VASCULAR RESISTANCE OF FOETAL + NEWLY VENTILATED LUNG OF LAMB
VASCULAR RESISTANCE OF FOETAL + NEWLY VENTILATED LUNG OF LAMB
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DOI：
10.1113/jphysiol.1964.sp007361
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发表时间：
1964-01-01
影响因子：
5.5
通讯作者：
ROSS, BB
中科院分区：
文献类型：
--
作者：
CASSIN, S;DAWES, GS;ROSS, BB
平均 O2 解离曲线是根据来自干酪切片的成熟胎儿羔羊的血液计算的。所有实验中脐带均完好无损。个别胎羔未扩张的肺部经常出现无法解释的肺血流量和血管阻力的大的、无法解释的变化，而动脉PQ2或PCO2没有显着变化。对22只羔羊的数据进行多元回归分析表明，具有较高PCO2和较低PO2的羔羊往往具有较高的肺血管阻力。首次用含 1% CO2 的 N2 进行肺部通气导致肺血管阻力下降，动脉 PO2 略有下降，但 PCO2 无显着变化。氮气通气导致血管阻力进一步下降，动脉 PCO2 降低；空气通气导致血管阻力进一步下降，PO2 上升。在空气或 N2 存在的情况下，向通气气体中添加 7% CO2 会引起大约相同程度的血管收缩。仅右肺通气（气体混合物引起动脉 PO2 或 PCO2 变化，与双肺通气时观察到的变化类似）导致不通气左肺血管阻力发生类似变化。结论是胎儿肺的血管张力是可变的，并且它受其他因素以及动脉PCO2和PO2的控制。
The mean O2 dissociation curve was calculated on blood from mature fetal lambs, delivered by Casearean section. The umbilical cord was intact in all experiments. Large, unexplained changes in pulmonary blood flow and vascular resistance were often seen in the unexpanded lungs of individual fetal lambs, with no significant change in arterial PQ2 or PCO2- Multiple regression analysis of data from 22 lambs indicated that lambs with a higher PCO2 and lower PO2 tended to have a higher pulmonary vascular resistance. First ventilation of the lungs with 1% CO2 in N2 caused a fall in pulmonary vascular resistance with a small decrease in arterial PO2 and no significant change in PCO2. Ventilation with N2 caused a further fall in vascular resistance and a decrease in arterial PCO2; ventilation with air caused a still further fall in vascular resistance and a rise in PO2. Addition of 7% CO2 to the ventilating gas caused about the same degree of vasoconstriction in the presence of air or of N2. Ventilation of the right lung only (with gas mixtures which caused changes in the arterial PO2 or PCO2 similar to those observed when both lungs were ventilated) led to similar changes in vascular resistance in the un-ventilated left lung. It was concluded that the vascular tone of the fetal lung is variable, and that it is controlled by other factors as well as the arterial PCO2 and PO2.