Adrogué H J, Chap Z, Okuda Y, Michael L, Hartley C, Entman M, Field J B
Department of Medicine, Veterans Administration Medical Center, Houston, Texas.
Am J Physiol. 1988 Dec;255(6 Pt 1):E812-23. doi: 10.1152/ajpendo.1988.255.6.E812.
The determinants of the altered glucoregulation in acidosis were investigated in anesthetized dogs. Because CO2 rapidly equilibrates and its effects are mediated by pH changes, CO2 inhalation was examined. Plasma acid-base composition, glucose, insulin, glucagon, and blood flows were evaluated before and after an intravenous glucose load (1.2 +/- 0.1 g/kg body wt) in normal and acidotic dogs with flow probes and catheters chronically implanted in the portal circulation. A simultaneous infusion of phentolamine (5 micrograms.kg-1.min-1), propranolol (3.5 micrograms.kg-1.min-1), both, or none was used. All acidemic dogs had lower hepatic extraction of insulin and greater hyperglycemia after the glucose challenge; thus the adrenergic system is not critical for these responses. Because arterial insulin levels were either normal (propranolol) or increased (all others) in acidosis, insulin resistance was likely. Insulin infusion (2 and 4 mU.kg-1.min-1) with euglycemic clamp and [3-3H]glucose documented that acidemia decreases peripheral glucose utilization and the insulin suppression of hepatic glucose production. Acidemia also enhances plasma glucagon levels, yet this effect plays a limited role in the observed hyperglycemia.
在麻醉犬身上研究了酸中毒时糖调节改变的决定因素。由于二氧化碳迅速达到平衡且其作用由pH变化介导，因此对吸入二氧化碳进行了检测。在正常犬和酸中毒犬中，通过长期植入门静脉循环的血流探头和导管，在静脉注射葡萄糖负荷（1.2±0.1 g/kg体重）前后评估血浆酸碱组成、葡萄糖、胰岛素、胰高血糖素和血流量。同时输注酚妥拉明（5微克·千克⁻¹·分钟⁻¹）、普萘洛尔（3.5微克·千克⁻¹·分钟⁻¹）、两者或都不输注。所有酸血症犬在葡萄糖激发后胰岛素的肝摄取较低且高血糖更严重；因此，肾上腺素能系统对这些反应并不关键。由于酸中毒时动脉胰岛素水平要么正常（普萘洛尔组）要么升高（其他所有组），胰岛素抵抗很可能存在。采用正常血糖钳夹技术和[3-³H]葡萄糖进行胰岛素输注（2和4 mU·千克⁻¹·分钟⁻¹）表明，酸血症会降低外周葡萄糖利用以及胰岛素对肝葡萄糖生成的抑制作用。酸血症还会提高血浆胰高血糖素水平，但这种作用在观察到的高血糖中起的作用有限。
