Abstract
Coronary blood flow regulation was studied in dogs with an intact or chronically decentralized
intrinsic cardiac nervous system. We also examined the effect of angiotensin-converting
enzyme inhibition (ACEI) on coronary autoregulatory pressure–flow relations and distribution
of blood flow since the renin–angiotensin system may play a critical role in vasoregulation.
Myocardial oxygen demand was reduced in the chronic decentralized dogs compared to
the control dogs. The lower pressure limit of the autoregulatory pressure–flow relation
was similar for the control and chronic decentralized dogs (47±2 and 44±7 mm Hg, respectively;
p=NS). After ACEI, the lower pressure limit shifted leftward to 40 mm Hg (p=0.001) in both groups. Concomitant blockade of cyclooxygenase, bradykinin catabolism
and nitric oxide synthase had no further effect on the lower pressure limit. Total
myocardial blood flow was lower (p=0.001) in the chronic decentralized dogs compared to the control dogs, while transmural
distribution of blood flow was preserved in both groups. The results show that even
though myocardial oxygen requirements are lower in the chronically decentralized heart
compared to controls, coronary autoregulation is maintained at levels observed in
normally innervated hearts. The present findings indicate that intrinsic cardiac neurons
contribute to coronary autoregulatory control and myocardial blood flow distribution
even in the absence of cardiac connections to the central nervous system. In addition,
in the chronic decentralized dog, ACEI allows the heart to work at lower coronary
perfusion pressures while myocardial blood flow distribution is preserved.
Keywords
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to Autonomic Neuroscience: Basic and ClinicalAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
References
- Activity of in vivo atrial and ventricular neurons in chronically decentralized canine hearts.Am. J. Physiol. 1991; 260: H713-H721
- Modulation of intrinsic cardiac neuronal activity by nitric oxide donors induces cardiodynamic changes.Am. J. Physiol. 1995; 268: R403-R413
- Gross and microscopic anatomy of the human intrinsic cardiac nervous system.Anat. Rec. 1997; 247: 289-298
- Differential selectivity of cardiac neurons in separate intrathoracic autonomic ganglia.Am. J. Physiol. 1998; 274: R939-R949
- Interference of angiotensin-converting enzyme inhibition with vasoactive peptides in the coronary circulation of dogs.J. Cardiovasc. Pharmacol. 1995; 25: 756-762
- Acute and long-term effects of angiotensin converting enzyme inhibition on larger arteries and cardiac hypertrophy: mechanical and structural parameters.J. Hypertens. Suppl. 1994; 12: S21-S29
- Comparison of renin and converting enzyme inhibition in sodium-deficient dogs.Hypertension. 1985; 7: I66-I71
- Effect of lack of noradrenaline on myocardial oxygen consumption in denervated dog hearts.Cardiovasc. Res. 1987; 21: 515-520
- Myocardial tissue pressure and blood flow during coronary sinus pressure modulation in anesthetized dogs.J. Appl. Physiol. 1992; 73: 2184-2191
- Effects of cardiac sympathetic innervation on coronary blood flow.N. Engl. J. Med. 1997; 336: 1208-1215
- Inhibition of glycolysis in the denervated dog heart.Circ. Res. 1980; 47: 338-345
- Coronary circulation in the conscious dog with cardiac neural ablation.Circ. Res. 1972; 31: 129-144
- ANG II modifies cardiomyocyte function via extracardiac and intracardiac neurons: in situ and in vitro studies.Am. J. Physiol. 1997; 272: R766-R775
- Nitric oxide modulates signaling between cultured adult peripheral cardiac neurons and cardiomyocytes.Am. J. Physiol. 1995; 269: C504-C510
- Effects of perfluorochemical hemodilution on coronary blood flow distribution in dogs.Circulation. 1988; 78: 746-753
- Chemical modulation of in situ intrinsic cardiac neurones influences myocardial blood flow in the anaesthetised dog.Cardiovasc. Res. 1994; 28: 1403-1406
- Interpretation of changes in coronary flow that accompany pharmacologic interventions.Circulation. 1987; 75: 34-38
- Metabolic mapping of a cardiac reflex mediated by sympathetic ganglia in dogs.Am. J. Physiol. 1985; 249: R317-R322
- Varying elastance concept may explain coronary systolic flow impediment.Am. J. Physiol. 1989; 257: H1471-H1479
- Release of a prostaglandin E-like substance from canine kidney by bradykinin.Circ. Res. 1972; 31: 36-43
- Effects of pressure gradients between branches of the left coronary artery on the pressure axis intercept and the shape of steady state circumflex pressure–flow relations in dogs.Circ. Res. 1985; 56: 11-19
- Potentiation of endothelium-dependent relaxations to bradykinin by angiotensin I converting enzyme inhibitors in canine coronary artery involves both endothelium-derived relaxing and hyperpolarizing factors.Circ. Res. 1992; 71: 137-144
- Contrasting effects of blockade of nitric oxide formation on resistance and conductance coronary vessels in conscious dogs.Cardiovasc. Res. 1996; 31: 555-567
- Intrapericardial denervation of the heart.J. Surg. Res. 1980; 29: 101-109
- Myocardial angiotensin receptors in human hearts.Basic Res. Cardiol. 1998; 93: 37-42
- Interactions between ANG II, sympathetic nervous system, and baroreceptor reflexes in regulation of blood pressure.Am. J. Physiol. 1992; 262 ([editorial]): E763-E778
- The role of autoregulation and tissue diastolic pressures in the transmural distribution of left ventricular blood flow in anesthetized dogs.Circ. Res. 1979; 45: 804-815
- Coronary vasodilator reserve impairment distal to systolic coronary artery compression in dogs.Cardiovasc. Res. 1983; 17: 96-105
- Myocardial blood flow regulation relative to left ventricle pressure and volume in anesthetized dogs.Can. J. Physiol. Pharmacol. 1999; 77: 902-908
- Effect of angiotensin inhibition on the coronary artery lower pressure limit in anesthetized dogs.Can. J. Physiol. Pharmacol. 2000; 78: 892-896
- Splenic contraction-induced increases in arterial O2 reduce requirement for CBF in conscious dogs.Am. J. Physiol. 1995; 269: H491-H503
- Modulation of coronary autoregulatory responses by nitric oxide. Evidence for flow-dependent resistance adjustments in conscious dogs.Circ. Res. 1993; 73: 232-240
- Chronic decentralization of the heart differentially remodels canine intrinsic cardiac neuron muscarinic receptors.Am. J. Physiol. 2001; 281: H1919-H1930
- Neuronally induced augmentation of cardiac output.Can. J. Cardiol. 1999; 15: 1361-1366
- Coronary vasodilation induced by angiotensin-converting enzyme inhibition in vivo: differential contribution of nitric oxide and bradykinin in conductance and resistance arteries.Circulation. 1996; 93: 1734-1739
- Metabolic alterations in the chronically denervated dog heart.Cardiovasc. Res. 1998; 37: 160-170
- Mechanisms of supersensitivity to sympathomimetic amines in the chronically denervated heart of the conscious dog.Circ. Res. 1985; 57: 55-64
- Coronary vasodilating drug effects or normal coronary blood flow regulation?.J. Cardiothorac. Vasc. Anesth. 1998; 12: 450-456
- Chronic cardiac denervation affects the speed of coronary vascular regulation.Cardiovasc. Res. 1999; 44: 615-622
- Evidence for angiotensin-converting enzyme- and chymase-mediated angiotensin II formation in the interstitial fluid space of the dog heart in vivo.Circulation. 1999; 99: 2583-2589
- Hoe 140 a new potent and long acting bradykinin-antagonist: in vivo studies.Br. J. Pharmacol. 1991; 102: 774-777
- Endothelium dependent vasomotor responses to endogenous agonists are potentiated following ACE inhibition by a bradykinin dependent mechanism.Cardiovasc. Res. 1994; 28: 209-214
Article info
Publication history
Accepted:
December 14,
2001
Received in revised form:
November 29,
2001
Received:
October 26,
2001
Identification
Copyright
© 2002 Elsevier Science B.V. Published by Elsevier Inc. All rights reserved.