Hettrick D A, Pagel P S, Kersten J R, Tessmer J P, Bosnjak Z J, Georgieff M, Warltier D C
Department of Anesthesiology, Medical College of Wisconsin, and the Zablocki VA Medical Center, Milwaukee 53226, USA.
Anesthesiology. 1998 Nov;89(5):1166-73. doi: 10.1097/00000542-199811000-00017.
Clinical interest in xenon has been rekindled recently by new recycling systems that have decreased its relative cost. The cardiovascular effects of xenon were examined in isoflurane-anesthetized dogs before and after the development of rapid left ventricular (LV) pacing-induced cardiomyopathy.
Dogs (n = 10) were chronically instrumented to measure aortic and LV pressure, LV subendocardial segment length, and aortic blood flow. Hemodynamics were recorded, and indices of LV systolic and diastolic function and afterload were determined in the conscious state and during 1.5 minimum alveolar concentration isoflurane anesthesia alone and combined with 0.25, 0.42, and 0.55 minimum alveolar concentration xenon in dogs with and without cardiomyopathy.
Administration of xenon to healthy dogs anesthetized with isoflurane decreased heart rate and increased the time constant (tau) of isovolumic relaxation but did not alter arterial and LV pressures, preload recruitable stroke work slope, and indices of LV afterload. Chronic rapid LV pacing increased the baseline heart rate and LV end-diastolic pressure, decreased arterial and LV systolic pressures, and produced LV systolic and diastolic dysfunction. Administration of xenon to isoflurane-anesthetized, cardiomyopathic dogs did not alter heart rate, arterial and LV pressures, myocardial contractility, and indices of early LV filling and regional chamber stiffness. More pronounced increases in tau were accompanied by increases in total arterial resistance during administration of xenon to isoflurane-anesthetized cardiomyopathic compared with healthy dogs.
The results indicate that xenon produces minimal cardiovascular actions in the presence of isoflurane in dogs with and without experimental dilated cardiomyopathy.
最近，新型循环系统降低了氙气的相对成本，从而重新引发了临床对氙气的兴趣。在快速左心室（LV）起搏诱导的心肌病发生前后，对异氟烷麻醉的犬进行了氙气的心血管效应研究。
对10只犬进行长期仪器植入，以测量主动脉和左心室压力、左心室心内膜下节段长度和主动脉血流量。记录血流动力学，并在清醒状态下以及仅使用1.5最低肺泡浓度异氟烷麻醉时，以及在患有和未患有心肌病的犬中，联合使用0.25、0.42和0.55最低肺泡浓度氙气时，测定左心室收缩和舒张功能及后负荷指标。
对用异氟烷麻醉的健康犬给予氙气可降低心率并增加等容舒张时间常数（tau），但不改变动脉和左心室压力、可招募前负荷的搏功斜率以及左心室后负荷指标。慢性快速左心室起搏增加了基线心率和左心室舒张末期压力，降低了动脉和左心室收缩压，并导致左心室收缩和舒张功能障碍。对异氟烷麻醉的心肌病犬给予氙气不会改变心率、动脉和左心室压力、心肌收缩力以及左心室早期充盈和局部心室僵硬度指标。与健康犬相比，对异氟烷麻醉的心肌病犬给予氙气时，tau的增加更为明显，同时总动脉阻力也增加。
结果表明，在患有和未患有实验性扩张型心肌病的犬中，在异氟烷存在的情况下，氙气对心血管的作用极小。
