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心房利钠因子对急性容量扩张的清醒恒河猴的影响。

Effects of atrial natriuretic factor in conscious rhesus monkeys with acute volume expansion.

作者信息

Lee K C, Greenwood J M, Wendt R L, Lappe R W

机构信息

Department of Experimental Therapeutics, Wyeth-Ayerst Research, Princeton, New Jersey.

出版信息

Am J Hypertens. 1990 Apr;3(4):262-7. doi: 10.1093/ajh/3.4.262.

Abstract

The renal and hemodynamic responses to intravenous anaritide, a human atrial natriuretic factor [102-126] at 0.3 to 20 micrograms/kg in conscious rhesus monkeys with and without acute extracellular hypervolemia were analyzed and compared. Acute isotonic saline loading (intravenous bolus at 10 mL/kg plus continuous infusion at 0.25 mL/kg/min 30 min prior to and maintained throughout experiment) significantly augmented urine output (UV) and urinary Na+ excretion rate (UNaV) by 31% and 91%, respectively. Radial mean arterial pressure (MAP) and heart rate (HR) were not affected by volume expansion. Anaritide at doses higher than 0.3 micrograms/kg reduced MAP in a dose-dependent fashion in euvolemic monkeys. In contrast, reduction in MAP was observed only at the highest dose (20 micrograms/kg) of anaritide in hypervolemic monkeys. The hypotensive responses to anaritide at 20 micrograms/kg in euvolemic and hypervolemic animals were similar (-26 +/- 5 v -24 +/- 5 mm Hg, respective maximum changes in MAP). UV and UNaV were increased by anaritide at 3 to 20 micrograms/kg in both euvolemic and hypervolemic monkeys; however, the increases at each effective dose of anaritide were greater or tended to be greater in hypervolemic rhesus monkeys compared with euvolemic rhesus monkeys. Compared to vehicle responses, HR was not affected by anaritide in either group of animals. In conclusion, acute extracellular hypervolemia potentiates the renal but suppresses the hypotensive responses to anaritide in conscious rhesus monkeys.

摘要

分析并比较了清醒恒河猴在有或无急性细胞外液量过多情况下,静脉注射0.3至20微克/千克人心房利钠因子[102 - 126](阿那利肽)后的肾脏和血流动力学反应。急性等渗盐水负荷(实验前30分钟静脉推注10毫升/千克并在整个实验过程中以0.25毫升/千克/分钟持续输注)分别使尿量(UV)和尿钠排泄率(UNaV)显著增加31%和91%。桡动脉平均动脉压(MAP)和心率(HR)不受容量扩张影响。剂量高于0.3微克/千克的阿那利肽使血容量正常的猴子的MAP呈剂量依赖性降低。相比之下,在细胞外液量过多的猴子中,仅在阿那利肽最高剂量(20微克/千克)时观察到MAP降低。血容量正常和细胞外液量过多的动物对20微克/千克阿那利肽的降压反应相似(MAP的最大变化分别为-26±5和-24±5毫米汞柱)。阿那利肽在3至20微克/千克剂量时使血容量正常和细胞外液量过多的猴子的UV和UNaV均增加;然而,与血容量正常的恒河猴相比,细胞外液量过多的恒河猴在阿那利肽各有效剂量下的增加幅度更大或趋于更大。与溶媒对照反应相比,两组动物的HR均不受阿那利肽影响。总之,急性细胞外液量过多增强了清醒恒河猴对阿那利肽的肾脏反应,但抑制了其降压反应。

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