Höhne Claudia, Boemke Willehad, Schleyer Nora, Francis Roland C, Krebs Martin O, Kaczmarczyk Gabriele
Experimental Anesthesia, Clinic of Anesthesiology and Surgical Intensive Care Medicine, Campus Virchow-Klinikum, Charité, D-13353 Berlin, Germany.
J Appl Physiol (1985). 2002 May;92(5):2097-104. doi: 10.1152/japplphysiol.00719.2001.
Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis and sodium, potassium, and bicarbonate excretion. With a low sodium intake, the excretion of the anion bicarbonate may be limited by the lower excretion rate of the cation sodium through activated sodium-retaining mechanisms. This study investigates whether the short-term renal compensation of hypoxia-induced respiratory alkalosis is impaired by a low sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low-sodium (LS = 0.5 mmol sodium x kg body wt-1 x day-1) or high-sodium (HS = 7.5 mmol sodium x kg body wt-1 x day-1) diet. The dogs breathed spontaneously via a ventilator circuit during the experiments: first hour, normoxia (inspiratory oxygen fraction = 0.21); second to fourth hour, hypoxia (inspiratory oxygen fraction = 0.1). During hypoxia (arterial PO2 34.4 +/- 2.1 Torr), plasma pH increased from 7.37 +/- 0.01 to 7.48 +/- 0.01 (P < 0.05) because of hyperventilation (arterial PCO2 25.6 +/- 2.4 Torr). Urinary pH and urinary bicarbonate excretion increased irrespective of the sodium intake. Sodium excretion increased more during HS than during LS, whereas the increase in potassium excretion was comparable in both groups. Thus the quick onset of bicarbonate excretion within the first hour of hypoxia-induced respiratory alkalosis was not impaired by a low sodium intake. The increased sodium excretion during hypoxia seems to be combined with a decrease in plasma aldosterone and angiotensin II in LS as well as in HS dogs. Other factors, e.g., increased mean arterial blood pressure, minute ventilation, and renal blood flow, may have contributed.
急性缺氧会导致通气过度和呼吸性碱中毒，常伴有利尿增加以及钠、钾和碳酸氢盐排泄增多。在钠摄入量较低时，由于激活了保钠机制，阳离子钠的排泄率降低，阴离子碳酸氢盐的排泄可能会受到限制。本研究探讨低钠摄入是否会损害缺氧诱导的呼吸性碱中毒的短期肾脏代偿。对9只清醒、行气管切开术的狗进行了两次研究，分别给予低钠（LS = 0.5 mmol钠×kg体重-1×天-1）或高钠（HS = 7.5 mmol钠×kg体重-1×天-1）饮食。实验期间，狗通过通气回路自主呼吸：第一小时，常氧（吸入氧分数 = 0.21）；第二至第四小时，缺氧（吸入氧分数 = 0.1）。在缺氧期间（动脉血氧分压34.4±2.1托），由于通气过度（动脉血二氧化碳分压25.6±2.4托），血浆pH值从7.37±0.01升至7.48±0.01（P < 0.05）。无论钠摄入量如何，尿pH值和尿碳酸氢盐排泄均增加。高钠组的钠排泄增加幅度大于低钠组，而两组的钾排泄增加幅度相当。因此，低钠摄入并未损害缺氧诱导的呼吸性碱中毒在第一小时内快速出现的碳酸氢盐排泄。缺氧期间钠排泄增加似乎与低钠组和高钠组狗血浆醛固酮和血管紧张素II的降低有关。其他因素，如平均动脉血压升高、分钟通气量增加和肾血流量增加，可能也起到了作用。
