J.Samuel M. Oliveira

Cardiac noradrenaline in experimental rat envenomation with africanized bee venom

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.

An unusual case of Budd-Chiari syndrome. A case report

The authors report a rare case of congenital Budd-Chiari syndrome in a twenty-eight-year-old male mongoloid. The patient was submitted to azygous- portal disconnection, because of the syndrome of portal hypertension suppos edly due to cirrhosis of the liver. He died of hemorrhage of the liver on the third postoperative day. Autopsy revealed a congenital fibrotic obstruction of all su prahepatic veins, with a wide, round ligament containing a functional umbilical vein, which had been routinely ligated during surgery. An extensive review of the literature showed no similar report. The authors speculate that the inadver tent interruption of the round ligament, which until then had served as a path way for venous draining of the liver, followed by ligation of the anastomoses between the portal and azygous systems, was the factor that triggered the lethal outcome. Thus, this appears to be the first case of congenital Budd-Chiari syn drome predominantly maintained at the expense of the round ligament of the liver, with a patent vascular branch.

Congenital absence of the circumflex coronary artery associated with dilated cardiomyopathy.

We report the first autopsied case of congenital absence of the left circumflex coronary artery. The patient was a 12-year-old girl in whom the clinical diagnosis was idiopathic dilated cardiomyopathy. This type of heart disease is uncommon among children. The coexistence of the two conditions therefore suggests a possible aetiologic relationship between them. The pathological findings, however, do not support such an association. Rather, they suggest that they co-exist by chance.

Cardiomyopathy in rats with Walker 256 tumor: The potential role of microvascular disease in its genesis

Considering that diffuse abnormalities of myocardial microcirculation with transient ischemia have been suggested to play a role in the genesis of myocytolytic necrosis, characteristic lesion of dilated or congestive cardiomyopathies, and the bloodstream is the most common pathway for dissemination of cancer cells, which gain access to the microcirculation, the present study was undertaken to search for morphologic and electrocardiographic evidence of myocardial damage associated with microcirculatory disease in rats experimentally inoculated with the Walker 256 tumor. Young albino rats inoculated intramuscularly with the Walker 256 tumor developed a cardiomyopathy characterized by diffuse small foci of myocytolytic necrosis, decreased thickness of the mean left midventricular wall associated with reduced size of the minor diameter of myocytes, and electrocardiographic abnormalities reflecting the myocardial damage, correlated with the presence of a microvascular disease, characterized by intramyocardial microvessels (less than 50 μm in diameter) partially or totally occluded because of entrapment of tumor cells and fibrin-platelet/tumor cell-cellular debris thrombi. The occlusive or subocclusive small vessel lesions preceded the development of the myocytolytic necrosis, suggesting that the microvascular disease would play an important role in the process of focal micronecrosis and consequent electrocardiographic changes. However, it must be taken into account that the tumor thromboemboli can generate related factors that could promote cell injury and cell death. In conclusion, the hematogenic dissemination of Walker 256 cells promotes the development of an experimental cardiomyopathy attributable, at least in part, to microvascular obliterative changes in the myocardium.

Beneficial effects of gangliosides on the natural history of acute chagasic myocarditis in rats

This study was designed to investigate the effects of ganglioside treatment on acutely Trypanosoma cruzi-infected rats with emphasis on the heart. Newly weaned Wistar rats were infected with T. cruzi (Colombian strain, 50,000 parasites/kg body weight injected intraperitoneally). Two groups of 25 infected rats received daily injections of saline or ganglioside (10 mg/kg body weight) intraperitoneally between the 14th and 30th days after infection. Two groups of 10 noninfected rats were similarly treated. On day 31, all surviving rats were killed. Hearts were collected for histopathology and norepinephrine assay. An arbitrary score for myocardial microscopic lesions was used to characterize each heart wall. Mortality was recorded throughout the experimental period. Seven of 25 (28%) ganglioside-treated and 14 of 25 (56%) saline-treated rats died spontaneously (p = 0.02). The histological score was 5.4 ± 3.2 for ganglioside-treated and 7.9 ± 3.0 for saline-treated rats (p < 0.05). No difference was detected in myocardial norepinephrine content. Thus, ganglioside treatment decreases mortality and myocardial inflammation in acute chagasic myocarditis in rats.