© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Comparative reactivity and mechanical properties of human isolated internal mammary and radial arteries
aDepartment of Internal Medicine, Broussais Hospital, Paris, France
bINSERM (U.337), 15, rue de l'Ecole de Médecine, 75270 Paris Cedex 06, France
* Corresponding author. Tel. (+33-1) 44 07 90 30; Fax (+33-1) 44 07 90 40.
Received 14 April 1997; accepted 26 September 1997
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Abstract |
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 Top Abstract 1 Introduction2 Material and method3 Results4 DiscussionReferences |
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Objective: The aim of this study was to analyse the arterial wall mechanics and the vasoreactive properties of the radial artery in comparison with those of the internal mammary artery and to discuss their implications for coronary bypass grafts. Methods: Measurements of pressure and diameter were obtained from cylindrical segments, whereas measurements of reactivity were obtained from ring segments from the same arteries. We used an echo-tracking technique of high resolution enabling to investigate, in vitro, the diameter and the wall thickness of arterial cylindrical segments. Furthermore, the compliance, distensibility and incremental elastic modulus of the radial and of the mammary arteries were determined for a wide range of transmural pressure (0–200 mmHg) in presence and absence of norepinephrine (NE). Results: Our results show that NE caused vasoconstriction of the two arteries. Strain was found significantly higher for the radial artery than for the internal mammary artery at any given value of stress both in the presence and in the absence of NE. In presence of NE, compliance for radial artery, in the overall transmural pressure range, did not change, whereas, distensibility was significantly increased and the elastic modulus was significantly decreased. Under the same conditions, the distensibility of the mammary artery tended to decrease and its elastic modulus to increase. In parallel, the vasoreactive properties of the two arteries confirmed the previous results showing that radial artery developed a significant higher tension to vasoconstricting agents (KCl, NE and phenylephrine (PHE)) and higher relaxation to isradipine than internal mammary artery. Moreover, radial artery displayed a lesser sensivity to sodium nitroprusside than internal mammary artery. Furthermore, sensitivity to NE was found to be 7-fold higher for radial artery than for internal mammary artery. Conclusion: Taken together, data on the mechanical and reactive properties of radial and internal mammary arteries show why the radial artery displayed a higher potential for spasm than the internal mammary artery and why the use of Ca2+ channel blocker can decrease the incidence of occlusion and spasm.
KEYWORDS Internal mammary artery; Radial artery; Viscoelastic property; Vasoreactivity; Norepinephrine; Epinephrine; Isradipine
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1 Introduction |
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TopAbstract1 Introduction2 Material and method3 Results4 DiscussionReferences |
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Considerable interest has emerged during the last decade in the use of arterial graft conduits in coronary artery bypass surgery. This interest resulted in part from the well demonstrated, superior long-term survival of internal mammary artery over the traditionally used saphenous vein bypass grafts [19, 24].
Despite advances in surgical technique and therapy, occlusions due to thromboses and/or vasospasm remain a frequent occurrence of reoperative coronary bypass in patients with exhausted venous reserve grafts [19, 24]. Recently, the use of radial artery as possible alternative conduit has become more popular than before with the introduction of antispastic drugs. Success is now reported even if arterial spasms on post-operative angiograms is present [1, 5, 20].
If the success of the bypass procedure is dependent on the adaptive changes in the conduit that ensue under the new hemodynamic conditions it is also dependent on the conduit itself [4]. In order to evaluate this latter point we have, in the present study, compared the mechanical properties and the vasoreactivity of segments of radial and internal mammary arteries used for coronary bypass grafts under in vitro conditions. Arterial vasoreactivity has been determined with the classical technique based on the study of the isometric tension developed in ring segments [6, 8, 9]. However, if this methodology allows to measure changes in tension applied to ring in response to vasoactive agents, it does not provide any information on stiffness. To resolve this problem we have used a high resolution ultrasonic echo-tracking device [10, 25]designed to evaluate the viscoelastic properties of the human radial arteries through the determination of the pressure–diameter and pressure–distensibility curves for this artery [15, 18].
In the present study we have compared the mechanical properties of the radial and internal mammary arteries in presence and absence of NE at different transmural pressures and determined the stress–strain relationships, changes in arterial diameter and changes in indices of stiffness of each artery segment. We then, have evaluated the reactivity of the vessels to the vasoactive agents KCl, NE and PHE and the capability of the arteries to relax in the presence of isradipine, a Ca2+ channel antagonist, sodium nitroprusside, an endothelium-independent vasodilator, and carbamylcholine, an endothelium-dependent vasodilator.
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2 Material and method |
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2.1 Study design
Mechanical properties of the internal mammary and the radial arteries were determined in vitro in the presence and absence of NE using: (i) a high resolution ultrasonic device allowing to preserve the geometry of the vessel and to measure internal diameter and wall thickness, and (ii) the organ chambers using classical artery ring preparations to analyze their capability to contract and relax in the presence of vasoactive compounds. For the experimental design, 14 radial artery and 27 internal mammary artery segments (100 mm length) were obtained for coronary grafting in 32 patients with coronary heart disease. Age was 61±2 years (mean±standard error of the mean). Systolic and diastolic blood pressure was 143±6 and 87±5 mmHg, respectively. Pre-operative drug treatment involved beta-blocking agents in 15 patients, calcium entry blockers in 19 patients, isosorbide dinitrate in 13 patients, miscellaneous in 16 patients. The entire study was approved by the Ethical Committee of Broussais Hospital, Paris and was conform with the principles outlined in the Declaration of Helsinki.
2.2 Determination of the mechanical properties of radial and internal mammary arterial segments
The ultrasound system used in this ex vivo study was similar to that previously described and validated in vivo for the non invasive measurement of pulsatile changes of internal diameter [15, 17, 18]and intima-media thickness of the radial artery [10, 11]. This high resolution echo-tracking device was used primarily to acquire back-scatter radio frequency data from the radial artery at the wrist and, in the present investigation, was applied to in vitro measurements.
After surgical excision, each vessel was immediately placed in a cold (4°C) Krebs solution at pH 7.2±0.2 of the following composition (mM): NaCl 118.0; KCl 4.6; CaCl2·2H2O 2.5; KH2PO4 1.2; MgSO4 1.2; glucose 11.1; NaHCO3 25.0, bubbled with a gas mixture of 95% O2/5% CO2. After removing fat and loose tissue from the adventitia, each terminal portion of the segment was gently cannulated and then perfused in a perfusion system consisting of a reservoir (an i.v. bag) connected to the vessel and to a pressure transducer (Gould, Cleveland, OH, USA). Pressurization of the vessel was achieved by inflating a cuff around the reservoir and closing the vessel by turning a stopcock positioned distal to the artery. Since all arteries display longitudinal retraction when they are harvested, the length of each arterial segment was measured carefully before excision. Because the longitudinal retraction was 10±8%, the vessel was stretched after cannulation to 110% of its retracted length and maintained at this fixed length throughout the study. Before measuring the arterial diameter and wall thickness, the artery was inflated several times to a pressure of up 250 mmHg to exclude the excessive hysteresis found during the first inflation. Pressure–diameter curves were obtained by increasing intraluminal pressure in 25 mmHg steps from 0 to 200 mmHg. The transmural pressure was maintained at each level until the vessel segment exhibited a steady diameter for at least 2 min. At each level of transmural pressure, internal diameter and wall thickness were measured. After baseline determinations, NE (10–5 M) was added to the Krebs–Ringer perfusate within the lumen of the vessel and determinations were repeated [10, 11, 15, 17, 18]. At the end of the procedure all vessels were perfused with 10% formaldehyde for 30 min, at 100 mmHg, for histomorphometric analysis such as thickness of the vessel wall.
Three basic assumptions were used for the calculation of the arterial mechanical properties. Firstly, the vessel was considered as cylindrical. Secondly, the arterial wall was considered as incompressible as previously described [12]. Thirdly, since the length of the vessel was maintained constant, the arterial volume (Vi) was calculated as the lumen cross-sectional area (LCSA) per unit length. Thus, according to classical formula [9, 22]and using calculated values of the internal arterial diameter (Di) and thickness (h) from 0 to 200 mmHg, Vi was calculated at each transmural pressure, as: Vi=LCSA(per unit length)=3.14xDi2/4. Unstressed internal diameter (D0) and volume (V0 or LCSA0) were defined as diameter or volume at zero pressure and measured, respectively, under control and NE conditions. The compliance (C) of the observed arterial segment was defined, as: C=
Vi/P where, Vi (or LCSA) is the change in volume induced by a transmural pressure variation of P (25 mmHg) in a segment of 1 mm length of the artery. The vessel distensibility (Dist) can be defined, for each step of transmural pressure as the compliance (C) divided by the unstressed volume (V0) evaluated under control and NE conditions (Dist=C/V0). According to the Laplace's law, the wall tension (T), i.e., the tangential wall force per unit length, was given by the formula: T=PxDi/2 where P is the transmural pressure. Thus, the tangential wall stress (s) was defined for each step of transmural pressure by: s=T/h. Strain was calculated as (Di–D0)/D0. Finally the stress–strain relationship was established and the incremental elastic modulus (Einc) was calculated as the slope of the stress–strain relationship.
Mathematical procedures were used to establish the compliance and distensibility transmural pressure curves and the stress–strain curves. Firstly, the relationship between LCSA (y axis) and transmural pressure (x axis) was established from a fitting of the experimental data according to a polynomial equation of the 3rd order (y=ax3+bx2+cx+d) as previously described by others [3]. The experimental data were predicted by the model at 99±1%. Then, the compliance and distensibility curves were calculated as the derivative of the LCSA pressure and LCSA/LCSA0–pressure curves. For the study of the stress–strain relationship, the same polynomial model was also used with a fitting of 99.8±1.7%.
2.3 Organ chamber experiments [16]
Arterial segments were dissected free and cleaned of connective tissues under a dissection microscope (Leica Stereozoom 4) in an ice cold Krebs–Ringer solution (pH 7.2±0.2; 4°C) of the following composition (mM): NaCl 118.0; KCl 4.6; CaCl2·2H2O 2.5; KH2PO4 1.16; MgSO4 1.2; glucose 11.1; NaHCO3 25.0 and cut into rings of 3–4 mm length. Radial and internal mammary artery segments harvested from the same patients were studied in parallel. They were mounted on two stainless wires in a 20 ml organ bath and connected to transducers (Hugo Sachs Electronic type 351 and Marty Technologie). Isometric contractions variations were recorded on a Mac Lab using Chart v3.4 software (AD Instruments). Solution of the bath was aerated by a gas mixture 95% O2/5% CO2 at 37±1°C. All vessels were passively stretched to a resting tension of 4 g, which is the optimal tension found to generate maximal isometric contractions. After 90 min equilibration, rings were exposed to KCl 80 mM during 15 min. After a washout, cumulative concentrations of NE from 10–9 to 10–4 M were added to the bath. The response of functional endothelium was evaluated by the ability of the rings precontracted by phenylephrine (PHE) at 10–5 M to relax in presence of carbamylcholine at 10–5 M. The endothelium independent relaxation was tested by addition of sodium nitroprusside at 10–5 M to arteries precontracted by PHE at 10–5 M. Some segments were then exposed to a maximum depolarizing KCl concentration (80 mM) and, when the plateau was reached increased concentrations of the calcium-entry blocker isradipine (10–9–10–5 M) were added.
The drugs used, potassium chloride, sodium nitroprusside (sodium nitroferricyanide), carbamylcholine (carbamylcholine chloride), norepinephrine bitartrate (Arterenol), phenylephrine (phenylephrine hydrochloride), were from Sigma Chimie, St Quentin Fallavier, France. Isradipine (PN 200-110) was a gift of Sandoz. The drugs concentrations are expressed as final molar (M) or millimolar (mM) concentration in the bath solution. The drugs were either dissolved daily in distilled water at 10–2 M and keep at 4°C before use (carbamylcholine, norepinephrine, phenylephrine) or in dimethyl sulfoxide for isradipine.
2.4 Statistical analysis
For the study of the arterial mechanical properties, statistical analysis were performed using Statview SE 1.03 software (Abacus concepts, Berkeley, CA, USA). For each artery, diameter, stress and indices of stiffness (compliance, distensibility, elastic modulus) were studied before and after NE at different levels of transmural pressure or strain, using a two-way analysis of variance. This procedure has also been used to compare the two arteries at a given value of transmural pressure (50, 100, 150 mmHg).
For artery rings, response to cumulative concentrations of NE was expressed in mg and relaxation to isradipine was expressed as percentage of the maximum tension induced by 80 mM KCl. Curves fitting and EC50 values were estimated using of Boltzman equation and the Origin v 4.0 software (MicrocalTM software), with the following equation:
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Data were evaluated for statistical significance by applying the t-test for unpaired values, the Kruskall–Wallis test for non parametric data and ANOVA.
For the overall study, values were considered statistically significant at P<0.05.
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3 Results |
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3.1 Mechanical properties of the arteries
3.1.1 Changes in the arterial diameter and stiffness in presence of 10–5 M NE
In baseline conditions, and in presence of NE the effects of the transmural pressure on the diameter and stiffness was studied at 50, 100 and 150 mmHg. The radial artery was thicker than the mammary artery and had a larger diameter whatever the transmural pressure studied (Table 1). For example at a transmural pressure of 100 mmHg thickness was 290±86 µm and 209±35 µm (P<0.05) for radial and internal mammary arteries, respectively. Addition of NE (Table 1) induced a significant diameter reduction and no change in compliance for both radial and internal mammary arteries. The two arteries were different in regard to their distensibility and their elastic modulus as shown in Table 1. Radial artery displayed a significant increase in distensibility (P<0.05) in presence of NE, whereas, the internal mammary artery distensibility did not change. Under the same conditions, the elastic modulus of the radial artery was significantly decreased (P<0.05) and slightly increased in the mammary artery. In presence of NE, the intima-media thickness, measured histomorphometrically at 100 mmHg, was significantly increased from 290±86 µm to 329±91 µm and from 209±35 µm to 221±4 2 µm (P<0.05) for radial and internal mammary arteries, respectively.
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3.1.2 Mechanical properties of radial and internal mammary arteries at different transmural pressures in presence and absence of NE
In baseline conditions (Table 1) the diameter of the radial artery was larger than that of the internal mammary artery whatever the transmural pressure studied. As the transmural pressure increased from 50 to 150 mmHg, the internal diameter of both arteries increased and the pressure-diameter relationships were more or less curvilinear. All these effects were highly significant (Table 1). The compliance decreased with the pressure but the decrease was significantly more important for radial artery than for internal mammary artery. Distensibility decreased with the increase in pressure for radial artery but did not change in internal mammary artery. Under the same conditions, the elastic modulus increased with increased pressure, but the increase was not significantly different for the two arteries.
In presence of NE (Table 1) the diameter increased significantly for each transmural pressure studied. The increase was significantly more important for radial than for internal mammary arteries. Under the same conditions in presence of NE, compliance decreases significantly in parallel to the increase in pressure. The decrease was greater for the radial arteries than for the internal mammary arteries (P=0.01). Similar results were obtained for distensibility, which increased in presence of NE but decreased with the increase in pressure.
The radial artery elastic modulus, increased in parallel to the increase pressure and decreased in presence of NE, whereas, the internal mammary artery elastic modulus was lightly increased by the pressure and by the NE, at 100 and 150 mmHg.
Taken together, these results indicate that NE, by reducing baseline diameters reset the pressure-induced dilation and that this resetting was more pronounced for the internal mammary artery than for the radial artery. Whereas, NE limited the pressure induced decrease in compliance in the radial artery, it had no significant effect on the internal mammary artery. By contrast, NE amplified the pressure-dependent decrease in distensibility in the internal mammary artery. While NE increased the radial artery distensibility, it had little effect on the response to pressure. Finally, NE increased the elastic modulus of internal mammary artery and decreased that of radial artery at pressure ranging between 100 and 150 mmHg.
3.1.2.1 Changes in the stress–strain relationship
Fig. 1, shows, that in baseline conditions, a positive relationship was observed between stress and strain according to a curvilinear curve for both radial and internal mammary arteries. For a given stress, strain was found to be significantly higher (P<0.05) for the radial than for the internal mammary arteries.
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) and internal mammary (
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) arteries in presence (In presence of NE at 10–5 M, the stress–strain curves were shifted to the right. This shift was not significant with the internal mammary artery whereas, its was highly significant for the radial artery (P<0.02).
3.2 Reactivity properties of the artery rings
NE, PHE and KCl have been used to analyse the reactivity of IMA and RA rings. High K+ solution induced maximum contraction velocity, independently of the endothelial function, by smooth cell depolarisation, whereas, maximum developed contraction in presence of both PHE and NE was dependent on both endothelial and smooth muscle function [26, 27]. Under the latter conditions we have evaluated the effects of compounds such as carbamylcholine through the endothelial function and sodium nitroprusside on the smooth muscle through Ca2+ recapture. Isradipine, a slow voltage-dependent Ca2+ channel blocker which is highly dependent on the membrane potential, was studied after smooth muscle depolarisation in presence of high K+ solution (80 mM).
3.2.1 Sensitivity and maximum tension to NE
Fig. 2 shows, the effects of increased concentrations of NE on arteries coming from six different patients. At 10–5 M, radial arteries developed stronger maximum contraction than internal mammary arteries. Mean values were 2.14±0.50 g and 0.95±0.25 g, respectively (P<0.05) (Fig. 2 and, inset A). Sensitivity to NE was calculated by evaluation of the effective drug concentration producing 50% maximum contraction (EC50). EC50 values were (1.5±1.1)x10–6 M and (11.0±2.3)x10–6 M for the radial and the internal mammary arteries, respectively (P<0.05) (Fig. 2). Under the same conditions the maximum contraction force to 80 mM KCl was determined, radial arteries (n=5) showed stronger contraction (11.4±4.3 g) than internal mammary arteries (3.4±0.9 g) (n=10). Maximum developed contractions were also significantly different (P<0.05) (Fig. 2, inset B).
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3.2.2 Endothelium-independent and -dependent responses
Endothelium-independent response of both vessels was evaluated by addition of sodium nitroprusside at 10–5 M after precontraction induced by PHE 10–5 M (Fig. 3). Relaxations observed were 1.5±0.3 g and 0.5±0.1 g for radial and internal mammary arteries, respectively (P<0.05). Under these conditions, the maximal relaxation induced in response to the addition of sodium nitroprusside were 75±7% and 102±9% of the tension developed in presence of 10–5 M PHE for the radial and the internal mammary arteries, respectively (P<0.05) (Fig. 3). Similarly, the endothelium dependent relaxation observed in presence of carbamylcholine (10–5 M) was significantly different for radial and internal mammary arteries with a value of 0.7±0.2 g and 0.04±0.05 g, respectively. The presence of functional endothelium estimated as the percentage of maximal relaxation induced by carbamylcholine (10–5 M) on developed tension induced by PHE (10–5 M), was 35±12% and 4±4% (P<0.01) for radial and internal mammary arteries, respectively (Fig. 3).
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P<0.05, **P<0.01 for radial versus internal mammary arteries.3.2.3 Sensitivity and maximum relaxation force to isradipine
The maximum relaxation to 10–5 M isradipine expressed as the percentage of contraction obtained with KCl 80 mM, was –102±3% for the radial artery and –61±9% for the internal mammary artery. Significant differences in force of relaxation were found between 10–7 M and 10–5 M isradipine (P<0.05) (Fig. 4). On the other hand, EC50 values, for isradipine on radial and internal mammary arteries, were similar with a value of 40±2 nM and 10±6 nM, respectively (NS).
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4 Discussion |
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TopAbstract1 Introduction2 Material and method3 Results4 DiscussionReferences |
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In the present study, we have used two approaches to investigate the vasoreactivity and the mechanical properties of straight segments of large arteries in vitro. The investigation of mechanical properties was performed in the presence of preserved geometry of the vessel, whereas vasoreactivity was studied on vascular rings at isometric tensions.
In this study, arterial segments were obtained from patients with coronary heart disease under treatment with mainly beta-blocking and vasodilating agents. These drugs act mainly on vascular smooth muscle, which constitutes a significant proportion of the wall mass, particularly for the radial artery.
The possibility that these compounds might have modified the in vitro vasoreactivity of the vessels does not seem likely. However, considering the complex nature of this problem it was decided to record mechanical properties and vasoreactivity under conditions in which the variable effects of intracellular and extracellular factors were minimized as much as possible by doing before any measurement of arterial diameter and tension several washes followed by 90 min equilibration at 37°C to exclude all remaining ex-vivo pharmacological effect linked to drug treatment. Such measurements thus represent the intrinsic properties of these arteries recorded under the conditions of the experiments. Furthermore, the distribution of the classes of drugs is not different between IMA and RA preparations in accord with a Chi-square testing value of 2.12 (3DF). In this context our experiments demonstrate that differences exist in functional properties between the two arteries.
The first consideration related to our results concerns the geometry of the vessels. In these studies, we directly determined the internal diameter and the intima-media-thickness of cylindrical arterial segments. This type of measurement is in contrast with previous in vitro studies, in which external diameter was measured and thickness deduced from the dry weight and the density of the vessel wall [7]. Since arterial thickness is known to decrease in proportion to an increase in transmural pressure, we should expect, under these conditions, that the internal diameter will increase more than the external diameter. This will induce small differences in calculated tangential stress, determined either from the internal or external diameter. Since intima-media thickness was directly measured in the present study, all approximations derived from the determinations of dry-weight arterial mass were avoided. Furthermore, since the initial length of the vessel remained constant, only circumferential stress had to be considered [8, 21].
The second issue concerning the present study is the use of NE as the vaso-active agent to produce contraction of arterial smooth muscle. On the basis of previous reports [2, 7, 9, 13, 22], and mostly on the basis of the data obtained from tissue bath experiments (Fig. 3), we chose the concentration of 10–5 M as the most appropriate concentration to obtain optimal smooth muscle contraction with both arteries for the mechanical study. The concentration of NE that produced 50% of the maximal contractile response (EC50) was determined for each vessel from the tissue bath experiments.
The last important consideration concerns the capability of the endothelium to relax the vessels. Because arterial segments were obtained from atherosclerotic subjects with coronary artery disease, and associated of cardiovascular risk factors, such as hypercholesterolemia, the problem was not to assess if endothelium had a ‘normal’ function, but rather, that this function was still present. This permitted an adequate comparison between the radial and the internal mammary arteries. Furthermore, the vessel relaxation induced by the addition of carbamylcholine was found equal to 35% for the radial artery and 4% for the mammary artery, indicating that the endothelium relaxation was linked to the NO pathway [27, 28]for the radial artery whereas, endothelium relaxation seemed either absent or differently regulated on the internal mammary artery. Under our experimental conditions, these differences appear arteries related.
The major finding of this study was that under NE, the incremental elastic modulus of the radial artery was decreased at any given value of transmural pressure, whereas that of the internal mammary artery was either unchanged or increased (Table 1). Such data differ somewhat from those previously published for the carotid artery of dogs and rats [8, 9, 14, 22]. They have reported a reduced elastic modulus under NE at any given value of transmural pressure and an increase of the elastic modulus (Einc) at any given value of strain. Such discrepancies have been previously discussed by others on the basis of methodological differences, including the value taken as the initial diameter, in the presence or absence of NE, or the effects of changes of wall thickness at different diameters [8, 9, 13, 22]. Nevertheless, the geometrical characteristics of the two arteries and the simple observation of the changes in diameter and stiffness before and after NE provided a good explanation for the difference in behavior of the two arteries in the presence and absence of NE.
It is not surprising that radial arteries display higher strain than internal mammary arteries with regard to their respective histomorphometry, since the radial artery is essentially composed of smooth muscle cells whereas the internal mammary artery consists of elastic material. Furthermore, mechanical differences found between the two arteries appear well correlated with the results obtained from the tissue bath experimentation using the arterial rings model. In this experimental condition, the radial arteries developed, in the presence of KCl and NE, a significantly higher tension than the internal mammary arteries and, for the two arteries, the contraction induced by KCl is much higher than that induced by NE (Fig. 2). These results also show, that there is a stronger response of the arteries to depolarizing stimuli than that observed for the non depolarizing adrenergic receptor stimulation. To explain such results it is reasonable to assume that NE mobilizes mainly intracellular Ca2+ whereas KCl depolarization mobilizes both extracellular and intracellular Ca2+ pools. Furthermore, under the same conditions radial arteries display a significantly higher sensitivity to NE than internal mammary arteries since the EC50 value for NE was 7-times higher for radial arteries than for internal mammary arteries. Such differences can in part explain why the radial artery is more prone to spasm in response to a circulating vasoconstrictor agents, such as NE in comparison to the internal mammary artery which displays a lower affinity and lower maximum developed tension to NE (Fig. 2).
Results obtained in response to antispastic drugs are of interest since maximal relaxation in response to sodium nitroprusside for radial artery reached 75±7% of the tension developed by 10–5 M PHE whereas, internal mammary artery, under the same conditions, is completely relaxed in presence of sodium nitroprusside with a value of 102±9% (P<0.05) (Fig. 3). By contrast, the maximum relaxation induced by the calcium channel blocker isradipine, is more effective on the radial artery (99±4%) than on the internal mammary artery (61±9%) (Fig. 4). This difference in the efficacy (% of relaxation) of isradipine is not accompanied by changes in the affinity of the calcium channel binding site for the calcium channel blocker, isradipine.
These results point out the difference in the capability of the two arteries to relax in presence of sodium nitroprusside and isradipine. Under our in vitro conditions, we show that sodium nitroprusside is more effective in the internal mammary artery than in the radial artery, and that the calcium channel blocker, isradipine, is more effective on the radial artery than on the internal mammary artery to relax the contraction induced by KCl. Since the action of these two antispastic agents is not endothelium dependent, it is reasonable to assume that, such difference could be directly related to the nature of the artery wall composition. However, another possible explanation for the difference in function of these vessels may also include an altered endothelial function, observed in the study in response to carbamylcholine, due either to an altered response of the muscarinic receptor itself or some other primary dysfunction of the endothelium linked to unknown atherosclerotic change especially for internal mammary artery.
The last point concerns the response to carbamylcholine (Fig. 3). For the reasons discussed above, these data are difficult to interpret. They show that radial arteries have a significantly higher percentage of endothelium (35%) than internal mammary arteries (4%) and/or the ability to release NO is substantially higher for the radial arteries. This detail might play a major role in situations of vasoconstrictor stress. Indeed, several studies have emphasized that strong interactions may be observed between catecholamine release and NO at the arterial level [26, 29]. Furthermore, NO donors are known to increase markedly the arterial distensibility, independent of mechanical factors [13]. This mechanism, may also explain why radial arteries increase their distensibility and decrease their elastic modulus more than internal mammary artery in response to NE.
In conclusion, the present study has analysed both the mechanical and the reactivity properties of the human radial and internal mammary arteries which are often used for coronary graft bypass. The radial artery in contrast to the internal mammary artery develops at any value of stress a higher strain, higher distensibility and lower elastic modulus in presence of NE. These differences in behavior between the two arteries are not only due to the smooth muscle mass but also to the differences between the two arteries in term of sensitivity and reactivity to vasoactive compounds such as KCl and NE and antispastic agents, such as sodium nitroprusside and isradipine. Finally, our study suggests that perioperative spasm is probably better prevented by calcium entry-blocking drugs in radial artery than in internal mammary artery, although a clinical trial would clearly be required.
Time for primary review 15 days.
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Acknowledgements |
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This study was performed with the help of INSERM (Institut National de la Santé et de la Recherche Medicale, Paris), the Fondation pour la Recherche Médicale and the Ministère de la Recherche. We thank Mrs. A. Safar and S. Derly for skillful technical help. We gratefully acknowledge Professor P. Bruneval for histologic expertise, Professor C. Acar for providing radial and internal artery samples and Professor Smulyan for all his advice on the manuscript.
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