Bonsignore M R, Jerome E H, Staub N C
J Appl Physiol (1985). 1987 Jun;62(6):2147-53. doi: 10.1152/jappl.1987.62.6.2147.
Since it is not clear whether alpha-adrenergic receptors can modulate lung microvascular liquid and protein leakiness, we studied the effects of alpha-adrenergic receptor stimulation or blockade on lung filtration under base-line conditions and during the acute lung injury caused by a 4-h infusion of venous air emboli in six unanesthetized, chronically instrumented sheep with lung lymph fistulas. During the experiments we continuously infused the alpha-adrenergic receptor agonist phenylephrine hydrochloride (1.0 microgram X kg-1 X min-1 iv) or the alpha-adrenergic receptor antagonist phentolamine mesylate (1.0 mg X kg-1 X min-1 iv), and we measured pulmonary vascular pressures, cardiac output, lung lymph flow, and the lymph-to-plasma protein concentration ratio. During air embolism, alpha-receptor stimulation increased pulmonary vascular resistance and decreased lung lymph flow by 25%; alpha-receptor blockade had the opposite effects. During recovery, neither agent significantly affected pulmonary hemodynamics or lymph flow. Our results indicate that alpha-adrenergic receptors are active during air embolism and modulate pulmonary filtration by causing arteriolar constriction, which reduces the surface area or the perfusion pressure in the pulmonary microvascular bed. They may also affect venous smooth muscle tone. We found no evidence that alpha-adrenergic receptors modulate lung microvascular liquid or protein leakiness directly.
由于尚不清楚α-肾上腺素能受体是否能调节肺微血管液体和蛋白质渗漏，我们在6只未麻醉、长期植入仪器且有肺淋巴瘘的绵羊中，研究了α-肾上腺素能受体刺激或阻断在基线条件下以及在静脉空气栓塞4小时引起的急性肺损伤期间对肺滤过的影响。在实验过程中，我们持续静脉输注α-肾上腺素能受体激动剂盐酸去氧肾上腺素（1.0微克·千克⁻¹·分钟⁻¹静脉注射）或α-肾上腺素能受体拮抗剂甲磺酸酚妥拉明（1.0毫克·千克⁻¹·分钟⁻¹静脉注射），并测量肺血管压力、心输出量、肺淋巴流量以及淋巴与血浆蛋白浓度比。在空气栓塞期间，α受体刺激增加了肺血管阻力，并使肺淋巴流量减少了25%；α受体阻断则产生相反的效果。在恢复过程中，两种药物均未显著影响肺血流动力学或淋巴流量。我们的结果表明，α-肾上腺素能受体在空气栓塞期间具有活性，并通过引起小动脉收缩来调节肺滤过，这会减少肺微血管床的表面积或灌注压力。它们还可能影响静脉平滑肌张力。我们没有发现证据表明α-肾上腺素能受体直接调节肺微血管液体或蛋白质渗漏。
