Pulmonary vascular and airway responses to systemic vasoconstrictors in anesthetized BALB/c mice
Pulmonary vascular and airway responses to systemic vasoconstrictors in anesthetized BALB/c mice
复制标题
麻醉 BALB/c 小鼠的肺血管和气道对全身血管收缩剂的反应
DOI：
10.1097/fjc.0000000000000199
复制
发表时间：
2015
影响因子：
3
通讯作者：
Toga H
中科院分区：
文献类型：
--
作者：
Wang M;Shibamoto T;Shinomiya S;Yamamoto Y;Kurata Y;Kuda Y;Tanida M;Toga H
目前还没有通过直接测量心输出量和肺循环中的流入和流出压力来研究血管活性物质对体内小鼠肺血管阻力（PVR）的影响的系统研究。在麻醉的BALB/c小鼠中，我们测定了PVR、总外周阻力（TPR）和气道压力（AWP）对血管紧张素II、内皮素1、加压素、苯肾上腺素和血栓素A2类似物U46619的反应。测量肺动脉压、左心房压和主动脉血流量。TPR增加剂量依赖性地响应于连续给药的所有血管收缩剂，除了加压素，降低TPR在最高剂量为100 nmol/kg。在高剂量的血管收缩剂，肺动脉压和AWP增加，由于增加肺动脉压，如单独的肺动脉压升高实验所示。当高剂量时PVR短暂增加时，PVR不增加而是降低。然而，内皮素-1，血管紧张素II，和U46619增加PVR。100 nmol/kg的加压素增加AWP，但不升高AUC。总之，这里研究的高剂量血管收缩剂间接地施加了短暂的肺血管扩张和AWP增加的行动，由于强烈的全身血管收缩引起的肺充血。然而，内皮素-1，血管紧张素II，和U46619引起肺血管收缩，加压素收缩麻醉的BALB/c小鼠的气道。
There is no systematic study in which the effects of vasoactive substances were investigated on pulmonary vascular resistance (PVR) in in vivo mouse by directly measuring cardiac output and the inflow and outflow pressures in the pulmonary circulation. We determined the responses of PVR, total peripheral resistance (TPR), and airway pressure (AWP) to angiotensin II, endothelin-1, vasopressin, phenylephrine, and thromboxane A 2 analog U46619 in anesthetized BALB/c mice. Pulmonary arterial pressure, left atrial pressure (LAP), and aortic blood flow were measured. TPR increased dose-dependently in response to consecutive administration of all vasoconstrictors except vasopressin which reduced TPR at the highest dose of 100 nmol/kg. At high doses of vasoconstrictors, pulmonary arterial pressure and AWP increased due to increased LAP, as demonstrated by the separate LAP elevation experiments. When LAP transiently increased at high doses, PVR did not increase but decreased. Nonetheless, enodothelin-1, angiotensin II, and U46619 increased PVR. Vasopressin at 100 nmol/kg increased AWP without LAP elevation. In conclusion, the high doses of the vasoconstrictors studied here exert indirectly a transient pulmonary vasodilatory and AWP increasing actions due to pulmonary congestion evoked by strong systemic vasoconstriction. Nevertheless, enodothelin-1, angiotensin II, and U46619 cause pulmonary vasoconstriction, and vasopressin constricts airway in anesthetized BALB/c mice.