Rose C E, Ragsdale N V, Carey R M
Department of Internal Medicine, University of Virginia School of Medicine, Charlottesville.
Miner Electrolyte Metab. 1992;18(1):24-34.
To evaluate the changes in atrial natriuretic polypeptide during acute hypoxemia and acute hypercapnic acidosis, conscious mongrel dogs with controlled sodium intake were evaluated in four protocols: (1) 80 min of acute hypoxemia (PaO2 = 34 +/- 1 mm Hg) followed by 40 min of combined hypoxemia and hypercapnic acidosis (PaO2 = 38 +/- 1 mm Hg, PaCO2 = 60 +/- 3 mm Hg, pH = 7.15 +/- 0.03) (n = 7); (2) 40 min of combined acute hypoxemia and hypercapnic acidosis (PaO2 = 36 +/- 1 mm Hg, PaCO2 = 56 +/- 2 mm Hg, pH = 7.20 +/- 0.03) induced immediately following control measurements (n = 5); (3) 120 min of acute hypercapnic acidosis (PaCO2 = 58 +/- 1 mm Hg, pH = 7.20 +/- 0.01) (n = 5), and (4) 120 min of normoxemia and normocapnia (n = 7). These studies did not observe any association between urinary sodium excretion and circulating atrial natriuretic polypeptide during acute blood gas derangements in conscious dogs. The natriuresis with acute hypoxemia or acute hypercapnic acidosis was unaccompanied by change in plasma atrial natriuretic polypeptide concentrations. Conversely, the rise in circulating atrial natriuretic polypeptide during combined acute hypoxemia and hypercapnic acidosis was not associated with an increase in urinary sodium excretion. These observations do not exclude a role for atrial natriuretic polypeptide in altering sodium excretion during acute blood gas derangements, since the effects of this autacoid on renal sodium excretion may have been offset by other counterregulatory mechanisms of sodium excretion activated during the acute blood gas derangement.
为评估急性低氧血症和急性高碳酸性酸中毒期间心房利钠多肽的变化，对有意识的、钠摄入量受控的杂种犬按照四种方案进行了评估：（1）急性低氧血症80分钟（动脉血氧分压[PaO2]=34±1毫米汞柱），随后是低氧血症合并高碳酸性酸中毒40分钟（PaO2=38±1毫米汞柱，动脉血二氧化碳分压[PaCO2]=60±3毫米汞柱，pH=7.15±0.03）（n=7）；（2）在对照测量后立即诱发急性低氧血症合并高碳酸性酸中毒40分钟（PaO2=36±1毫米汞柱，PaCO2=56±2毫米汞柱，pH=7.20±0.03）（n=5）；（3）急性高碳酸性酸中毒120分钟（PaCO2=58±1毫米汞柱，pH=7.20±0.01）（n=5），以及（4）常氧血症和正常碳酸血症120分钟（n=7）。这些研究未观察到清醒犬急性血气紊乱期间尿钠排泄与循环心房利钠多肽之间存在任何关联。急性低氧血症或急性高碳酸性酸中毒时的利钠作用并未伴随血浆心房利钠多肽浓度的变化。相反，急性低氧血症合并高碳酸性酸中毒期间循环心房利钠多肽的升高与尿钠排泄增加无关。这些观察结果并不排除心房利钠多肽在急性血气紊乱期间改变钠排泄方面的作用，因为在急性血气紊乱期间，这种自分泌物质对肾钠排泄的影响可能已被其他激活的钠排泄反调节机制所抵消。
