Renal hemodynamics and renal O2 uptake during hypoxia in the anesthetized rabbit

Summary The effects of hypoxic hypoxia on renal hemodynamics and metabolism have been studied in anaesthetized mechanically ventilated rabbits. Acute hypoxia (F₁O₂=0.10,PaO₂=35 torr) induces at constant mean arterial pressure a 45% decrease in RBF, GFR, and whereas free water clearance increases. These alterations were still apparent 50 min after resuming normal arterial oxygenation. In order to assess the role of the stimulation of catecholamine release in these observations, two other sets of experiments were performed: 1) the animals were ventilated with the same hypoxic gas mixture but after adrenergic blockade (phentolamine: 0.2 mg·kg·min^–1 i.v.), 2) hypoxia was induced by ventilating the animals with CO (F_ICO=0.002) at constantPaO₂. Increase in renal vascular resistance and reduction of renal O₂ uptake were still observed. This indicates that adrenergic stimulation cannot fully explain the renal vasoconstriction encountered in hypoxia. The role of a local vasoactive factor, especially that of the renin angiotensin system is discussed. The apparent O₂ cost of Na reabsorption was not greatly modified by any type of hypoxia and the Na:O₂ ratio remained close to the value observed in normoxic animals. This indicates that the kidney may adapt to hypoxia by reducing its O₂ demand keeping unaltered its tubular function and basal O₂ needs.     

Effect of succinic semialdehyde on some aspects of nitrogen metabolism in the brain tissue of hypoxic animals

Investigation of the concentrations of free ammonia, glutamine, and some free amino acids in the brain tissue of normal animals and of hypoxic animals receiving or not receiving succinic semialdehyde revealed a marked increased in the free ammonia and -alanine concentrations in hypoxia compared with normal, a small increase in the -aminobutyric acid, no change in the glutamic and aspartic acid concentrations, and a decrease in glutamine. If succinic semialdehyde was given before exposure to hypoxia the concentrations of free ammonia, glutamine, and -alanine were close to normal in this state. One possible mechanism of the antihypoxic effect of succinic semialdehyde is the conversion of this compound with the resulting synthesis of glutamic acid and glutamine, which leads to detoxication of the free ammonia that accumulates in the brain tissue during hypoxia.Institute of Pharmacology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR V. V. Zakusov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 81, No. 5, pp. 539–541, May, 1976     

Pathogenesis of the low cardiac output syndrome in postresuscitation states

Acute hypervolemia induced in experiments on dogs by infusion of dextran, did not produce decompensation of the circulation in animals whose cardiac output was sharply depressed in the postresuscitation period after circulatory arrest lasting 15 min. The increase in the venous return and change in the conditions of the peripheral circulation as a result of dextran administration temporarily increased the central venous pressure, caused a lasting increase in the arterial pressure, cardiac output, stroke volume, work of the left ventricle, and total oxygen consumption by the body, and lowered the peripheral vascular resistance. In model experiments on dogs subjected to isolated compression ischemia of the brain for 20 min, a low cardiac output syndrome also developed.Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Fedorov.Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 82, No. 7, pp. 787–789, July, 1976.     

Liver and Heart Mitochondrial Succinate Dehydrogenase Activity of Newborn Rats in Anoxic Hypoxia and Starvation

Succinate dehydrogenase activity was determined in the liver and heart of newborn rats after 3 and 48 hours' exposure to anoxic hypoxia (10% O₂) and after 48 hours' starvation. Control determinations were made on newborn animals of corresponding ages, full term foetuses (21 days), infantile (1 and 2 weeks) and full grown animals. Hypoxia for 3 h had no influence on succinate dehydrogenase activity at all in either the heart or liver mitochondria of the newborn animals. After 48 h no difference was observed in the liver between the hypoxic animals and the starved controls of the same age, though starvation itself had resulted in a significant increase in activity, as much as 42%. When liver mitochondrial succinate dehydrogenase in normal mitochondria was activated by preincubation mitochondria with the substrate, the activity increase obtained was greater than that resulting from starvation. The increase in activity in the heart of the hypoxic or starved animals was not significant (< 10%).     

Meconium-stained amniotic fluid

Passage of meconium usually occurs within 48 hours after birth. However, some fetuses may pass meconium in-utero leading to meconium staining of amniotic fluid (MSAF). The vast majority of fetuses pass meconium in-utero due to the physiological maturation of the fetal gut with advancing gestation leading to normal defaecation in utero. However, clinicians need to exclude ‘non-physiological’ causes of MSAF, especially an ongoing hypoxia or chorioamnionitis, to improve perinatal outcomes. Meconium aspiration syndrome (MAS) is a potentially serious fetal condition with increased risk of severe morbidity and mortality. The use of the cardiotocograph (CTG), timely recognition of ongoing hypoxia or infection, consideration of the overall clinical picture and avoidance of injudicious use of oxytocin may help avoid poor perinatal outcomes and resultant medico-legal consequences.     

Increased α1-adrenoceptor activity of the rat heart during adaptation to intermittent hypoxia

Research Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. Research Institute of Experimental Cardiology, All-Union Cardiologic Scientific Center, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR A. D. Ado.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 111, No. 6, pp. 570–572, June, 1991.     

Exercise breathing pattern during chronic altitude exposure

Summary Breathing pattern in response to maximal exercise was examined in four subjects during a 7-day acclimatisation to a simulated altitude of 4247 m (barometric pressure,PB = 59.5 kPa). Graded exercise tests to exhaustion were performed during normoxia (day 0), and on days 2 and 7 of hypoxia, respectively. Ventilation was significantly augmented in the hypoxic environment, as were both the mean inspiratory flow (V _T/T _I) and inspiratory duty cycle (T _I/T _TOT) components of it.V _I/T _I was increased due to a significant increase in tidal volume (VT) and a corresponding decrease in inspiratory time duration (TI). Throughout a range of exercise ventilation,T _I/T _TOT was increased due to an apparently greater decrease in expiratory time duration (T _E) with respect to TI. In all cases, the relation betweenV _T andT _I displayed a typical range 2 behaviour, with evidence of a range 3 occurring at very high ventilatory rates. There was essentially no difference observed in theV _T-T _I relation during exercise between the normoxic and hypoxic conditions. No significant changes were observed in the breathing pattern in response to exercise within the exposure period (from day 2 to day 7), although there was a discernible tendency to a higher stage 3 plateau by day 7 of altitude exposure.     

Influence of hypobaric hypoxia in infancy on the subsequent development of vasoconstrictive pulmonary vascular disease in the Wistar albino rat

A group of Wistar albino rats was injected subcutaneously with monocrotaline to induce vasoconstrictive hypertensive pulmonary vascular disease characterized by medial hypertrophy of small pulmonary arteries, the appearance of muscular pulmonary arterial vessels of arteriolar dimensions (less than 20 microns) in diameter), and exudative changes in the lung parenchyma. The vascular abnormalities were quantified by measuring the percentage medial thickness of small pulmonary arteries, the number of muscular pulmonary arterial vessels below 20 microns in diameter per cm2 of lung section and by determining the smallest arterial vessels in each case showing muscularity. A second group of rats was born in a decompression chamber and kept in hypobaric hypoxia for a month of the neonatal period, developing hypoxic hypertensive pulmonary vascular disease as a consequence. The animals in this group were allowed to recover in room air for a period of 3 months and were then injected with the same dose of monocrotaline as that given to the first group. The rats previously exposed to hypoxia exhibited an exaggerated response to the alkaloid, showing in particular many more small muscular pulmonary arterial vessels which were of a smaller diameter than those found in the eupoxic rats treated with the alkaloid. The experiment demonstrates the perinatal hypoxia exaggerates the effects of agents inducing vasoconstrictive pulmonary hypertension with a shift of the segment of the pulmonary arterial tree involved to the periphery as in hypoxia. Reports of a similar phenomenon are noted as occurring in babies born at high altitude, spending their infancy there and subsequently developing primary pulmonary hypertension later in life.     

低氧致鼠腺泡内肺动脉PDGF—B链蛋白表达的变化

目的：探讨血小板源性生长因子（ＰＤＧＦ）在低氧肺动脉高压血管构形重建发生中的作用。方法：应用免疫组化技术结合计算机图像分析，检测了低氧大鼠腺泡内肺动脉（ＩＡＰＡ）ＰＤＧＦ－Ｂ链蛋白表达水平。结果：常氧时，ＩＡＰＡ仅有ＰＤＧＦ－Ｂ链蛋白弱表达；低氧１天时，ＩＡＰＡ便有较强的ＰＤＧＦ－Ｂ链蛋白表达，定位于ＩＡＰＡ的内皮和中膜，低氧３天至１４天仅分布于中膜；低氧１、３、５、７、１４天各时间点ＰＤＧＦ－Ｂ链蛋白表达分别为常氧组的１．５３、１．５９、１．５６、１．６２和１．４２倍，差异有显著性（Ｐ＜０．０１）。结论：ＰＤＧＦ－Ｂ链蛋白可能参与了低氧肺动脉高压血管构形重建的发病过程