Takasu A, Yagi K, Okada Y
Department of Traumatology and Critical Care Medicine, National Defense Medical College, Saitama, Japan.
Resuscitation. 1995 Aug;30(1):69-73. doi: 10.1016/0300-9572(95)00864-p.
The role of endothelin-1 (ET-1) in the failure of cerebral circulation after cardiac arrest is unknown. We evaluated the effect of complete global cerebral ischemia that was induced on the plasma ET-1 concentration in 5 dogs, by occluding the ascending aorta and caval veins for 15 min. A fiberoptic catheter was inserted into the sagittal sinus for the continuous monitoring of venous oxygen saturation. Blood samples were collected before and at 0.5, 1, 2, 4, and 6 h after the ischemic insult. The ET-1 concentration in the sagittal sinus and abdominal aorta was assayed. Complete global cerebral ischemia resulted in a significant 3-fold increase in the sagittal sinus concentration of ET-1 (P < 0.01) that was associated with a significant decrease in the sagittal sinus venous oxygen saturation (P < 0.01); the arterial ET-1 concentration remained unchanged. The difference between arterial and venous ET-1 concentrations during the hypoperfusion phase subsequent to the ischemic insult may result from an increased secretion of ET-1 by the cerebrovasculature and a decrease in the clearance of ET-1 in the cerebral circulation. The result suggests that ET-1 may contribute to the failure of cerebral circulation after cardiac arrest.
内皮素-1（ET-1）在心脏骤停后脑循环衰竭中的作用尚不清楚。我们通过阻断5只犬的升主动脉和腔静脉15分钟，评估了完全性全脑缺血对血浆ET-1浓度的影响。将一根光纤导管插入矢状窦，用于连续监测静脉血氧饱和度。在缺血损伤前以及损伤后0.5、1、2、4和6小时采集血样。检测矢状窦和腹主动脉中的ET-1浓度。完全性全脑缺血导致矢状窦中ET-1浓度显著增加3倍（P < 0.01），这与矢状窦静脉血氧饱和度显著降低相关（P < 0.01）；动脉ET-1浓度保持不变。缺血损伤后低灌注期动脉和静脉ET-1浓度的差异可能是由于脑血管系统中ET-1分泌增加以及脑循环中ET-1清除减少所致。结果表明，ET-1可能促成心脏骤停后脑循环衰竭。
