Weissman M L, Sonnenschein R R, Rubinstein E H
Am J Physiol. 1978 Jul;235(1):H72-81. doi: 10.1152/ajpheart.1978.235.1.H72.
Vascular responses in the hindlimb muscles of anesthetized paralyzed cats during systemic asphyxia were studied. The cats were ventilated with 10% O2-10% CO2-80% N2 for 10-20 min periods, while blood flow to the skinned hindlimb was monitored (electromagnetic flowmeter). Mean arterial pressure rose and hindlimb flow typically fell during asphyxia, implying increased vascular resistance. After sympathetic denervation of the hindlimb, resistance increased in some groups of animals, and did not change in others during asphyxia. Functional adrenalectomy did not alter these response characteristics. Resistance also did not changes significantly if the control resistance was first increased to the predenervation level by electrically pacing the lumbar sympathetic chain. In contrast, pronounced vasodilatation occurred during asphyxia after blocking of the alpha receptors in the hindlimb (phenoxybenzamine) or after systemic catecholamine depletion (reserpine). We conclude that the vasoconstriction in innervated muscle during asphyxia was caused in part by increased discharge of sympathetic constrictor nerves to the muscle vasculature, with augmentation from a humoral alpha agonist of nonadrenal origin, possibly norepinephrine released from sympathetic nerves throughout the body.
研究了全身窒息期间麻醉瘫痪猫后肢肌肉的血管反应。猫用10%氧气-10%二氧化碳-80%氮气通气10至20分钟，同时监测去皮后肢的血流（电磁流量计）。窒息期间平均动脉压升高，后肢血流通常下降，这意味着血管阻力增加。后肢交感神经去节后，一些动物组的阻力增加，而另一些动物组在窒息期间阻力没有变化。功能性肾上腺切除并不改变这些反应特征。如果通过电刺激腰交感神经链首先将对照阻力增加到去节前水平，阻力也不会显著变化。相反，在后肢α受体阻断（酚苄明）或全身儿茶酚胺耗竭（利血平）后，窒息期间会出现明显的血管舒张。我们得出结论，窒息期间受神经支配肌肉的血管收缩部分是由交感缩血管神经向肌肉血管系统的放电增加引起的，非肾上腺来源的体液α激动剂（可能是全身交感神经释放的去甲肾上腺素）起增强作用。
