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Biomedical subjects

D V Priola

Publications and source records attributed to D V Priola.

At least 37 records · Page 2Linked to original sources
PubMed1983

Altered nicotinic sensitivity of AV node in surgically denervated canine hearts.

The responses of normal and cardiac-denervated (DNV) dogs to acetylcholine (ACh) and nicotine (NIC) were examined to determine if the intrinsic cardiac nerves (ICN) that modulate electrical conduction display denervation supersensitivity. Control (n = 18) and DNV (n = 18) animals were placed on cardiopulmonary bypass. Recording of intra-atrial (P-A), intraventricular (H-V), and atrioventricular (AV) nodal (A-H) conduction times were made from the region of the His bundle. ACh (0.1-10 micrograms) was used to produce muscarinic stimulation, whereas NIC (0.1-400 micrograms) was employed to stimulate the ICN. All drugs were administered intracoronary. No supersensitivity to either ACh or NIC was seen in the data from the P-A or H-V intervals of the His electrogram in the DNV animals. However, this group displayed approximately a 10-fold increase in the negative dromotropic effect of NIC on the AV node compared with control. No significant change in muscarinic sensitivity of the AV node was observed in the DNV animals. We conclude that 1) no denervation supersensitivity of the ICN mediating effects on intra-atrial and intraventricular conduction occurs; 2) the AV node itself does not show muscarinic supersensitivity following extrinsic denervation; 3) the ICN do display denervation supersensitivity as shown by a 10-fold increase in the effects of NIC on AV nodal conduction time.

Acetylcholine↗
PubMed1982

Responsiveness of intracardiac neurons to cholinergic stimulation in normal and thyroidectomized dogs.

Hypothyroidism alters the responsiveness of sympathetically innervated structures. The present work was done to determine if the responsiveness of the intrinsic cardiac nerves (ICN) to nicotine is also affected by thyroidectomy (THX). Mongrel dogs were anesthetized and an electrode catheter was advanced into the right atrium for recording His bundle activity (HB). A second cannula was placed into the carotid artery with its tip near the coronary ostia, so that the responses to the drugs injected would be confined to the heart. Changes in the A-H interval of the HB were recorded in response to both acetylcholine (ACH) 2-50 ug, and nicotine HCl (NIC) 5-100 ug, before and after beta blockade with metoprolol (1-4 mg). There were no important differences between the two groups in the responses of A-V nodal conduction to ACH over the dose range used. However, the THX animals showed an apparent increase in responsiveness to NIC; ie., ca. 5% decrease in A-H at 10 ug (control) compared to ca. 30% increase after THX. The apparent catecholamine-releasing effect of NIC was also enhanced in the THX animals. In addition, the responses to ACH and NIC were compared in animals both 'on' and 'off' cardiac bypass. The data suggest that hypothyroidism increases the effectiveness of nicotinic stimulation of intracardiac neurons.

Acetylcholine↗
PubMed1981

Cardiac catecholamine stores after cardiac sympathectomy, 6-OHDA, and cardiac denervation.

Sympathetic nerves are known to reach the heart via classical vagal pathways. Bilateral cervicothoracic sympathectomy (CS) might be expected therefore to leave significant amounts of releasable catecholamines in the myocardium if the vagi are left intact. Cardiac responses to tyramine (500 micrograms intracoronary) were compared in animals with CS, extrinsic cardiac denervation (CD), and chemical sympathectomy with 6-hydroxydopamine (6-OHDA). Dogs were placed on cardiopulmonary bypass and isovolumic pressures were recorded from the heart. In control animals, tyramine caused profound increases in rate (58%) and isovolumic pressures (86-170%). Ten CS animals demonstrated responses indistinguishable from control animals. Four CD and four 6-OHDA animals showed no response to tyramine. Cervical vagal stimulation after atropine in the CS animals produced tachycardia. Histofluorescent studies demonstrated the presence of significant numbers of cardiac adrenergic fibers in this group. The normal tyramine responsiveness of the CS animals was attributed to 1) significant numbers of vagal adrenergic fibers remaining in the heart after cervicothoracic sympathectomy, and 2) denervation supersensitivity, rendering the heart very responsive to the catecholamine that remains.

Animals↗
PubMed1978

The efficacy of practolol-induced beta1 adrenergic blockade in the canine heart.

The efficacy of adrenergic blockade with practolol was assessed by subjecting 6 adult mongrel dogs in a closed-chest procedure to bolus injections of isoproterenol (0.5 mcg/kg, i.v.) before and after practolol (2.0 mg/kg, i.v.). Following practolol both heart rate and pulse pressure responses were significantly reduced. It is suggested that significant beta1 receptor adrenergic blockade is achieved by practolol.

Animals↗
PubMed1978

Vagal stabilization of the ischemic canine ventricle.

To determine whether vagal activity during myocardial ischemia functions to stabilize the heart, the left anterior descending coronary artery in dogs was occluded for periods of 3 1/2 minutes with and without concurrent vagal stimulation. Bipolar electrograms were measured from the surface of the canine left ventricle within and outside the regions of intended ischemia. Ischemia in the absence of vagal stimulation depressed both the electrogram amplitude and the upstroke velocity of the electrogram signal. Vagal stimulation significantly decreased the absolute magnitude of the ischemia-induced decrease of the electrogram signal, which indicates that it tended to stabilize the insulted heart. This stabilizing influence however, was seen only in the presence of adrenergic blockade with practolol. The vagal response was only partially blocked by atropine, whereas it was abolished by lidocaine. These results suggest that a vagally mediated stabilization of the ischemic canine ventricle can occur and is unmasked only in the absence of sympathetic neural activity.

Animals↗
PubMed1977

Chronology and mode of reinnervation of the surgically denervated canine heart: functional and chemical correlates.

This study was undertaken to evaluate functionally the time and pattern of inotropic and chronotropic efferent cardiac reinnervation of the deneravated canine heart and to correlate functional data with regional myocardial catecholamine content and supersensitivity to norepinephrine. Our data indicate that efferent autonomic reinnervation takes place first in the atria, followed by a base-to-apex sequence in the ventricles, and that such reinnervation is functionally effective 9-12 mo after denervation. The return of neural function parallels the return of measurable quantities of myocardial norepinephrine and is accompanied by a decrease in supersensitivity to exogenous norepinephrine. The return to apparently complete functional reinnervation, however, cannot be quantitatively related to myocardial levels of catecholamine. Segmental myocardial supersensitivity to norepinephrine is sequentially reversed during progressive adrenergic reinnervation.

Adrenergic Fibers↗
PubMed1977

The intrinsic innervation of the canine heart: a functional study.

The intrinsic innervation of the heart has been described anatomically but seldom, functionally. These experiments were designed to verify and to evaluate the influence of intrinsic neural activation on the contractility of the atria and ventricles. Nine mongrel dogs underwent total cardiac denervation using the Geis two-stage technique. Following recovery, they were placed on total cardiopulmonary bypass. Balloons were inserted into each cardiac chamber, filled with saline, and used to record atrial and ventricular isovolumic pressures in response to intracoronary drug injections. The hearts were paced to avoid rate changes. Acetylcholine (ACh) (0.05-1.0 mug) was given to assess direct effects on the myocardium; nicotine (NIC) (25-200 mug) was used to produce indirect inotropic effects. d-Tubocurare (dTC) (1.0-2.5 mg) and tetrodotoxin (TTX) (10-30 mug) were used to differentiate the direct and the indirect effects. Both ACh and NIC produced qualitatively similar negative inotropic responses in both atria and ventricles. dTC usually produced a significantly greater blockade of responses to NIC than toACh. TTX administered to 12 other denervated dogs to differentiate direct and neurally mediated responses, completely blocked NIC-induced negative inotropy but did not change responses to ACh. The data show that (1) the intrinsic cardiac innervation can exert significant negative inotropic effects on atria and ventricles (10 to greater than 30%); (2) there is no functional evidence of participation by chromaffin cells in the inotropic responses to intrinsic nerve activation; (3) the negative inotropy produced by NIC is sensitive to dTC and, especially, TTX blockade. This is consistent with the mechanism of action being intrinsic neural stimulation.

Acetylcholine↗