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The concentration of cardiac tissue noradrenaline (NOR) was determined in Wistar rats injected with 1.5 microliters/100 g body weight Africanized bee venom (ABV) (LD50 = 0.8 microliter/100 g body weight by the intravenous route). The animals were injected with ABV by the intramuscular (IM), intraperitoneal (IP), subcutaneous (SC) and intravenous (IV) routes. Animals injected by the IM, IP and SC routes were sacrificed 4, 7 and 24 hours after injection. The animals injected by the IV route were sacrificed when they became apnoeic (within minutes). NOR levels in animals injected by the IM, IP and SC routes were inconstant and inconclusive. In contrast, animals injected with ABV by the IV route showed a significant decrease in NOR concentration when compared to their respective controls, suggesting tissue NOR release. It is suggested that the mechanism of death of the animals injected IV with ABV seems to be related, at least in part, to functional cardiac alterations secondary to stress-induced NOR release. As a consequence, cardiological monitoring of patients who are victims of multiple bee stings is recommended, together with a judicious evaluation of therapy involving drugs with a sympathomimetic action.

Extraction and measurement of biogenic amines (norepinephrine, dopamine, serotonin and histamine) were carried out on human ventricular myocardium obtained from autopsies of individuals divided in the three following groups: chronic Chagas' heart disease (with congestive heart failure: 16 cases, and with sudden and unexpected death: 13 cases); hypertensive heart disease (12 cases); and control patients (with no heart disease: 12 cases). The myocardial samples were obtained from the free walls of left and right ventricles and from the apex. A significant depletion of norepinephrine was detected in those with congestive failure. A poorly elevated level of dopamine was also seen in right ventricular and apical myocardium from those with failure. Left ventricular and apical concentration of serotonin were significantly elevated in the presence of hypertensive heart disease. The most important findings were obtained with histamine, which is increased in both groups of Chagasic patients. We believe that the approach here reported may provide useful informations on the pathogenetic mechanisms, thus far poorly understood, of chronic Chagas' heart disease.

Experimental protein-calorie malnutrition was produced in rats by feeding them a low-protein diet for 6 weeks. Control animals were fed a high-protein diet. The deficient rats showed severe restriction of body weight gain, fatty liver and hypoproteinemia. In addition the present study demonstrated that the experimentally-induced protein-calorie malnutrition brings about striking pathological and electrocardiographic changes as well as increased cardiac catecholamine levels. Based on this demonstration and considering the synchronism of morphological, electrophysiological and biochemical data, we postulated that nutritional stress to the heart raises the myocardium norepinephrine concentration, and continued exposure to high levels of catecholamines may play a role in the development of cardiac changes in protein-energy malnutrition.

The existing controversies on the pathogenesis of Chagas' heart disease can be simplified into two theories: (1) "neurogenic" which is concerned with the denervation of the ganglion cells of the heart (chiefly parasympathetic), theoretically resulting in a relative sympathetic overdrive to the heart, and (2) "immunoallergic", concerned with myocarditis, evoked by antibodies related to myocardial and/or parasite products. It is known that both patients and animals with Chagas' disease exhibit such serologic antibodies. Heart-specific antibodies are known to potentiate myocardial lesions caused by isoproterenol. This observation may provide clues in terms of a link between these two theories of the pathogenesis of Chagas' disease by virtue of two mutually potentiating mechanisms. To test the above hypothesis groups of control and T. cruzi-infected rats were submitted to either two s.c. injections of isoproterenol HCl (190 mg/kg) at 24 h intervals or saline solution. Ten days later, the survivors were killed, and gross heart lesions as well as a detailed histological grading of myocardial lesions were recorded. No differences were detected between control and T. cruzi-infected rats with respect to mortality, gross heart lesions, and myocardial histopathology after isoproterenol treatment. These results indicate no potentiation of myocardial lesions by isoproterenol in T. cruzi-infected rats.

The effect of mild acute exercise (swimming for 1 h), restraint for 1 h and fasting for 48 h on myocardial norepinephrine concentration was compared with rats "at rest" using 320 control and chronically T. cruzi-infected rats at 50, 110, 200 and 380 days of age. Ventricular norepinephrine concentrations of control and similarly aged T. cruzi-infected rats were different for 2 of 4 "at rest" groups. Significant and opposite differences in ventricular norepinephrine were observed for restrained T. cruzi-infected rats when compared to controls (-35% in 50-day old rats and +40% in 110-day old rats). Exercised, "at rest" and fasted control rats presented a significant age-dependent decrease of ventricular norepinephrine concentration, which was not observed for restrained control rats. Norepinephrine levels of pooled atria from 120-day old "at rest" T. cruzi-infected rats were significantly lower than those from non-infected controls, whereas no difference was found in serotonin levels. The lability of myocardial norepinephrine levels in T. cruzi-infected rats suggests, but does not demonstrate, that there is a disturbance of the cardiac sympathetic control.

The effect of long-term alcohol ingestion on the norepinephrine concentration of the heart was investigated in rats. The alcoholic animals showed a highly significant increase in cardiac norepinephrine concentration as compared with the corresponding controls. It is further suggested that continued exposure to high levels of norepinephrine may play a role in the development of cardiomyopathy in chronic alcoholism.

Experimental protein-calorie malnutrition was produced in rats by giving them a low-protein diet for 6 weeks. Control animals were fed a high-protein diet. The deficient rats showed severe restriction of body weight gain, fatty liver and hypoproteinaemia. In addition the present study demonstrates that the experimentally induced protein-calorie malnutrition brings about marked pathological changes and increased catecholamine levels in the hearts of rats. Based on this demonstration, and considering the synchronism of morphological and biochemical data, we postulate that the nutritional stress to the heart raises the myocardium noradrenaline concentration and the continued exposure to high levels of catecholamines may play a role in the development of cardiac changes in protein-energy malnutrition.

Experimental alcoholism was produced in rats by giving them 32% alcohol as the only source of liquid for 4, 12, and 24 weeks. Control rats were given no alcohol. After 12 and 24 weeks on test the alcohol-fed animals developed pathologic changes and tissue catecholamine alterations of the myocardium. However after 4 weeks there were no differences in myocardial structure and norepinephrine levels between alcohol-fed and control rats. The present experiments indicate that marked increase in norepheinephrine concentration accompanies morphologic evidence of myocardial degeneration and may play a role in the development of the alcoholic cardiomyopathy.

Resting electrocardiograms were recorded in 18 male adult rats injected subcutaneously with two doses of isoproterenol (200 mg.kg-1 body weight) 10 days before the animals were submitted to the ajmaline test (1 mg.kg-1 body weight iv). After the ajmaline test all rats were killed and the hearts examined histologically. Electrocardiographic changes were detected at rest in 72% of the isoproterenol injected rats: pathological Q waves, lengthening of the QRS complex, and QRS abnormality were found in 50%, 44%, and 44% of these animals respectively. Ajmaline induced similar changes in both control and isoproterenol treated rats (P wave enlargement (p less than 0.01 and p less than 0.001 respectively), increased PR interval (p less than 0.003 and p less than 0.001 respectively), and increased QaT interval (p less than 0.001 in both groups]. However, ajmaline caused an increase in heart rate only in isoproterenol treated rats (p less than 0.05). A pronounced increase in PR interval, not observed in control rats, was detected in one of five isoproterenol injected rats with a normal resting ECG but showing microscopical cardiac lesions. Apical aneurysm of the left ventricle was found in 16% of isoproterenol injected rats. A mononuclear inflammatory reaction was observed in 13 (72%) of the isoproterenol injected rats and was multifocal in at least three regions of the myocardium in six (46%) and disseminated throughout the myocardium in seven (53%) of these animals. When the electrocardiographic and pathological findings were compared, the ECG changes were found to have a 91% sensitivity, 83% specificity, and 91% positive predictive value.(ABSTRACT TRUNCATED AT 250 WORDS)

Noradrenaline levels and heart morphology were studied in animals with severe iron deficiency anaemia. This condition was induced by feeding rats an iron-deficient diet for 30 days from the time of weaning. Anaemia was indicated by the lowering of blood haemoglobin levels. Statistically significant decreases in myocardial noradrenaline levels associated with cardiac hypertrophy, as revealed by increased wet heart weight and increased size of cardiac muscle cells, were observed in anaemic rats compared with controls.

Catecholamine levels and weight of heart were studied in rats subjected to protein-calorie malnutrition and after a period of nutritional rehabilitation. Rats given a protein deficient diet (4% protein) for periods of 6 and 12 weeks showed a severe restriction of body weight gain. Nevertheless, even though the measured heart weight of deficient rats was significantly lower than the respective controls (16% protein), the deficient rats incurred "real" cardiac enlargement since the mean heart weight of the equal body weight controls was significantly different from that of the deficient animals. The mean heart weight of rats fed a high-protein diet for 6 weeks thereupon a 6-week period of protein deprivation was still less than that of controls, and the heart ratio was still greater than that of controls. However, the heart weight of rehabilitated rats was not significantly different from that of equal body weight controls. Serum protein and albumin levels in dificient rats were significantly decreased in comparison to rats fed a high-protein diet. While the serum protein levels of rehabilitated rats were lower than those of controls, the albumin levels were not different. The protein-calorie malnourished rats, which received a low-protein diet for 6 and 12 weeks, showed a significant increase in myocardium noradrenaline concentration. After a period of nutritional rehabilitation this change did not persist. These catecholaminergic alterations in heart may be responsible, at least in part, for the different cardiac abnormalities described as a result of protein-calorie dietary deficiency. It may also explain the "real" cardiac enlargement observed in deficient rats, according to the hypothesis that noradrenaline may be the ultimate myocardial hypertrophy hormone.

Isolated superfused rat atria release [3H]-acetylcholine when depolarized with 57 mM potassium. The depolarization-induced [3H]-acetylcholine overflow was significantly reduced in atria from chronically T. cruzi-infected rats with electrocardiographically characterized cardiopathy. This fact suggests the occurrence of functional alterations of cardiac parasympathetic control in these animals, probably related to cardiac ganglion cell destruction.