Stekiel W J, Willems W J, Harder D R, Lombard J H
Am J Physiol. 1980 Feb;238(2):H144-52. doi: 10.1152/ajpheart.1980.238.2.H144.
To clarify mechanisms leading to failure of compensatory vascular tone in splanchnic blood vessels during prolonged hypotensive stress, anesthetized rats were maintained at a constant mean arterial pressure of 35 mmHg by hemorrhage into an external reservoir until 40% autoinfusion of maximum bled volume. In vivo intracellular membrane potentials (Em) of small intestinal mesenteric veins (300--500 micrometers) were measured before and during the compensatory (bleedout) and decompensatory (autinfusion) phases of the hypotensive period to assess the state of vascular smooth muscle (VSM) excitation. During the compensatory phase, Em decreased from -41 +/- 1 mV (prehemorrhage) to -31 +/- 2 mV, and small venous pressures decreased significantly. The onset of cardiovascular decompensation was associated with hyperpolarization (-53 +/- 3 mV), vasodilation, and return of venous pressure to control levels. Although direct electrical stimulation of the VSM and norepinephrine suffusion still produced constriction late in the hypotensive period, venoconstrictor responses to perivascular nerve stimulation failed progressively. This study indicates that failure of adrenergic neuromuscular transmission contributes significantly to the loss of compensatory VSM tone during hemorrhage.
为了阐明在长时间低血压应激期间内脏血管代偿性血管张力衰竭的机制，将麻醉大鼠通过向外部储液器放血维持平均动脉压在35 mmHg恒定水平，直至自动回输最大放血量的40%。在低血压期的代偿期（放血）和失代偿期（自动回输）之前及期间，测量小肠肠系膜静脉（300 - 500微米）的体内细胞内膜电位（Em），以评估血管平滑肌（VSM）的兴奋状态。在代偿期，Em从出血前的-41 ± 1 mV降至-31 ± 2 mV，小静脉压力显著降低。心血管失代偿的开始与超极化（-53 ± 3 mV）、血管舒张以及静脉压力恢复到对照水平有关。尽管在低血压后期直接电刺激VSM和去甲肾上腺素灌注仍可产生收缩，但对血管周围神经刺激的静脉收缩反应逐渐失效。本研究表明，肾上腺素能神经肌肉传递功能衰竭在出血期间代偿性VSM张力丧失中起重要作用。
