Rose C E, Vance J E, Dacus W S, Brashers V L, Peach M J, Carey R M
Department of Internal Medicine, University of Virginia School of Medicine, Charlottesville 22908.
Circ Res. 1991 Jul;69(1):142-56. doi: 10.1161/01.res.69.1.142.
To evaluate our previous observation of renal vasoconstriction during combined acute hypoxemia and hypercapnic acidosis preceded by acute hypoxemia, we studied 13 conscious mongrel uninephrectomized dogs with chronic renal catheters and controlled sodium intake (80 meq/day for 4 days). Five dogs were studied during combined acute hypoxemia (PaO2, 37 +/- 1 mm Hg) and hypercapnic acidosis (PaCO2, 59 +/- 1 mm Hg; pH 7.20 +/- 0.01). Each dog was studied during infusion of 1) the intrarenal vehicle (n = 5), 2) the intrarenal alpha 1-antagonist prazosin (0.2 micrograms.kg-1.min-1, n = 5), 3) intrarenal [Sar1,Ala8]angiotensin II (70 ng.kg-1.min-1, n = 5), and 4) intrarenal prazosin and [Sar1,Ala8]angiotensin II (n = 4). Immediate induction of combined hypoxemia and hypercapnic acidosis after control measurements during intrarenal vehicle infusion resulted in a decrease in effective renal plasma flow and glomerular filtration rate, increase in renal vascular resistance, and decrease in filtered sodium load in the first 20 minutes of the blood gas derangement. Intrarenal administration of [Sar1,Ala8]angiotensin II failed to reverse the effects of the combined blood gas derangement on renal function. In contrast, intrarenal prazosin administration either alone or in combination with [Sar1,Ala8]angiotensin II abrogated the increase in renal vascular resistance, decrease in glomerular filtration rate, and fall in filtered sodium load. These studies identify a major role for alpha 1-adrenoceptors in the renal vasoconstriction during combined hypoxemia and hypercapnic acidosis.
为了评估我们之前观察到的在急性低氧血症合并高碳酸性酸中毒（此高碳酸性酸中毒发生于急性低氧血症之后）期间出现的肾血管收缩情况，我们对13只清醒的杂种单肾切除犬进行了研究，这些犬均留置有慢性肾导管，并控制钠摄入量（4天内每天80毫当量）。5只犬在急性低氧血症（动脉血氧分压[PaO2]，37±1毫米汞柱）合并高碳酸性酸中毒（动脉血二氧化碳分压[PaCO2]，59±1毫米汞柱；pH值7.20±0.01）期间接受研究。每只犬在输注以下物质时接受研究：1）肾内载体（n = 5），2）肾内α1拮抗剂哌唑嗪（0.2微克·千克-1·分钟-1，n = 5），3）肾内[Sar1,Ala8]血管紧张素II（70纳克·千克-1·分钟-1，n = 5），以及4）肾内哌唑嗪和[Sar1,Ala8]血管紧张素II（n = 4）。在肾内输注载体进行对照测量后，立即诱导低氧血症合并高碳酸性酸中毒，结果在血气紊乱的最初20分钟内有效肾血浆流量和肾小球滤过率降低，肾血管阻力增加，滤过钠负荷减少。肾内给予[Sar1,Ala8]血管紧张素II未能逆转血气紊乱合并症对肾功能的影响。相比之下，单独肾内给予哌唑嗪或与[Sar1,Ala8]血管紧张素II联合给予时，可消除肾血管阻力增加、肾小球滤过率降低以及滤过钠负荷下降的情况。这些研究确定了α1肾上腺素能受体在低氧血症合并高碳酸性酸中毒期间肾血管收缩中起主要作用。
