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Halothane, isoflurane, and sevoflurane reduce postischemic adhesion of neutrophils in the coronary system
C Kowalski1, S Zahler, B F Becker
1Institute of Anesthesiology, University of Munich, Germany.
Background:
Polymorphonuclear neutrophils (PMNs) contribute to postischemic reperfusion damage in many organs and tissues, a prerequisite being adhesion of PMNs to vascular endothelial cells. Because adhesion processes involve orderly interactions of membrane proteins, it appeared possible that "membrane effects" of volatile anesthetics could interfere. We investigated the effects of halothane, isoflurane, and sevoflurane on postischemic adhesion of human PMNs in the intact coronary system of isolated perfused guinea pig hearts.
Methods:
The hearts (n = 7-10 per group) were perfused in the "Langendorff" mode under conditions of constant flow (5 ml/min) using modified Krebs-Henseleit buffer equilibrated with 94.4% oxygen and 5.6% carbon dioxide. Global myocardial ischemia was induced by interrupting perfusion for 15 min. In the second minute of reperfusion (5 ml/min), a bolus dose of 6 x 10(5) PMNs was injected into the coronary system. The number of cells reemerging in the coronary effluent was expressed as a percentage of the total number of applied PMNs. Halothane, isoflurane, and sevoflurane, each at 1 and 2 minimal alveolar concentration (MAC), were vaporized in the gas mixture and applied from 14 min before ischemia until the end of the experiment.
Results:
Under nonischemic conditions, 24.7 +/- 1.3% of the injected neutrophils did not reemerge from the perfused coronary system. Subjecting the hearts to global ischemia augmented retention (36.4 +/- 2.8%, P < .05). Application of halothane reduced adhesion of neutrophils to 22.6 +/- 2.1% and 24.2 +/- 1.8% at 1 and 2 MAC, respectively (P < .05). Exposure to 1 and 2 MAC isoflurane was similarly effective, whereas basal adhesion was not significantly influenced. Sevoflurane-treated hearts (1 and 2 MAC) also showed decreased adhesion of PMNs (23 +/- 2.3% and 24.8 +/- 1.8%, respectively; P < .05) and an identical reduction resulted when sevoflurane (1 MAC) was applied only with the onset of reperfusion.
Conclusions:
Although the mechanism of action of volatile anesthetics remains unclear in these preliminary studies, their inhibitory effect on ischemia-induced adhesion of PMNs may be beneficial for the heart during general anesthesia.
Insights
Volatile anesthetics like halothane, isoflurane, and sevoflurane inhibit the adhesion of polymorphonuclear neutrophils (PMNs) to the heart during ischemia. This finding suggests a potential benefit for cardiac protection during general anesthesia.
Area of Science:
- Cardiovascular Physiology
- Anesthesiology
- Immunology
Background:
- Polymorphonuclear neutrophils (PMNs) contribute to reperfusion injury following ischemia.
- Adhesion of PMNs to vascular endothelial cells is a key step in this process.
- Volatile anesthetics' potential to modulate these adhesion processes was investigated.
Purpose of the Study:
- To investigate the effects of halothane, isoflurane, and sevoflurane on postischemic PMN adhesion.
- To assess the potential cardioprotective role of volatile anesthetics via modulation of PMN adhesion.
Main Methods:
- Isolated perfused guinea pig hearts were subjected to global myocardial ischemia.
- Human PMNs were introduced during reperfusion, and their adhesion was quantified.
- Hearts were exposed to halothane, isoflurane, or sevoflurane at 1 and 2 MAC.
Main Results:
- Global ischemia significantly increased PMN adhesion compared to non-ischemic conditions.
- Halothane, isoflurane, and sevoflurane significantly reduced ischemia-induced PMN adhesion at both 1 and 2 MAC.
- Sevoflurane demonstrated efficacy even when administered only at the onset of reperfusion.
Conclusions:
- Volatile anesthetics exhibit an inhibitory effect on ischemia-induced PMN adhesion in the heart.
- This inhibitory action may offer a beneficial effect for cardiac protection during general anesthesia.
- Further studies are needed to elucidate the precise mechanisms of action.