Wideman R F, Kochera Kirby Y, Forman M F, Marson N, McNew R W, Owen R L
Department of Poultry Science, University of Arkansas, Fayetteville 72701, USA.
Poult Sci. 1998 Feb;77(2):309-21. doi: 10.1093/ps/77.2.309.
Experiments were conducted to evaluate the pulmonary vascular responses of lightly anesthetized clinically healthy male broilers during acute metabolic acidosis induced by bolus i.v. injections or constant i.v. infusions of HCl. In Experiment 1, broilers received consecutive 1.5 mL i.v. bolus injections of 2.5% mannitol (volume control) and 0.4 N, 0.8 N, and 1.2 N HCl in 2.5% mannitol. Following each injection, equivalent concentrations of mannitol or HCl were infused i.v. at a rate of 0.05 mL/min.kg BW. In Experiment 2, repeated bolus injections of 2.5% mannitol and 1.2 N HCl were administered during ongoing constant infusion of 2.5% mannitol. The following variables were evaluated: pulmonary arterial pressure, pulmonary vascular resistance, mean arterial pressure, total peripheral resistance, cardiac output, stroke volume, heart rate, respiratory rate, hematocrit (HCT), and arterial blood gas (PaO2, PaCO2, pH, HCO3-). Mannitol alone did not alter any of the variables. The HCl loading protocols acidified the arterial blood to sustained (constant infusion) or transient (bolus injection) values averaging between pH 7.2 and 7.3. In both experiments, bolus injections of 1.2 N HCl caused transient increases in pulmonary vascular resistance and pulmonary arterial pressure, coincident with decreases in mean arterial pressure and cardiac output. When HCl was infused at a constant rate in Experiment 1, the arterial blood hydrogen ion concentration, [H+], was positively correlated with pulmonary arterial pressure and cardiac output, negatively correlated with mean arterial pressure and total peripheral resistance, and was not correlated with pulmonary vascular resistance. During constant i.v. infusion of mannitol or HCl in both experiments, pulmonary arterial pressure was positively correlated with pulmonary vascular resistance and cardiac output. Overall, bolus injections of 1.2 N HCl consistently triggered transient pulmonary vasoconstriction (increased pulmonary vascular resistance), leading to a transient increase in pulmonary arterial pressure in spite of opposing changes in cardiac output and mean arterial pressure. In contrast, equivalent or greater increases in [H+] during constant i.v. infusion of HCl caused a substantially lower increment in pulmonary arterial pressure, which, in, turn was primarily attributable to increases in cardiac output rather than pulmonary vascular resistance. Increments in either pulmonary vascular resistance or cardiac output induced by metabolic acidosis would be expected to contribute to the onset of pulmonary hypertension syndrome (PHS, ascites) in broilers.
进行实验以评估轻度麻醉的临床健康雄性肉鸡在通过静脉推注或持续静脉输注盐酸诱导的急性代谢性酸中毒期间的肺血管反应。在实验1中，肉鸡接受连续静脉推注1.5 mL 2.5%甘露醇（容量对照）以及在2.5%甘露醇中的0.4 N、0.8 N和1.2 N盐酸。每次注射后，以0.05 mL/min·kg体重的速率静脉输注等量浓度的甘露醇或盐酸。在实验2中，在持续静脉输注2.5%甘露醇期间重复静脉推注2.5%甘露醇和1.2 N盐酸。评估了以下变量：肺动脉压、肺血管阻力、平均动脉压、总外周阻力、心输出量、每搏输出量、心率、呼吸频率、血细胞比容（HCT）和动脉血气（PaO2、PaCO2、pH、HCO3-）。单独使用甘露醇未改变任何变量。盐酸加载方案将动脉血酸化至持续（持续输注）或短暂（静脉推注）值，平均pH在7.2至7.3之间。在两个实验中，静脉推注1.2 N盐酸导致肺血管阻力和肺动脉压短暂升高，同时平均动脉压和心输出量降低。在实验1中以恒定速率输注盐酸时，动脉血氢离子浓度[H+]与肺动脉压和心输出量呈正相关，与平均动脉压和总外周阻力呈负相关，与肺血管阻力无相关性。在两个实验中，在持续静脉输注甘露醇或盐酸期间，肺动脉压与肺血管阻力和心输出量呈正相关。总体而言，静脉推注1.2 N盐酸始终引发短暂的肺血管收缩（肺血管阻力增加），尽管心输出量和平均动脉压发生相反变化，但仍导致肺动脉压短暂升高。相比之下，在持续静脉输注盐酸期间[H+]等量或更大幅度的增加导致肺动脉压升高幅度明显较低，这反过来主要归因于心输出量的增加而非肺血管阻力的增加。代谢性酸中毒引起的肺血管阻力或心输出量的增加预计会导致肉鸡发生肺动脉高压综合征（PHS，腹水）。
