© 1997 by European Society of Cardiology
Copyright © 1997, European Society of Cardiology
Perfusion-induced changes in cardiac contractility and oxygen consumption are not endothelium-dependent
Laboratory for Physiology, Institute for Cardiovascular Research. ICaR-VU, Free University of Amsterdam, Van der Boechorststraat 7, 1081 HT Amsterdam, Netherlands
Objective: Are substances released from rat coronary endothelial cells responsible for the increase in contractility and oxygen consumption (Gregg phenomenon) seen with an increase in cardiac perfusion? Methods: In an isovolumically contracting, Langendorff, crystalloid perfused rat heart (n = 6) at 27 °C, coronary flow was changed (from 4.4 to 15.4 ml · min–1 · gWW–1) before and after the endothelium was made dysfunctional by Triton X-100. Vascular endothelium and smooth muscle function were tested with bradykinin (BK, 1 µM, an endothelium-dependent dilator) and papaverine (PAP, 1 µM, an endothelium-independent dilator) in a preconstricted vascular bed (vasopressin, VP, 3 nM). Results: Before Triton X-100, coronary resistance (at constant flow) decreased significantly in response to BK and to PAP. After Triton X-100 treatment the dilatory response to BK was abolished while the PAP response was still present, suggesting endothelial dysfunction with intact smooth muscle function. Due to Triton X-100 treatment, coronary resistance increased significantly. Therefore coronary flow changes were also applied during a similar increase in coronary resistance induced by VP infusion (3 nM) before Triton X-100 treatment. During control, developed left ventricular pressure (dev Plv) increased with 68 ± 21% and oxygen consumption (Vo2) increased with 122 ± 25% in response to the maximal increase in coronary flow. During increased coronary resistance with and without functional endothelium, dev Plv increased by 57 ± 16 and 64 ± 22%, respectively, and Vo2 increased by 126 ± 21 and 103 ± 20%, respectively, in response to the maximal increase in flow. These changes were not significantly different from control. Conclusion: The results suggest that the arterial endothelium is not involved in the Gregg phenomenon.
KEYWORDS Gregg's phenomenon; Coronary resistance; Triton X-100; Bradykinin; Papaverine; Vasopressin; Rat, heart
* Corresponding author. Tel. +31 20 444-8110/8123; Fax +31 20 444-8255. m.dijkman.physiol{at}med.vu.nl
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  N. Westerhof, C. Boer, R. R. Lamberts, and P. Sipkema Cross-talk between cardiac muscle and coronary vasculature. Physiol Rev, October 1, 2006; 86(4): 1263 - 1308. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. R. Lamberts, M. H. P. van Rijen, P. Sipkema, P. Fransen, S. U. Sys, and N. Westerhof Coronary perfusion and muscle lengthening increase cardiac contraction: different stretch-triggered mechanisms Am J Physiol Heart Circ Physiol, October 1, 2002; 283(4): H1515 - H1522. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. G. McLean, D. Aston, D. Sarkar, and A. Ahluwalia Protease-Activated Receptor-2 Activation Causes EDHF-Like Coronary Vasodilation: Selective Preservation in Ischemia/Reperfusion Injury: Involvement of Lipoxygenase Products, VR1 Receptors, and C-Fibers Circ. Res., March 8, 2002; 90(4): 465 - 472. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Rastaldo, N. Paolocci, A. Chiribiri, C. Penna, D. Gattullo, and P. Pagliaro Cytochrome P-450 metabolite of arachidonic acid mediates bradykinin-induced negative inotropic effect Am J Physiol Heart Circ Physiol, June 1, 2001; 280(6): H2823 - H2832. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. R. Giraldez, A. Panda, and J. L. Zweier Endothelial dysfunction does not require loss of endothelial nitric oxide synthase Am J Physiol Heart Circ Physiol, June 1, 2000; 278(6): H2020 - H2027. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. Bian and H.F. Downey Right coronary pressure modulates right ventricular systolic stiffness and oxygen consumption Cardiovasc Res, April 1, 1999; 42(1): 80 - 86. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A. Dijkman, J. W. Heslinga, P. Sipkema, and N. Westerhof Perfusion-induced changes in cardiac contractility depend on capillary perfusion Am J Physiol Heart Circ Physiol, February 1, 1998; 274(2): H405 - H410. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. R. Lamberts, M. H. P. van Rijen, P. Sipkema, P. Fransen, S. U. Sys, and N. Westerhof Increased coronary perfusion augments cardiac contractility in the rat through stretch-activated ion channels Am J Physiol Heart Circ Physiol, April 1, 2002; 282(4): H1334 - H1340. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. G. McLean, D. Aston, D. Sarkar, and A. Ahluwalia Protease-Activated Receptor-2 Activation Causes EDHF-Like Coronary Vasodilation: Selective Preservation in Ischemia/Reperfusion Injury: Involvement of Lipoxygenase Products, VR1 Receptors, and C-Fibers Circ. Res., March 8, 2002; 90(4): 465 - 472. [Abstract] [Full Text] [PDF]
|
|