[Respiration disorders in comatose states].
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The level of hormones, metabolites, toxins and biologically active substances that reflects the degree of endogenous intoxication increases drastically in acute ischemia and revascularization of the extremity and decreases upon hemosorption (HS). This can be accounted for by their adsorption on the sorbent. According to the data of electron microscopy this pathology is accompanied by morphological signs of the "shock lung". Upon HS dystrophic and destructive changes in lung capillaries and alveolar epithelium are minimum. It is believed that surfactant release from second type pneumocytes promotes to the extension of alveoli and decrease of atelectasis. The early application of HS is pathogenetically grounded.
Experiments on 11 dogs under hypoventilation hypoxia (a decrease in the respiratory minute volume by 40-50%) were made to study the efficacy of membrane oxygenation using a membrane Sever-OMP oxygenator of the blood under the conditions of minor perfusion (14-17% of the minute volume of circulation). The animals of the main series (7 dogs) with a veno-venous connection of the membrane oxygenator (MO) tolerated hypoxia quite well for 2 hours. The control animals died. The conclusion is made that membrane oxygenation with small volumes of perfusion (with the MO connected according to Seldinger) can be used in conjunction with artificial ventilation where the latter one is not effective enough.
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Increased prevalence of sleep-related breathing disorders has been reported in patients with essential hypertension and we have described disordered breathing in spontaneously hypertensive rats, an animal model of genetic hypertension. The mechanisms coupling hypertension to respiratory dysfunction during sleep remain, however, largely unknown. To determine if sleep-related respiratory disorder reflects cardiovascular derangement or, alternatively, represents an independent phenotype in hypertensive rats, we polygraphically recorded groups (n = 10) of genetically hypertensive, genetically normotensive, and phenotypically normotensive rats carrying a genetic background for hypertension. Apnea index was elevated more than 15-fold during NREM sleep in both animal groups carrying hypertension-related genes (p < 0.0001 for each) versus normotensive Wistar Kyoto rats. During REM sleep, a genetic background for hypertension was associated with an increased apnea index of at least 500% versus normotensive Wistar Kyoto rats (p < 0.0001 for each comparison). Still, overall mean respiratory rate, minute ventilation, and sleep architecture were equivalent among all animal groups. As expected, blood pressure and heart period were similar in both normotensive groups but elevated in the hypertensive animals. Persistent sleep-related breathing disorder despite effective cardiovascular normalization in the phenotypically normotensive but genetically hypertensive rats suggests that disordered breathing represents a genetically determined phenotype in these animals that is not secondary to the cardiovascular derangements. The model system described here may provide a powerful tool for investigation of the determinants of sleep-related breathing disorder.
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The actual therapy of choice for the common obstructive sleep-apnea syndrome is the application of continuous positive airway pressure (CPAP) via a nose-mask. This ventilation by positive pressure is explained in some detail. Mechanical ventilation for treatment of nocturnal respiratory failure in outpatients of various etiologies is covered in the companion paper by J. C. Chevrolet. Treatment of sleep disorders due to other pulmonary diseases such as bronchial asthma and others require treatment of the underlying disorder.
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