Biomedical subjects
Publications and source records attributed to O Sátori.
The case of a 64 year old man is presented by the authors whose spleen infarction developed in connection with atrial fibrillation was transformed into splenic abscess in spite of the applied conservative treatment. According to the overviewed literature the etiology, symptoms, diagnostic and therapeutic possibilities, as well as prognosis of these two entities related to spleen are described hereby.
Rat hearts were isolated from control animals (C), following 2.5 hours of hemorrhagic hypotension (Sh) and from rats pretreated with 10 mg/kg dexamethasone (Sh + D), and they were perfused by the modified Langendorff technique. Dexamethasone pretreatment prevented the development of depression of left ventricular mechanical performance and increase of coronary resistance, but the reduction of O2 consumption observed in Sh hearts was not influenced by the synthetic glucocorticoid. Sh animals exhibited elevation of blood inorganic phosphate level, which was significantly diminished in Sh + D rats. Zonal lesions of myofilaments and mitochondria were not seen in electron micrographs of Sh + D hearts, but there was an increase in the number of cellular glycogen particles following dexamethasone pretreatment. The protection of contractile function and coronary circulation during shock cannot be the result of direct inotropic or coronary dilating action, since addition of dexamethasone (10 mg/liter) to the perfusate of C hearts did not alter contractility and coronary resistance. It is assumed that systemic hemodynamic and local cellular effects lead to the protection of myocardial integrity, which may contribute to the general beneficial action of dexamethasone in hemorrhagic shock.
The effect of dexamethasone administration on cerebrocortical NADH fluorescence, blood flow and blood volume, intracellular oxygen tension and electrocorticogram (ECoG) was studied in anaesthetized cats in two sets of experiments. Haemorrhagic shock was induced by stepwise decrease of mean arterial blood pressure from the control level a to 80, 60 and 40 mmHg. The bleeding was followed by reinfusion of the shed blood. The method of producing shock was identical in the untreated and dexamethasone treated groups. Dexamethasone was administered in the control period. The results are summarized as follows: (a) Dexamethasone, given in pharmacological doses failed to alter blood flow or blood volume, NADH fluorescence and the intracellular oxygen tension in the cerebral cortex of the cat; (b) Haemorrhagic shock resulted in a marked increase of cytoplasmic NADH fluorescence in the untreated group, while these changes were much smaller in the dexamethasone pretreated animals; (c) Dexamethasone pretreatment significantly reduced the extent of shock-induced cortical vasodilatation. In some experiments the brain cortex became ischaemic at 40 mmHg MABP; (d) Dexamethasone pretreatment failed to eliminate the shock-induced decrease in cortical intracellular oxygen tension and the irreversible deterioration of ECoG. It is suggested that the decrease in cortical cytoplasmic NAD reduction and the concomitant lactate acidosis might be involved in the ability of dexamethasone to control oedema during shock and other pathological conditions.
Authors studied the ultrastructure of the myocardium of rats treated with Dexamethasone in experimental haemorrhagic shock of 2.5 hours duration. The perfusion was performed on the Langendorff cannula. After preliminary treatment with Dexamethasone no characteristic morphological picture of the shock developed, but a marked accumulation of glycogen was observed. Authors believe that morphological pictures unambiguously evidence the anti-shock effect of Dexamethasone.
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