Biomedical subjects
Publications and source records attributed to D Popovici.
For the causal understanding of some evolutive morphological particularities at the level of the lateral wall of orbits (in mammals and in man), the authors have resorted to biomechanical interpretations of bony structures at the cranium level. To this effect some stress factors as well as the modeling effect on the local bone morphogenesis have been analysed.
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A great many apparently unrelated disorders present similar clinical features. Among pathogenetic mechanisms which could explain this phenomenon we studied, in some metabolic and endocrine diseases, the possible role of zinc (Zn) in correlation with lipid peroxidation (oxygen radicals). In the patients with Zn depletion (14 cases) the production of malondialdehyde (MDA) (marker for lipid peroxidation) was higher than in controls (10 subjects). Zincemia 57.62 vs 100 micrograms/dl, p less than 0.001, MDA 1.24 vs 0.7 nM/l, p less than 0.01. The clinical tests used were the gustative test for ZnSO4 1% and a clinical severity score. Between Zn and MDA levels a strong correlation was found in hypercortisolism cases, "r" = -0.82, p less than 0.01. After Zn therapy the MDA levels lowered by 23.55%, and the clinical score and gustative test improved significantly: chi 2 = 16.98, p less than 0.01 (for gustative test), chi 2 = 31.84, p less than 0.001 (for clinical score). These results suggest that the clinical features could be attributed both to Zn depletion and to oxygen radicals excess. However, only in the cases with hypercortisolemia (endogenous and exogenous) does the Zn-peroxide relationship seem significant. This fact suggests that in the course of corticosteroid therapy, Cushing's syndrome and reactive hypercortisolism Zn supplementation should be beneficial.
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A 48-year old female patient, thyroidectomized 4 weeks previously, returns as an emergency with arterial hypertension (AH), atrial fibrillation, cardio congestive failure; after a common therapy which included cardiotonics and diuretics, the patient's condition was improved, but quite unexpectedly she developed 5 cardiac syncopes within 3 hours (pulse and arterial pressure fall, electric asystole) with a dramatic Adams-Stokes syndrome requiring external resuscitation maneuvers. High speed infusion with glucose and ascorbic acid 2,500 mg given intravenously appeared to have stopped the imminence of an attack, but only after corticosteroids both in bolus and infused a stable sinusal rhythm was obtained. Intensive corticotherapy was preferred to sympathicomimetic drugs which are at risk for ventricular arrhythmia. Corticosteroids are the therapy of choice because they prevented the production of oxygen derived free radicals whose accumulation causes bradycardia and finally heart arrest.
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The endocrine system becomes involved in the physiopathologic mechanisms of essential arterial hypertension (EAH) by the interference of hormones with the pressor and depressor substances. A "depressor" pharmacodynamic model with beta-blockers based on the variations of hormone-dependent data offers a series of characteristics for assessing the vasoconstrictive and volemic components, evolution (accelerated for instance) and treatment. Hormone data are also useful for avoiding errors and for increasing the efficiency and control of the therapy. It is not uncommon for EAH to become endocrine-dependent, for instance: increase in aldosterone secretion by activation of the renin-angiotensin (RA) system or of the hypophysis- corticoadrenal system and the adreno-sympathetic system, transforms the relatively "benign" evolution of EAH into an "accelerated" one. The incidence of hyperreactive corticoadrenal (with or without altered steroidogenesis), corticoadrenal hyperplasia or adenoma, is in reality higher than commonly diagnosed.
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The authors have studied on 25 cases of hypercorticism, one of the mechanisms of producing arterial hypertension, the renin-angiotensin system. The study showed that in only 20% of the cases plasma renin activity was high whereas in the remaining 80% other mechanisms were responsible for the hypertension. In the cases in which the plasma activity of renin was high, by studying the changes in the value of electrolytes we were able to derive some understanding of the mechanism of action of the RA2A system. Thus, the literature data show that sometimes the excess of glucocorticoids causes hypertension by activating directly the RA2A system and concomitently inhibiting the renin-kalikrein system (RKKS) and PgS; at other times, the excess of glucocorticoids is exerted on the same renin-angiotensin system, but via ACTH and ADH, the electrolytes values being those that demonstrate the borrowed mechanism.