Bedford J J, Leader J P
Department of Physiology, University of Otago Medical School, Dunedin, New Zealand.
Am J Physiol. 1993 Jun;264(6 Pt 2):R1164-79. doi: 10.1152/ajpregu.1993.264.6.R1164.
Rats were exposed to osmotic stress either acutely, over periods of 1 or 4 h, or chronically, over several days. In acute experiments, hyposmolality was induced by intraperitoneal infusion of dilute glucose or mannitol solutions, whereas hyperosmolality was induced by use of sodium chloride, concentrated glucose or mannitol solutions, or urea. Chronic hypernatremia was induced by daily administration of sodium chloride to water-deprived animals; chronic hyponatremia was induced by daily injection of antidiuretic hormone supplemented with glucose. Animals were made hyperglycemic using streptozotocin or uremic by ureteral ligation. Where appropriate, animals were anesthetized with thiobutabarbital (Inaktin) or ether. In acute experiments, analysis of the composition of the cardiac ventricle, diaphragm, liver, and renal cortex showed no evidence of cell volume regulatory processes involving transmembrane movement of potassium ions. There was a small but significant increase in free amino acids [measured as ninhydrin-positive substance (NPS)] in cardiac muscle exposed to hypertonic solutions of sodium chloride and glucose but not when plasma osmolality was raised using mannitol. In cerebral cortical tissue, after 4 h of exposure to acute hypertonicity by infusion of sodium chloride or glucose, there was a significant increase in tissue potassium content and a slight increase in NPS content. In chronic experiments, tissue analysis revealed good evidence for cellular volume readjustment only in cerebral cortex and heart. In the cortex, levels of free amino acids, principally taurine and glutamate (plus glutamine), showed large increases during hypernatremia and hyperglycemia and corresponding decreases during hyposmolality. In heart the principal amino acid present was taurine, and it, together with aspartate and glutamate (plus glutamine), showed large changes under osmotic stress. Other tissues analyzed showed only small changes in composition.
大鼠急性暴露于渗透应激1小时或4小时，或慢性暴露于渗透应激数天。在急性实验中，通过腹腔注射稀释的葡萄糖或甘露醇溶液诱导低渗，而通过使用氯化钠、浓缩葡萄糖或甘露醇溶液或尿素诱导高渗。通过每天向缺水动物给予氯化钠诱导慢性高钠血症；通过每天注射补充葡萄糖的抗利尿激素诱导慢性低钠血症。使用链脲佐菌素使动物发生高血糖，或通过输尿管结扎使动物发生尿毒症。在适当情况下，用硫喷妥巴比妥（Inaktin）或乙醚麻醉动物。在急性实验中，对心室、膈肌、肝脏和肾皮质的成分分析表明，没有证据显示存在涉及钾离子跨膜移动的细胞体积调节过程。暴露于高渗氯化钠和葡萄糖溶液的心肌中，游离氨基酸[以茚三酮阳性物质（NPS）衡量]有小幅但显著的增加，但使用甘露醇提高血浆渗透压时则没有增加。在大脑皮质组织中，通过输注氯化钠或葡萄糖急性暴露于高渗状态4小时后，组织钾含量显著增加，NPS含量略有增加。在慢性实验中，组织分析仅在大脑皮质和心脏中发现了细胞体积重新调整的有力证据。在皮质中，游离氨基酸水平，主要是牛磺酸和谷氨酸（加谷氨酰胺），在高钠血症和高血糖期间大幅增加，在低渗状态下相应降低。在心脏中，主要存在的氨基酸是牛磺酸，它与天冬氨酸和谷氨酸（加谷氨酰胺）在渗透应激下显示出很大变化。分析的其他组织仅显示成分有微小变化。
