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首页> 外文期刊>American Journal of Physiology >Urotensin II causes fatal circulatory collapse in anesthesized monkeys in vivo: a 'vasoconstrictor' with a unique hemodynamic profile.
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Urotensin II causes fatal circulatory collapse in anesthesized monkeys in vivo: a 'vasoconstrictor' with a unique hemodynamic profile.

机译：降压肽II导致体内麻醉的猴子的胎儿循环衰竭：具有独特血流动力学特征的“血管收缩剂”。

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摘要

Urotensin II (UII) is a vasoactive peptide that has recently emerged as a likely contributor to cardiovascular physiology and pathology. Acute infusion of UII into nonhuman primates results in circulatory collapse and death; however, the exact cause of death is not well understood. This study was undertaken to elucidate the mechanism underlying the fatal cardiovascular event on UII application in vivo in nonhuman primates. To this end, cynomolgus monkeys (n = 4) were anesthetized and tracheal intubation was performed. One internal jugular vein was cannulated for administration of drugs, and one femoral artery for recording of blood pressure and heart rate using a transonic pressure transducer. Cardiac parameters were not significantly changed after administration of 0.003 nmol/kg human UII. A bolus of human UII (0.03 nmol/kg) caused a decrease of heart rate (HR) (13%), mean blood pressure (MBP) (18%), and first-order derivative of left ventricular pressure (dP/dt) (11%). Carotid and coronary blood flowwere reduced by 9% and 7%, respectively; 0.3 nmol/kg of human UII resulted in a further reduction of HR (50.3%), MBP (65%), dP/dt (45%), carotid (38%), and coronary blood flow (30%), ultimately leading to cardiovascular breakdown and death. Pulmonary pressure, however, was increased by 30%. Plasma histamine levels were found to be unaffected by administration of UII. Our results indicate that systemic administration of human UII has negative inotropic and chronotropic effects and reduces total peripheral resistance ultimately leading to severe myocardial depression, pulmonary hypertension, and fatal circulation collapse in nonhuman primates. We suggest that successful design of UII antagonists might offer a new therapeutic principle in treating cardiovascular diseases.
机译：Urotensin II（UII）是一种血管活性肽，最近被发现可能是心血管生理学和病理学的贡献者。将UII急性注入非人类灵长类动物会导致循环衰竭和死亡。然而，确切的死亡原因尚不清楚。进行这项研究是为了阐明在非人类灵长类动物体内进行UII致死性心血管事件的潜在机制。为此，将食蟹猕猴（n = 4）麻醉并进行气管插管。使用跨音压换能器插入一根颈内静脉用于给药，插入一根股动脉以记录血压和心率。给予0.003 nmol / kg人UII后，心脏参数没有明显改变。一剂人UII（0.03 nmol / kg）导致心率（HR）（13％），平均血压（MBP）（18％）和左心室压力的一阶导数（dP / dt）降低（11％）。颈动脉和冠状动脉血流量分别减少了9％和7％; 0.3 nmol / kg的人类UII导致HR（50.3％），MBP（65％），dP / dt（45％），颈动脉（38％）和冠状动脉血流量（30％）进一步降低，最终导致导致心血管衰竭和死亡。但是，肺压增加了30％。发现血浆组胺水平不受UII的影响。我们的结果表明，人类UII的全身性给药具有负性变力和变时作用，并降低了总外周阻力，最终导致非人灵长类动物出现严重的心肌抑制，肺动脉高压和致命性循环衰竭。我们建议UII拮抗剂的成功设计可能提供治疗心血管疾病的新治疗原则。

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  • 1. Monkey urotensin II [P] . 外国专利： US2002058323A1 . 2002-05-16

    机译：猴尾加压素II

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