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%).     

Hypertension and sleep apnoea

SUMMARY  Epidemiological data indicate a link between sleep-disordered breathing and elevation of arterial pressure. Previous studies suggest increased activity of the sympathetic nervous system in patients with sleep apnoea. The response of muscle sympathetic nerve activity was further investigated in normal, awake subjects following exposure to 20 minutes of asphyxia. Sympathetic nerve traffic increased during exposure and remained elevated even after the return to room air breathing. These findings raise the possibility that this sustained elevation of sympathetic nerve traffic could play a role in the development of daytime hypertension in patients with sleep-disordered breathing.     

The effect of tolbutamide on cerebral blood flow during hypoxia and hypercapnia in the anaesthetized rat

The increase in blood flow in the cerebral cortex of the anaesthetized rat during hypoxia and hypercapnia was investigated. Cerebral blood flow (CBF) was measured using the hydrogen clearance method with acutely implanted platinum electrodes. Hypoxia (PaO₂ 35.3±2.4 Torr) and hypercapnia (PaCO₂ 68.1±5.1 Torr) increased basal CBF from 76.3±9.0 ml/100g/min to 168.1±20.1 ml/100g/min and 162.4±31.9 ml/100g/min respectively. The sulphonylurea tolbutamide (1mM in 1%DMSO) had no significant effect on CBF in hyperoxia or in hypercapnia. However, it attenuated the increase of CBF during hypoxia by 66 ±11% (P<0.01). This suggests that opening of tolbutamide-sensitive potassium channels may be involved in the process of hypoxic vasodilation in the rat cerebral cortex.     

The Effects of Ante- and Postnatal Hypoxia on the Central Nervous System and Their Correction with Peptide Hormones

Ante- and postnatal hypoxia significantly worsened the postnatal development of animals. The posthypoxic behavioral model included hyperactivity and decreased learning ability, these being typical manifestations of attention deficit disorder. A peptide constellation prevented and significantly improved posthypoxic postnatal development and eliminated the majority of negative behavioral changes.     

兔急性脑缺氧时脑及脑脊液内腺嘌呤核苷含量的变化

本文报告了由低张性低氧血症所致兔急笥脑缺氧时脑组织内腺苷、次黄嘌呤核苷及次黄嘌呤水平分别从正常对照的５３．３±２．９、１１５．６±１１．８及１８６．５±１０．３增至８１６．４±５９．０、１０４９．７±３７．５及７０４．４±５５．３μＭ／ｇ（Ｘ±ＳＤ），各组间Ｐ值均＜０．０１至０．０５。同步测定的脑脊液中三种腺嘌呤核苷水平分别从正常对照的１．６±０．８、５．１±１．０及１３３．９±５０．８增至７．０     

慢性低氧大鼠肾上腺皮质球状带的变化

将Ｗｉｓｔａｒ大鼠喂养在逐渐降低的常压低氧条件下，用氮气和空气的混合气体调节氧含量。氧浓度由正常逐步降低为１５％、１２％、１０％、８％，最后降至７％，实验共进行１１２ｄ，结果显示低氧动物体重下降，肾上腺重量减少，肾上腺皮质球状带萎缩，脂质丢失，球状带细胞线粒体肿胀和空泡变性，溶酶体增多，表明在慢性常压低氧中，当吸入气氧含量降至７％时，可导致肾上腺皮质球状带细胞超微结构改变，从而影响醛固酮的合成与分     

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.     

Changes in Hemodynamics and Respiration in Rats with Different Resistance to Acute Hypoxia

Effects of acute hypoxia on hemodynamics and respiration were studied in acute experiments on narcotized rats. The animals were divided into groups characterized by high, low-, and medium- resistance to hypoxia by the time of respiration arrest during inhalation of gas mixture containing 3% O2. Hemodynamic parameters of highly resistant animals were higher than in low-resistant rats throughout the entire hypoxic period. The development of a rare (with prolonged inspiratory phase) respiratory rhythm in highly resistant rats is an adaptive reaction, which allows them longer tolerate hypoxia compared to low-resistant animals.     

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.