Effect of hypoxemia on the cardiovascular response to intracranial hypertension in postnatal lambs.
Effect of hypoxemia on the cardiovascular response to intracranial hypertension in postnatal lambs.
复制标题
低氧血症对产后羔羊颅内高压心血管反应的影响。
DOI：
10.1152/ajpheart.1993.265.5.h1557
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Traystman,RJ
中科院分区：
文献类型：
--
作者：
Kearney,ML;Backofen,JE;Koehler,RC;JonesJr,MD;Traystman,RJ
与出生后的绵羊相比，胎羊的颅内压大幅升高会导致更强大的外周血管收缩和更好的脑氧耗(CMRO2)维持。胎儿暴露在较低的氧分压下。我们验证了这样一种假设，即出生后羔羊的低PO2增强了外周血管收缩，并更好地维持了脑灌注压和CMRO2。用戊巴比妥钠麻醉2-7日龄羔羊，分别用室内空气(n=7)或低氧混合气(n=7)进行呼吸，使动脉血氧饱和度降至50%(n=7)。通过脑室输液将颅内压升高到基线平均动脉压的3-5毫米汞柱内30分钟，在正常氧[11+/-3(SE)毫米汞]组和低氧(14+/-2毫米汞)组最初引起类似的动脉压升高。血浆儿茶酚胺在低氧组升高更快。然而，血浆加压素水平仅因低氧而显著升高，且不能随着颅内压升高而进一步升高。此外，在动脉压的稳态升高方面，两组之间没有显著差异，微球确定的流向肠、肾、皮肤和肌肉的血流量在两组中都没有减少。因此，两组患者的脑灌流压、局部脑血流量和CMRO2均有相似的降低。因此，低氧血症不能增强出生后的升压反应。低氧血氧分压不太可能是胎儿产生强大库欣反应的主要机制。
Large increases in intracranial pressure in fetal sheep result in more potent peripheral vasoconstriction and better maintenance of cerebral O2 consumption (CMRO2) than in postnatal sheep. The fetus is exposed to a lower PO2. We tested the hypothesis that low PO2 in postnatal lambs potentiates peripheral vasoconstriction and better maintains cerebral perfusion pressure and CMRO2. Pentobarbital-anesthetized lambs, 2-7 days old, were ventilated with either room air (n = 7) or a low O2 mixture to reduce arterial O2 saturation to 50% (n = 7). Elevation of intracranial pressure to within 3-5 mmHg of baseline mean arterial pressure for 30 min by ventricular fluid infusion initially caused a similar increase in arterial pressure in the normoxic [11 +/- 3 (SE) mmHg] and hypoxic (14 +/- 2 mmHg) groups. Plasma catecholamines increased more rapidly in the hypoxic group. However, plasma vasopressin levels were substantially elevated by hypoxia alone and failed to increase further with elevated intracranial pressure. Moreover, there was no significant difference between groups in the steady-state increase in arterial pressure, and microsphere-determined blood flow to intestines, kidney, skin, and muscle did not decrease in either group. Consequently, cerebral perfusion pressure, regional cerebral blood flow, and CMRO2 were reduced similarly in both groups. Therefore, hypoxemia failed to potentiate the postnatal pressor response. Low PO2 is unlikely to be the major mechanism for the potent Cushing response in the fetus.