Blake C I, Banchero N
Respir Physiol. 1985 Sep;61(3):357-68. doi: 10.1016/0034-5687(85)90078-7.
Ventilation and oxygen consumption were measured in awake, unrestrained and unintubated guinea pigs during chronic and acute exposure to cold or hypoxia. Specific VE and VO2 in acute and chronic exposure to cold were more than twice that of animals in normal environmental temperatures. Increased ventilation was mainly due to a 70% greater VT in cold. Cold-acclimated guinea pigs returned acutely to normal temperatures, maintained higher VE and VO2 than that of control animals. Acclimation to cold did not result in respiratory advantages over that of control animals acutely exposed to cold. In hypoxia-acclimated guinea pigs, specific VE was 30% higher than that of control animals due to an elevation in VT; however, VO2 was similar in both groups of animals. In contrast, acute hypoxia did not increase VE in control animals. This lack of ventilatory response to acute hypoxia apparently causes the marked erythropoiesis and the severe increase in hematocrit observed throughout chronic exposure to hypoxia. The high blood viscosity resulting from the increased hematocrit contributes to the right ventricular hypertrophy and cardiac failure in guinea pigs chronically exposed to hypoxia.
在清醒、未束缚且未插管的豚鼠处于慢性和急性冷暴露或低氧暴露期间,测量了通气和氧消耗。急性和慢性冷暴露时的特定通气量(VE)和氧耗量(VO2)是处于正常环境温度动物的两倍多。通气增加主要是由于冷环境中潮气量(VT)增大了70%。冷适应的豚鼠急性恢复到正常温度后,其VE和VO2仍维持在高于对照动物的水平。冷适应并未使豚鼠相对于急性暴露于寒冷的对照动物在呼吸方面具有优势。在低氧适应的豚鼠中,由于VT升高,特定VE比对照动物高30%;然而,两组动物的VO2相似。相比之下,急性低氧并未使对照动物的VE增加。对急性低氧缺乏通气反应显然导致了在整个慢性低氧暴露过程中观察到的显著红细胞生成和血细胞比容的严重增加。血细胞比容增加导致的高血液粘度促成了慢性低氧暴露豚鼠的右心室肥大和心力衰竭。