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首页> 外文期刊>shock >EFFECTS OF HYPERTONIC-HYPERONCOTIC INFUSION ON THE HUMAN ATRIAL NATRIURETIC FACTOR IN A STANDARDIZED CLINICAL TRIAL
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EFFECTS OF HYPERTONIC-HYPERONCOTIC INFUSION ON THE HUMAN ATRIAL NATRIURETIC FACTOR IN A STANDARDIZED CLINICAL TRIAL

机译:EFFECTS OF HYPERTONIC-HYPERONCOTIC INFUSION ON THE HUMAN ATRIAL NATRIURETIC FACTOR IN A STANDARDIZED CLINICAL TRIAL

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摘要

Hypertonic-hyperoncotic solutions (HHT) are presently being utilized to resuscitate patients in shock. However, so far, the effects of HHT on human atrial natriuretic factor (hANF) have not yet been investigated in a clinical trial. The effects of HHT on hANF were studied in a standardized preoperative and clinical setting in patients undergoing aneurysmectomy. Twenty-three conscious patients were included in two groups: 11 HHT and 12 HES (HHT: 7.5% NaCl/10% HES 200; HES: .9% NaCl/10% HES 200). Stepwise infusion of 50 mL was titrated preoperatively according to individual Frank-Starling relationships. Central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) were determined before, during and after volume application. hANF, cGMP were also measured before and 1,10, 30, 60, and 120 min after administration. The volumes necessary to produce the same volume status were: 213.6 ± 63.6 mL of HHT, 409.9 ± 136.2 mL of HES (p.001). The sodium load was 273.9 ± 81.5 mmol of [HHT], 63.1 ± 21.0 mmol of [HES] (p.001). The data before and after volume loading were: PCWP: 7.9 ± 3.9 to 14.9 ± 4.3 mmHg of [HHT], 7.9 ± 5.2 to 14.5 ± 4.3 mmHg of [HES] (p.001); CVP: 3.5 ± 2.3 to 6.9 ± 2.9 mmHg of [HHT], 3.3 ± 3.1 to 7.5 ± 3.2 mmHg of [HES] (p.001); hANF: 42.5 ± 11.7 to 81.6 ± 30.8 pg/mL [HHT] (p.01), 42.0 ± 11.2 to 74.1 ± 47.6 pg/mL [HES] (p.05); cGMP: 4.4 ± 1.2 to 10.5 ± 4.2 nM [HHT] (p.01), 4.9 ± 1.7 to 12.6 ± 5.8 nM [HES] (p.001). The changes in CVP and PCWP were identical after infusion of HHT or HES in normovolemic patients. The increased hANF levels produced by identical atrial dilation with different dosages. Furthermore, plasma-hANF excretion was due to an acute volume expansion of the right atrium. Acute sodium load had no effects on hANF excretion.

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