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Biomedical subjects

C Hollmann

Publications and source records attributed to C Hollmann.

7 recordsLinked to original sources
PubMed1991

Beneficial effects of volatile anesthetics on decrease in coronary flow and myocardial contractility induced by oxygen-derived free radicals in isolated rabbit hearts.

Oxygen-derived free radicals have been implicated in reperfusion injury whereas volatile anesthetics have been shown to enhance myocardial recovery during reperfusion. To explore the mechanism by which these agents improve myocardial recovery, we measured the effect of volatile anesthetics on the free radical-induced reduction in left ventricular pressure (LVP), coronary flow, and endothelium-dependent dilation induced by acetylcholine (Ach). Isolated rabbit hearts were perfused in a Langendorff apparatus. Isovolumetric LVP and coronary flow were measured throughout the study. Oxygen-derived free radicals were produced by the electrolysis (direct current of 0.6 mA) of the perfusate. The following volatile anesthetics were used: halothane 0.5 or 1.0%, isoflurane 0.7 or 1.4%, and enflurane 1.0 or 2.0%. Oxygen free radicals induced a significant decrease in systolic LVP and coronary flow. Pretreatment of the heart with enflurane 1.0 or 2.0%, halothane 1.0%, or isoflurane 0.7% attenuated the effect of the free radicals on both systolic LVP and coronary flow. Free radicals reduced the dilating response induced by 0.1 microM Ach with or without addition of volatile anesthetics. These data suggest that the volatile agents have beneficial effects on the free radical cell damage pathway and that this protection is not related to the preservation of endothelium-dependent dilation.

Anesthetics↗
PubMed1991

Electrophysiologic effects of bupivacaine in the isolated rabbit heart.

To assess the direct electrophysiologic effects of bupivacaine, we examined the spontaneous sinus rhythm and induced rapid and premature atrial and ventricular pacing in 11 isolated rabbit hearts perfused in the Langendorff apparatus with varying concentrations (designated by []) of bupivacaine (control, n = 2; 0.3 microgram/mL, n = 3; 1.5 micrograms/mL, n = 3; 3.0 micrograms/mL, n = 3). There was no change in sinus node automaticity or sinus node recovery time at any concentration and no evidence of abnormal automaticity. Depression of conduction was reflected by prolongation of the PR interval at the following concentrations: 1.5 micrograms/mL (65.0 ms before, 96.6 ms after) and 3.0 micrograms/mL (61.6 ms before, 103.3 ms after) and increase in atrial and ventricular pacing thresholds at 3.0 micrograms/mL (atrial: 0.86-8.6 mA, ventricular: 2.0-10.0 mA). No spontaneous tachyarrhythmias occurred; 2:1 spontaneous atrioventricular block (n = 1) and a decrease in maximal paced rate with 1:1 anterograde or retrograde atrioventricular conduction were noted at all concentrations of bupivacaine. Thus bupivacaine did not change automaticity but had a depressant effect on conduction at the atrial, ventricular, and atrioventricular levels, providing a basis for clinically occurring atrioventricular block and reentrant arrhythmias.

Action Potentials↗
PubMed1991

Isoproterenol corrects the effects of bupivacaine on the electrophysiologic properties of the isolated rabbit heart.

The purpose of this study was to test the hypothesis that isoproterenol could reverse bupivacaine toxicity. In eight isolated rabbit hearts an electrophysiologic evaluation was performed then repeated during infusion of bupivacaine (1 microgram/mL) alone and bupivacaine plus isoproterenol (1-2 micrograms/mL). Bupivacaine alone increased electrocardiographic intervals (P wave, QRS complex, PR, AV, and QTc interval) and refractory periods of the myocardium and atrioventricular junction as well as the Wenckebach cycle and pacing thresholds. The addition of isoproterenol corrected partially or completely all bupivacaine-induced abnormalities, and decreased sinus cycle length, suggesting a potential therapeutic value in the treatment of bupivacaine intoxication.

Action Potentials↗