Olsson K, Hossaini-Hilali J, Cvek K
Department of Animal Physiology, Swedish University of Agricultural Sciences, Uppsala.
Acta Physiol Scand. 1994 May;151(1):83-90. doi: 10.1111/j.1748-1716.1994.tb09723.x.
Pressor doses of angiotensin II induced haemodilution in goats despite renal fluid losses. This study was undertaken to determine if this response is dose-dependent and correlated to the vasoconstrictor action of angiotensin II. Angiotensin II at the doses 0.025, 0.05 and 0.1 micrograms min-1 was given intravenously to five goats. Mean arterial blood pressure increased by 3, 10 and 20 mmHg, respectively, and the renal Na excretion rose. The haematocrit decreased by 7, 10, and 9% (percentage of control values) and the plasma protein concentration by 1% (n.s.), 4.5, and 3.5%, respectively. Infusions of phenylephrine (40 micrograms min-1; n = 6) caused an equivalent increase of blood pressure and renal Na excretion as angiotensin II (0.1 micrograms min-1), but the haematocrit increased by 16% and the plasma protein concentration by 6.5%. Infusions of atrial natriuretic peptide (1 microgram min-1) alone or together with angiotensin II (0.1 microgram min-1), or phenylephrine were also given (n = 6). Infusions of atrial natriuretic peptide alone did not change blood pressure, but renal Na excretion increased. The haematocrit rose by 10.5% and the plasma protein concentration by 7.6%. Adding atrial natriuretic peptide to the angiotensin II solution attenuated the rise of MAP and counteracted the haemodilution, but did not decrease the natriuresis. Infusions of phenylephrine plus atrial natriuretic peptide caused similar elevations of blood pressure and renal Na excretion as phenylephrine alone. The haematocrit rose by 24% and the plasma protein concentration by 13%. These results show that in the intact conscious goat rapid and marked changes in haematocrit and plasma protein concentration can be provoked by intravenous infusions of vasoactive agents and that these effects are not correlated to changes in arterial blood pressure or renal Na excretion.
尽管存在肾液丢失，但血管紧张素II的升压剂量仍可引起山羊血液稀释。本研究旨在确定这种反应是否呈剂量依赖性，并与血管紧张素II的血管收缩作用相关。以0.025、0.05和0.1微克/分钟的剂量将血管紧张素II静脉注射给5只山羊。平均动脉血压分别升高3、10和20 mmHg，肾钠排泄增加。血细胞比容分别下降7%、10%和9%（相对于对照值的百分比），血浆蛋白浓度分别下降1%（无统计学意义）、4.5%和3.5%。静脉输注去氧肾上腺素（40微克/分钟；n = 6）引起的血压升高和肾钠排泄增加与血管紧张素II（0.1微克/分钟）相当，但血细胞比容升高16%，血浆蛋白浓度升高6.5%。还分别给予了静脉输注心房利钠肽（1微克/分钟）单独或与血管紧张素II（0.1微克/分钟）或去氧肾上腺素联合使用（n = 6）。单独输注心房利钠肽不会改变血压，但肾钠排泄增加。血细胞比容升高10.5%，血浆蛋白浓度升高7.6%。将心房利钠肽添加到血管紧张素II溶液中可减弱平均动脉压的升高并抵消血液稀释，但不会减少钠尿。输注去氧肾上腺素加心房利钠肽引起的血压升高和肾钠排泄增加与单独输注去氧肾上腺素相似。血细胞比容升高24%，血浆蛋白浓度升高13%。这些结果表明，在完整清醒的山羊中，静脉输注血管活性药物可引起血细胞比容和血浆蛋白浓度的快速而显著变化，且这些效应与动脉血压或肾钠排泄的变化无关。
