循环降钙素基因相关肽的升高与猪内毒素休克期间血流动力学恶化相关。

Circulatory shock Pub Date : 1994-03-01
W A Arden, R R Fiscus, X Wang, L Yang, R Maley, M Nielsen, S Lanzo, D R Gross
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引用次数: 0

摘要

降钙素基因相关肽(CGRP)是一种有效的血管舒张神经肽,可能在感染性休克时血管功能障碍中起作用。用氯胺酮和异氟醚麻醉16头猪(25-50 kg),并静脉注射100微克/千克大肠杆菌脂多糖(LPS;n = 8)或生理盐水载体(n = 8)。分别从门静脉(PV)、肺动脉(PA)和颈动脉(CA)取血进行血流动力学测定和CGRP测定(pg/ml)。在给药前(基线)和给药后60min、120min和180min采集血液样本检测EDTA和抑肽酶。LPS使血流动力学指标明显恶化,各采样点血浆CGRP浓度显著升高(P < 0.01)。在任何时候,采样点之间都没有记录到显著差异。血浆CGRP浓度与平均动脉压、心脏指数和左室卒中功呈显著负相关。这些数据证实了我们之前关于内毒素大鼠CGRP升高的发现,并表明1)LPS是CGRP全身释放的有力刺激,2)血浆CGRP浓度升高与LPS休克期间心血管恶化有时间相关性,3)很少有证据表明门静脉循环是LPS休克期间循环CGRP水平的主要来源。血管活性神经肽,如CGRP,可能在感染性休克的发病机制中与其他血管功能障碍介质相互作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Elevations in circulating calcitonin gene-related peptide correlate with hemodynamic deterioration during endotoxic shock in pigs.

Calcitonin gene-related peptide (CGRP) is a potent vasodilatory neuropeptide, which may play a role in vascular dysfunction during septic shock. Sixteen pigs (25-50 kg) were anesthetized with ketamine and isoflurane in O2, and administered 100 micrograms/kg Escherichia coli lipopolysaccharide i.v. (LPS; n = 8) or saline vehicle (n = 8). Pigs were instrumented for hemodynamic determinations and blood sampling for CGRP assay (pg/ml) from the portal vein (PV) and the pulmonary (PA) and carotid (CA) arteries. Blood samples were collected into EDTA and aprotinin before (baseline) and at 60, 120, and 180 min after LPS administration. LPS caused significant deterioration in indices of hemodynamic function and a significant increase in plasma CGRP concentration at all sampling sites by 120 min (P < 0.01). No significant difference between sampling sites was recorded at any time. Plasma CGRP concentrations displayed significant negative correlations with mean arterial pressure, cardiac index, and left ventricular stroke work. These data confirm our previous findings of CGRP elevations in endotoxemic rats, and indicate that 1) LPS is a potent stimulus for the systemic release of CGRP, 2) increasing plasma CGRP concentrations temporally correlates with cardiovascular deterioration during LPS shock, and 3) there is little evidence that the portal circulation is a major source of circulating CGRP levels during LPS shock. Vasoactive neuropeptides, such as CGRP, may interact with other documented mediators of vascular dysfunction in the pathogenesis of septic shock.

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