Abstract
Intracoronary infusion of [4Cl-D-Phe6-Leu17]VIP caused modest significant inhibition of the coronary vasodilation produced by intraarterial VIP, but did not significantly inhibit serotonin-induced coronary vasodilation. In addition, infusion of [4Cl-D-Phe6-Leu17]VIP did not result in significant changes in baseline coronary resistance, heart rate or left ventricular dP/dt. These findings demonstrate that [4Cl-D-Phe6-Leu17]VIP is a competitive antagonist of VIP-induced vasodilation in the canine coronary circulation, but fail to demonstrate a significant role for VIP in the regulation of resting coronary vasomotor tone, and do not support the hypothesis that VIP is a mediator of serotonin-induced coronary arteriolar dilation.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 989-993 |
| Number of pages | 5 |
| Journal | Peptides |
| Volume | 12 |
| Issue number | 5 |
| DOIs | |
| State | Published - 1991 |
Bibliographical note
Funding Information:Studies were performed in seven adult mongrel dogs of either sex weighing approximately 25 kg. The clogs were premedicated with fentanyl (0.4 mg IM) and droperidol (20 mg IM), anesthetized with sodium pentobarbital (30-35 mg/kg IV), intubated, and ventilated with room air and supplemental oxygen using a mechanical respirator. Under sterile conditions, a left thoracotomy was made in the fifth intercostal space. A heparin-filled polyvinyl chloride catheter, 3.0 mm o.d., was advanced through the internal thoracic artery into the ascending aorta. The pericardium was then opened and the heart suspended in a pericardial cradle. Heparin-filled catheters were placed in the left atrium through the atrial appendage and into the left ventricle through a stab wound at the apical dimple; both were secured with purse-string sutures. A 2-3 cm proximal section of the left circumflex artery was dissected free from the epicardial surface. A 10 MHz Doppler flowmeter probe, with an internal diameter closely matching the arterial diameter, was fitted around the left IThis study was supported by U.S. Public Health Service Grants HL20598 and HL21872 from the National Heart, Lung and Blood Institute. Brian Quebbemann was the recipient of a Research Fellowship for Medical Students from the American Heart Association and Minnesota Medical Foundation.
Keywords
- 5-Hydroxytryptamine
- Coronary circulation
- Vasoactive intestinal peptide antagonist
- Vasodilation