Diabetic myocardial alterations in ultrastructure and function.

Myocardial samples taken from six healthy and six alloxan-diabetic dogs by means of percutaneous needle-biopsy were investigated electronmicroscopically. Specific increase in the number of collagen fibers and that of mitochondria were demonstrated beside the widening of Z bands. In the same experimental animals, a close, inverse correlation was detected (y = 0.

Contributions to the mechanism of action of beta-adrenergic stimulants.

Subcellar localization of ionic Ca was investigated by the Pb-acetate cytochemical method in rat myometrium on the 21st day of pregnancy, following oxytocin and Bricanyl treatment. Following Oxytocin treatment the amount of ionic Ca increased in the muscle cells of the uterus and decreased in the plasma membrane and mitochondria as compared with the control. Tocolytics given in the last four days of pregnancy caused a decrease in the cytoplasmic concentration of ionic Ca and increased the Ca++ content of Ca++ pools (plasma membrane, mitochondrium).

Comparative electron-microscopic investigation of postmortem human heart muscle biopsy.

Based on Harvard criteria findings, comparative morphological investigation on postmortem heart muscle biopsy following coronary insufficiency after sudden cardiac death have been reported. The subendothelial layer of the left ventricular wall has revealed a severe interstitial edema, various types of actin-myosin filamental destruction, mitochondrial damage, and disseminated muscle fiber necrosis. One of the first alterations observed was the change in transmembrane calcium and intracellular calcium metabolism.

Electron-cytochemical detection of endogenous nickel in the myocardium in acute carbon monoxide poisoning. Applicability of a new cytochemical technique in forensic medicine.

After acute carbon monoxide poisoning (inhalation, dogs; perfusion, rats; postmortem, humans) endogenous nickel was cytochemically detected in heart muscle by dimethylglioxime reaction. Dimethylglioxime cytochemical reaction, in each case at the COHb level, was always positive in experiments and in postmortem samples. A nickel ion accumulation in the heart muscle above 30 rel.

Endogenous nickel release as a possible cause of coronary vasoconstriction and myocardial injury in acute burn of rats.

The aim of the present study was to test the hypothesis that endogenous nickel release may play a role in myocardial depression in the acute phase of burn shock in rats. Serum nickel concentration (Se-Ni) measured by atomic absorption spectrophotometry, the sensitivity of isolated perfused hearts to exogenous nickel chloride (0.01 mumol/l), and ultrastructural myocardial alterations, as well as subcellular localization of endogenous Ni by the dimethylglyoxim method, were analyzed in the first week after standardized third-degree full thickness skin thermal burn covering 20-25% of the body surface.

Changes in myosin isozyme distribution induced by low doses of isoproterenol.

The Ca2+-activated myosin ATPase activity in isoproterenol-induced hypertrophied left ventricle increased by 20-30% while in Goldblatt rats hypertrophy occurred with a decreased myosin ATPase activity. In non-dissociating (pyrophosphate) gel electrophoresis isoproterenol treatment showed decreased V2 and V3 myosin isozymes; at the higher dose of isoproterenol (0.5 mg/kg body weight) only V1 was present.

Effect of nickel on uterine contraction and ultrastructure in the rat.

The in vitro effects of nickel chloride (NiCl2) on uterine contractile activity and ultrastructure were studied in uterine strips isolated from 20-day-pregnant Wistar rats. Ni2+ had a dual action on uterine spontaneous contractions. In low concentrations (10(-7) M to 10(-5) M), NiCl2 increased basal tone significantly but had no effect on the amplitude or frequency of development of isometric force.

Cytochemical detection of nickel in the myocardium after acute carbon monoxide intoxication.

The dimethylglyoxim cytochemical method was used for detecting endogenous nickel (Ni) in the canine and human myocardium. Electrondense deposits were observed in the myocardial cells and the wall and lumen of capillaries of the dog heart when after CO-intoxication the blood COHb level exceeded 30%. Energy-dispersive microanalysis proved the presence of Ni in the reaction product.

Topographical patterns of ultrastructural changes in the rat brain during methionine sulphoximine convulsions.

Ultrastructure of the cerebral and cerebellar cortex, hippocampus and nucleus facialis was examined in albino rats during MSO convulsions. Three, 6 and 12 h after peritoneal injection of the drug (600 mg/kg) perfusion and dissection were done. Convulsions appeared 4-5 h, status epilepticus 8-9 h after drug administration.

New findings concerning the pathogenesis of acute carbon monoxide (CO) poisoning.

The pathomechanism of carbon monoxide (CO) poisoning was studied by means of cardiopathological and neuropathological investigations in experimental CO intoxication. It has been shown that besides CO-hemoglobin association, the binding of CO to cytochromes is a significant factor. The latter is thought to be responsible for the cytotoxic phenomena.

Electron cytochemical detection of nickel ions under pathological conditions in the rat heart.

A newly developed electron cytochemical method for using dimethylglyoxim for visualization of nickel particles in the heart muscle is described. Application of the method under hypoxic conditions in carbon monoxide poisoning is considered.

Multilamellar bodies in rat cerebellar Purkinje cells.

Multilamellar bodies appearing in the rat's cerebellar Purkinje cells were studied ultrastructurally in methionine sulphoximine convulsions, hypovolaemic shock and carbon monoxide poisoning. It is concluded that multilamellar bodies are pathological formations due to toxic hypoxic factors.

Protection of functional and structural integrity of the rat myocardium by dexamethasone in hemorrhagic shock.

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.

Electroncytochemical studies on changes of the adenylcyclase activity following experimental hypoxia and ischaemia in perfused rat hearts.

Changes in activity and localization of adenylcyclase were studied in rat heart perfused according to LANGENDORFF after N2-and CO-hypoxia and ischaemia. Under hypoxic conditions an increase of adenylcylase activity was found in the first minutes. Following 3 h nitrogen or 30 min CP perfusion the intensity of reaction was diminished.

[Effect of dexamethasone on the ultrastructure of the myocardium in experimental hemorrhagic shock].

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.