Search PubMed⌕ Search

PubMed · 1725899

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

Abstract

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.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M Tanguay, G Blaise, L Dumont, G Beique, C Hollmann. 1991. Beneficial effects of volatile anesthetics on decrease in coronary flow and myocardial contractility induced by oxygen-derived free radicals in isolated rabbit hearts.. https://doi.org/10.1097/00005344-199112000-00012

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Early detection of anthracycline cardiotoxicity in a rabbit model: left ventricle filling pattern versus troponin T determination.

Anthracycline cardiotoxicity represents a serious risk of anticancer chemotherapy. The aim of the present pilot study was to compare the potential of both the left ventricular (LV) filling pattern evaluation and cardiac troponin T (cTnT) plasma levels determination for the early detection of daunorubicin-induced cardiotoxicity in rabbits. The echocardiographic measurements of transmitral LV inflow as well as cTnT determinations were performed weekly for 10 weeks in daunorubicin (3 mg/kg weekly) and control groups (n=5, each). Surprisingly, no significant changes in LV-filling pattern were observed through the study, most likely due to the xylazine-containing anesthesia, necessary for appropriate resolving of the E and A waves. In contrast to the echographic measurement, the dP/dt(min) index obtained invasively at the end of the study revealed a significant impairment in LV relaxation, which was further supported by observed disturbances in myocardial collagen content and calcium homeostasis. However, at the same time cTnT plasma levels were progressively rising in the daunorubicin-treated animals from the fifth week (0.024+/-0.008 microg/l) until the end of the experiment (0.186+/-0.055 microg/l). Therefore, in contrast to complicated non-invasive evaluation of diastolic function, cTnT is shown to be an early and sensitive marker of anthracycline-induced cardiotoxicity in the rabbit model.

Anesthetics↗

Identification of a molecular target mediating the general anesthetic actions of pentobarbital.

Barbiturates were introduced into medical practice in 1934. They are widely used today as general anesthetics. Although in vitro studies revealed that the activity of a variety of ligand-gated channels is modulated by barbiturates, the target(s) mediating the anesthetic actions of barbiturates in vivo are unknown. Studying pentobarbital action in beta3(N265M) mice harboring beta3-containing GABAA receptors insensitive to a variety of general anesthetic agents, we found that the immobilizing action of pentobarbital is mediated fully, and the hypnotic action is mediated in part by this receptor subtype. It was surprising that the respiratory depressant action of pentobarbital is indistinguishable between beta3(N265M) and wild-type mice and thus is mediated by other as-yet-unidentified targets. Whereas the target for the immobilizing and hypnotic actions of pentobarbital seems to be the same as for etomidate and propofol, these latter agents' respiratory depressant actions are mediated by beta3-containing GABAA receptors. Thus, in contrast to etomidate and propofol, pentobarbital can elicit respiratory depression by a beta3-independent pathway. Pentobarbital reduced heart rate and body temperature to a slightly smaller extent in beta3(N265M) mice compared with wild-type mice, indicating that these actions are largely mediated by other targets. Pentobarbital-induced increase of heart rate variability and prolongation of ECG intervals are seen in both beta3(N265M) mice and wild-type mice, suggesting that they are not dependent on beta3-containing GABAA receptors. In summary, we show a clear pharmacological dissociation of the immobilizing/hypnotic and respiratory/cardiovascular actions of pentobarbital.

Anesthetics↗