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Biomedical subjects

D Godin

Publications and source records attributed to D Godin.

32 records · Page 2Linked to original sources
PubMed1985

Sinus node responses to perfusion pressure changes, ischaemia and hypothermia in the isolated blood-perfused dog atrium.

Sinus node responses to perfusion pressure changes, ischaemia and hypothermia were evaluated in 22 isolated blood-perfused dog atria. Sinus cycle length (SCL) was measured and sinoatrial conduction time (SACT) was estimated using the premature atrial stimulation technique (PAS) and the constant atrial pacing method (CAP). There was a good correlation between the results obtained with both techniques (r = 0.8297) but CAP had less depressing action on sinus node automaticity. Increasing the perfusion pressure from 100 to 200 mmHg did not influence estimated SACT nor SCL. However, a reduction in perfusion pressure (from 100 to 50 mmHg) markedly shortened SCL without significantly decreasing estimated SACT. Lowering temperature from 37 to 25 degrees C caused a linear increase in estimated SACT and SCL. Occlusion of the sinus node artery induced a sinus tachycardia which was not blocked by sotalol. Estimated SACT was significantly shorter 1 min after occlusion and longer 3 min after occlusion; this increase was significantly inhibited by atropine infusion. Thus, the increase in estimated SACT seen after occlusion might be related to cholinergic activity. However, the sinus tachycardia following a decrease in perfusion pressure might be due to activation of the stretch-receptors while the one seen after reduction in blood flow and occlusion of the sinus node artery seems more likely to be a consequence of ischaemia.

Animals↗
PubMed1985

Abnormalities of in vitro responses to polyclonal activation of peripheral blood lymphocytes in patients with active sarcoidosis.

A variety of immunological abnormalities have been described in patients with sarcoïdosis. At the blood level, both hypo and hyper immune responsiveness seem to coexist and were related to abnormal T cell and macrophage functions by using allogenic cocultures and/or lymphocyte fractionation. We tested several components of cell mediated responses with two in vitro models: (a) the pokeweed mitogen activation of B cells which is T cells and macrophage dependent; (b) the Epstein-Barr virus (EBV) activation of B cells which is T cell- and macrophage-independent. We confirm previous data showing that PWM induced Ig Production of peripheral blood lymphocytes (PBL) of patients with sarcoïdosis is significantly reduced compared with normal PBL. However, this is associated with an increase of IgG, IgM synthesis of EBV-infected PBL in these sixteen patients. Thus, there is no evidence for a complete B cell defect in sarcoïd PBL. Furthermore, by using limiting dilution analysis of antibody secreting cells, there is an increase of precursor B cells EBV infectable in PBL of sarcoïd patients but T cells are effective in reducing EBV-induced B cell proliferation. Finally, these abnormalities are concomitant to the disease, disappear with it, and are apparently not correlated with the stage or the activity of sarcoïdosis.

Adult↗
PubMed1985

Catecholamine release and ventricular arrhythmias during coronary occlusion and reperfusion in the dog.

In anesthetized dogs, 60-min occlusions of either the proximal (n = 14), distal (n = 8) left circumflex (LCX), or left anterior descending (LAD, n = 10) arteries were followed by reperfusion. Coronary sinus and aortic norepinephrine and epinephrine plasma concentrations were measured. The ventricular arrhythmias were ventricular premature depolarizations (VPDs), unsustained ventricular tachycardia (VT) (greater than or equal to 3 and less than 20 VPDs), sustained VT (greater than or equal to 20 VPDs), and ventricular fibrillation (VF). A gradual twofold increase (p less than 0.05) in myocardial norepinephrine overflow followed occlusion in all three groups. The increases in the amounts of norepinephrine released in the coronary sinus blood during reperfusion were significant and proportional to the size of the occluded area: proximal LCX, from 0.236 +/- 0.038 to 1.528 +/- 0.490 ng/mL of plasma (p less than 0.001); LAD, from 0.180 +/- 0.027 to 0.795 +/- 0.286 ng/mL (p less than 0.05); distal LCX, from 0.215 +/- 0.039 to 0.404 +/- 0.110 ng/mL (p less than 0.05). Aortic epinephrine concentrations were significantly increased only by LAD occlusion; at 15 min, the value had increased to 0.187 +/- 0.053 ng/mL from an initial value of 0.069 +/- 0.029 ng/mL (p less than 0.001). Two phases of ventricular arrhythmias followed both occlusion and reperfusion. Phase 1 postocclusion was characterized by VPDs and phase 2 by VPDs and unsustained VT. Sustained VT was seen only in phase 1 postreperfusion, whereas unsustained VT was seen in phase 2. VF was seen in 50, 35, and 25% of the dogs with proximal LCX, LAD, and distal LCX occlusion and reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Intracardiac electrophysiological study of S-2395 in intact and chemically sympathectomized dogs.

S-2395 is a new, long-acting, non-selective beta-receptor blocking agent without apparent intrinsic cardiodepressive action and no receptor selectivity. Its electrophysiological actions were studied in intact and chemically sympathectomized dogs. In normal dogs, S-2395 very slightly increased atrial monophasic action potential (MAPa) duration, atrioventricular functional (FRP) and ventricular effective (ERP) refractory periods. The onset of the atrial supernormal conduction phenomenon (SNCP) was delayed and the ventricular SNCP was abolished. These results are consistent with the action of low concentrations of beta-blocking agents. In contrast S-2395 reduced the ventricular MAPv and increased the ERP/MAPv ratio of sympathectomized animals. Such modifications are usually seen with concentrations higher than necessary for simple beta-receptor blockade. In conclusion S-2395, like several others beta-blockers, had minor effects on the classical electrophysiological parameters of normal dogs. However, it suppressed ventricular SNCP and had a more pronounced action in sympathectomized dogs who are known to have higher levels of circulating catecholamines and who present post-synaptic supersensitivity. The SNCP has been linked with re-entrant arrhythmias. Considering that beta-blockers prevent arrhythmias specially in hyperadrenergic states, the suppression of the ventricular SNCP by S-2395 could thus be the mechanism by which this drug and possibly other beta-blockers might exert their antiarrhythmic action.

Adrenergic beta-Antagonists↗
PubMed1983

Electrophysiological effects of ouabain in 6-hydroxydopamine pretreated dogs.

Chemical sympathectomy and bilateral vagotomy were used to evaluate the contribution of each division of the autonomic nervous system in the electrophysiological actions of ouabain. Intact and chemically sympathectomized dogs were given successive and cumulative doses of ouabain until toxicity became manifest (ventricular extrasystoles and (or) ventricular tachycardia). An additional group of normal and sympathectomized animals was also submitted to bilateral vagotomy in the presence of a therapeutic dose of ouabain. Sinus cycle length, AH interval of the His bundle electrogram, atrioventricular junctional effective and functional refractory periods were increased by ouabain at therapeutic doses. These effects were no different in sympathectomized dogs than in intact dogs, indicating the absence of any significant contribution of efferent sympathetic neural activity. However, our results suggested that vagal enhancement was the main mechanism whereby ouabain produced sinus bradycardia and depression of atrioventricular conduction. Sympathectomy with 6-OHDA did not modify nor abolish ouabain toxicity. However, toxic doses were significantly higher in sympathectomized animals than in normal animals. Considering that increasing heart rate by cardiac pacing or vagotomy significantly lowered toxic doses of ouabain in both intact and sympathectomized dogs, it is possible that sympathectomy could influence ouabain toxicity by altering heart rate alone.

Animals↗
PubMed1983

Acute effects of amiodarone in the isolated dog heart.

Direct injection of amiodarone (10-1000 micrograms) into the sinus node artery of the isolated blood-perfused dog atrium produced dose-dependent negative inotropic and chronotropic responses that were unaffected by atropine. Intraarterial amiodarone also had a negative inotropic action on isolated left ventricular muscle preparations electrically paced at 1.5 to 2.0 Hz. A continuous infusion of 100 micrograms/min of amiodarone significantly suppressed the positive chronotropic effect of norepinephrine whether expressed in percent change or in absolute values; its positive inotropic effect expressed in percent change was not suppressed but rather enhanced by amiodarone. Calcium chloride induced positive chronotropic and inotropic effects expressed in percent change were, respectively, slightly suppressed and enhanced by amiodarone. Intravenous injection of amiodarone (5 mg/kg) decreased the heart rate and blood pressure of the support dog and produced a negative inotropic response in the isolated left ventricular muscle preparation perfused with arterial blood from the support dog. These results suggest first, that amiodarone has direct negative inotropic and chronotropic effects that are not mediated by cholinergic mechanisms and second, that it has a depressive action on norepinephrine and calcium-induced positive chronotropic effects and an enhancing action on their positive inotropic effects.

Amiodarone↗
PubMed1982

Electrophysiology of the chemically sympathectomised dog.

The contribution of the sympathetic nervous system in the definition of various electrophysiological variables was studied in chemically sympathectomised dogs. Chemical sympathectomy was obtained following intravenous injection of 50 mg X kg-1 of 6-hydroxydopamine. Sympathectomised dogs presented significant increases in: basic sinus period, sino-atrial conduction time (SACT), AH and HV intervals of the His bundle electrogram, atrial functional (AFRP) and effective (AERP) refractory periods, atrio-ventricular node functional (AVNFRP) and effective (AVNERP) refractory periods, ventricular functional (VFRP) and effective (EVRP) refractory periods and atrial (AMAP) and ventricular (VMAP) monophasic action potential durations. Corrected sinus recovery time (CSRT) was not affected by chemical sympathectomy. Neither was the atrial ERP/MAP duration ratio. This new form of sympathectomy affects all the levels of the cardiac conduction system. Such results are in accordance with those obtained with surgical sympathectomy or the use of beta-blocking agents.

Animals↗
PubMed1980

Compared effects of enflurane and of halothane on the intracranial pressure and the cerebral perfusion pressure in the dog.

In this study, we compare the values of the systemic arterial pressure (S.A.P.), of the intracranial pressure (I.C.P.) and of the cerebral perfusion pressure (C.P.P.) -- (C.P.P. = P.A.S. -- I.C.P.) -- in the anesthetized dog, artificially ventilated, before and after vaporization with two halogenated anesthetics, enflurane and halothane at different concentrations. The measures were made in a group of ten dogs in normoventilation and intracranial normotension conditions, in one hypercapnic dog with intracranial hypertension, and in four dogs after injection of sodium laurylsulfate in the internal carotide to induce cerebral edema. In normocapnic dogs, enflurane and halothane increase the I.C.P., decrease the S.A.P. and the C.P.P. Under enflurane 0.5%, the I.C.P., the S.A.P., and the C.P.P. show no significant variations. The increase in I.C.P. is due to the cerebral vasodilator effect of the anesthetics. At equal concentrations, halothane is more hypotensive than enflurane, and the changes in C.P.P. induced by both anesthetics depend more on the variations in S.A.P. than on the variations in I.C.P. In the hypercapnic dog, the vaporization of enflurane and of halothane further enhance the increase in I.C.P., since the vasodilator effect of the anesthetics is added to that of hypercapnia. The S.A.P. and the C.P.P. drop in relation to the concentrations of vaporization used. After sodium laurylsulfate, the administration of enflurane and halothane is accompanied by a drop in S.A.P. and in C.P.P. In this group, the decrease in I.C.P. recorded in two thirds of the cases can be explained by the hypotensive effect of the anesthetics which decreased the hydrostatic pressure in the cerebral vascular bed, a maintenance element of the edema.

Anesthesia, Inhalation↗