Nishiwaki K, Rock P, Stuart R S, Nyhan D P, Peterson W P, Murray P A
Department of Anesthesiology/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287-4961.
J Appl Physiol (1985). 1993 Jul;75(1):256-63. doi: 10.1152/jappl.1993.75.1.256.
Our objective was to determine whether chronic denervation associated with left lung autotransplantation (LLA) results in an alteration in sympathetic beta-adrenoreceptor regulation of the pulmonary circulation in conscious dogs. Continuous left pulmonary vascular pressure-flow (LPQ) plots were generated in conscious dogs 2-4 wk post-LLA and in sham-operated control conscious dogs. We tested the hypothesis that endogenous sympathetic beta-adrenoreceptor activation via circulating catecholamines acted to attenuate the chronic increase in pulmonary vascular resistance post-LLA. Administration of the sympathetic beta-adrenoreceptor antagonist propranolol had no significant effect on the LPQ relationship post-LLA. We also tested the hypothesis that pulmonary vascular reactivity to sympathetic beta-adrenoreceptor activation would be increased post-LLA. The thromboxane analogue U-46619 was used to acutely preconstrict (P < 0.01) the pulmonary circulation in control dogs; this preconstriction shifted the LPQ relationship to the same position measured post-LLA. Under these conditions, cumulative doses of the beta-adrenoreceptor agonist isoproterenol caused pulmonary vasodilation (P < 0.01) in the control group but had no effect post-LLA. However, after acute preconstriction with U-46619, the pulmonary vasodilator response (P < 0.01) to isoproterenol post-LLA was not significantly different from that in the control group. These differential responses to isoproterenol with and without acute preconstriction indicate that a significant component of the chronic increase in pulmonary vascular resistance post-LLA is mediated by passive nonvasoactive mechanisms. Moreover, sympathetic beta-adrenoreceptor reactivity of the pulmonary circulation is not enhanced by chronic denervation resulting from the LLA procedure.
我们的目的是确定与左肺自体移植（LLA）相关的慢性去神经支配是否会导致清醒犬肺循环交感β-肾上腺素能受体调节的改变。在LLA术后2 - 4周的清醒犬以及假手术对照清醒犬中生成连续的左肺血管压力-流量（LPQ）图。我们检验了以下假设：内源性交感β-肾上腺素能受体通过循环儿茶酚胺激活，可减轻LLA术后肺血管阻力的慢性增加。给予交感β-肾上腺素能受体拮抗剂普萘洛尔对LLA术后的LPQ关系无显著影响。我们还检验了以下假设：LLA术后肺血管对交感β-肾上腺素能受体激活的反应性会增加。血栓素类似物U - 46619用于急性预收缩（P < 0.01）对照犬的肺循环；这种预收缩将LPQ关系转变为与LLA术后测量的相同位置。在这些条件下，β-肾上腺素能受体激动剂异丙肾上腺素的累积剂量在对照组中引起肺血管舒张（P < 0.01），但在LLA术后无作用。然而，在用U - 46619急性预收缩后，LLA术后对异丙肾上腺素的肺血管舒张反应（P < 0.01）与对照组无显著差异。这些对有无急性预收缩时异丙肾上腺素的不同反应表明，LLA术后肺血管阻力慢性增加的一个重要组成部分是由被动非血管活性机制介导的。此外，LLA手术导致的慢性去神经支配并未增强肺循环的交感β-肾上腺素能受体反应性。
