Sarkar Joy, Golden Patrick J, Kajiura Lauren N, Murata Lee-Ann M, Uyehara Catherine F T
*Departments of Surgery and †Clinical Investigation, Tripler Army Medical Center, Hawaii.
Shock. 2015 May;43(5):475-82. doi: 10.1097/SHK.0000000000000325.
Vasopressors are gaining renewed interest as treatment adjuncts in hemorrhagic shock. The ideal vasoconstrictor will increase systemic blood pressure without increasing pulmonary vascular resistance (PVR), which hinders pulmonary perfusion and exacerbates hypoxemia. However, the selectivity of pressors for pulmonary versus systemic vasoconstriction during hemorrhage has not been characterized. The purpose of this study was to test the hypothesis that vasopressin (VP) has distinct effects on pulmonary versus systemic hemodynamics, unlike the catecholamine vasopressors norepinephrine (NE) and phenylephrine (PE). Anesthetized and ventilated pigs were assigned to resuscitation with saline only (n = 7) or saline with VP (n = 6), NE (n = 6), or PE (n = 6). Animals were hemorrhaged to a target volume of 30 mL/kg and a mean arterial pressure of 35 mmHg. One hour after the start of hemorrhage, animals were resuscitated with saline up to one shed blood volume, followed by either additional saline or a vasopressor. Hemodynamics and oxygenation were measured hourly for 4 h after the start of hemorrhage. Vasopressin increased systemic vascular resistance (SVR) while sparing the pulmonary vasculature, leading to a 45% decrease in the PVR/SVR ratio compared with treatment with PE. Conversely, NE induced pulmonary hypertension and led to an increased PVR/SVR ratio associated with decreased oxygen saturation. Phenylephrine and crystalloid had no significant effect on the PVR/SVR ratio. Sparing of pulmonary vasoconstriction occurs only with VP, not with administration of crystalloid or catecholamine pressors. The ability of VP to maintain blood oxygenation indicates that VP may prevent hypoxemia in the management of hemorrhagic shock.
血管升压药作为失血性休克治疗辅助药物正重新受到关注。理想的血管收缩剂应在不增加肺血管阻力（PVR）的情况下提高全身血压，因为肺血管阻力会阻碍肺灌注并加重低氧血症。然而，出血期间血管升压药对肺血管收缩与全身血管收缩的选择性尚未得到明确。本研究的目的是检验以下假设：与儿茶酚胺类血管升压药去甲肾上腺素（NE）和去氧肾上腺素（PE）不同，血管加压素（VP）对肺血流动力学和全身血流动力学有不同影响。将麻醉并通气的猪分为仅用生理盐水复苏组（n = 7）或用生理盐水加VP组（n = 6）、NE组（n = 6）或PE组（n = 6）。动物出血至目标血量为30 mL/kg且平均动脉压为35 mmHg。出血开始1小时后，用生理盐水复苏动物，直至回输一个失血量，随后再给予额外生理盐水或一种血管升压药。出血开始后每小时测量血流动力学和氧合情况，持续4小时。血管加压素增加全身血管阻力（SVR），同时不影响肺血管，与用去氧肾上腺素治疗相比导致PVR/SVR比值降低45%。相反，去甲肾上腺素诱发肺动脉高压，并导致PVR/SVR比值升高，同时氧饱和度降低。去氧肾上腺素和晶体液对PVR/SVR比值无显著影响。仅血管加压素可避免肺血管收缩，而晶体液或儿茶酚胺类血管升压药则不能。血管加压素维持血液氧合的能力表明，血管加压素可能在失血性休克的治疗中预防低氧血症。
