Journal
AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL
Volume 187, Issue -, Pages 70-75Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.autneu.2014.11.003
Keywords
Intrinsic cardiac neurons; Nitric oxide donor; Nitric oxide synthase isoforms; Myocardial blood flow; Acute cardiac decentralization
Categories
Funding
- Heart and Stroke Foundation of Quebec
- Quebec Heart Institute Research Foundation
Ask authors/readers for more resources
The sympathetic nervous system and nitric oxide (NO) contribute to regulation of vascular tone, blood flow regulation and cardiac function. Intrinsic cardiac neurons are tonically influenced by locally released NO and exogenous NO donors; however, the role of intact central neural connections remains controversial. We investigated the effects of S-nitroso-N-acetylpenicillamine (SNAP) administered into an intracoronary artery near the ventral interventricular ganglionated plexus (VIVGP) to evaluate distribution of myocardial blood flow (MBF) and ventricular function in normal and acute cardiac decentralized dogs. MBF was measured with microspheres during infusion of SNAP (100 mu M, IC) after systemic administration of 7-nitroindazole (nNOS blacker) followed by N-omega-nitro-L-arginine methyl ester (LN; non-selective NOS blacker). Cardiac dynamics were not significantly affected by cardiac decentralization; several of these parameters (aortic systolic and diastolic pressures) were significantly increased after systemic administration of LN. Overall SNAP administered to the VIVGP increased blood flow in the anterior LV wall (vs. posterior LV wall) without affecting other cardiodynamic factors. In cardiac decentralized dogs subepicardial blood flow to the anterior LV wall during LN + SNAP was diminished resulting in a significantly higher inner:outer blood flow ratio (index of blood flow uniformity across the LV wall). LV function was not affected by acute cardiac decentralization; however, LV ejection fraction decreased markedly after LN (reduced NO bioavailability). These results validate earlier claims that reduced NO bioavailability imposes an upper limit on myocardial blood flow regulation and its transmural distribution. These effects are exacerbated after disconnection of intrinsic cardiac neurons from intact central neuron connections. (C) 2014 Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available