Baum V C
Department of Anesthesiology, University of California, Los Angeles.
Anesth Analg. 1992 Jun;74(6):865-9. doi: 10.1213/00000539-199206000-00015.
The inhaled anesthetics impair transsarcolemmal calcium entry (ICa) in myocardial cells, although the mechanism of this interaction is not known. This inhibition of calcium entry has been implicated in the myocardial depression of the volatile anesthetics. To further characterize this interaction and to evaluate whether a calcium channel agonist could attenuate or prevent the inhibition of calcium entry, the effect of the calcium channel agonist BAY K8644 on the impairment of ICa by halothane was evaluated in single guinea pig ventricular myocytes. Calcium currents were evoked by means of the whole-cell voltage-clamp technique. Baseline peak ICa was higher in the cells exposed to 5 microM BAY K8644 (311 vs 206 pA/cm2, P less than 0.04). On exposure to 1% halothane, peak ICa was impaired to an identical degree whether or not cells were exposed to BAY K8644 (78% and 79% of baseline value). This is consistent with the suggestion that the effects of these agents on ICa are nonspecific. However, the increase in ICa suggests that appropriate calcium channel agonists might serve to ameliorate the myocardial depressant effects of halothane.
吸入麻醉药会损害心肌细胞的跨肌膜钙内流（ICa），尽管这种相互作用的机制尚不清楚。钙内流的这种抑制作用与挥发性麻醉药引起的心肌抑制有关。为了进一步描述这种相互作用，并评估钙通道激动剂是否可以减弱或防止钙内流的抑制，在单个豚鼠心室肌细胞中评估了钙通道激动剂BAY K8644对氟烷所致ICa损害的影响。通过全细胞电压钳技术诱发钙电流。暴露于5 microM BAY K8644的细胞中基线峰值ICa较高（311对206 pA/cm2，P<0.04）。暴露于1%氟烷时，无论细胞是否暴露于BAY K8644，峰值ICa均受到相同程度的损害（分别为基线值的78%和79%）。这与这些药物对ICa的作用是非特异性的这一观点一致。然而，ICa的增加表明合适的钙通道激动剂可能有助于改善氟烷的心肌抑制作用。
