Experimental Argentine hemorrhagic fever: myocardial involvement in Cebus monkey.

Four Cebus apella monkeys, to test a recently proposed model for testing neurovirulence of Junín virus (JV) strains, were intracerebrally infected with 10(5) LD50 of the XJ clone 3 strain of JV. There were no significant electrocardiographic abnormalities or gross lesions, but all infected monkeys exhibited a varying degree of histologic myocardial lesions including focal lymphoblastic infiltrates, vascular ruptures, and mild interstitial reactive change. One Cebus showed lymphocytic infiltrates in the caudal portion of the A-V node without specific cell involvement. These preliminary results demonstrate cardiac involvement in experimental infection of the Cebus monkey with Junín virus.

Aging jejunal vascular ectasia as a cause of persistent intestinal bleeding.

Undiagnosed gastrointestinal bleeding is a major problem in medical practice. This paper describes a patient with vascular intestinal ectasia who had repeated severe intestinal hemorrhages for two years, and required surgery. Vascular intestinal ectasia was demonstrated radiologically, histologically and by electron microscopy in a 25 cm upper jejunum resection. The absence of ultrastructural alterations in intestinal vessels points out that the term "aging vascular ectasia" (Moore Type I) seems preferable, when Rendu Ossler, Von Willebrand and intestinal hemangioma are discarded.

Effects of lorcainide and amiodarone on stress-induced myocardial damage in the rat.

This paper is concerned with the effects of Lorcainide (LCN) and Amiodarone (AMD) on stress-induced myocardial lesions in rats. Forty rats were used. The first group (G-1) was used as a control (n = 10) and animals were injected with saline. Animals in group 2 (G-2) (n = 15) received AMD 10 mg per kilogram, and animals in group 3 (G-3) (n = 15) received LCN 3 mg per kilogram. During five minutes before the injections, the rats were submitted to a stress, consisting of intermittent cold water jets (6 degrees C). Animals were sacrificed one hour after injection, and the hearts were histologically studied. The relative areas of necrotic myocardium were assessed by Bertazzoli's modified method. In G-1, myocytolysis in the subendocardium of left ventricle (score: 2.2 +/- 0.79), contraction bands (1.2 +/- 1.03) and subendocardial myocardial damage (0.8) were common findings. In groups G-2 and G-3, the lesions described were found, but to a lesser degree; subendocardial myocytolysis: 1.6 +/- 0.63 and 1.07 +/- 0.4; contraction bands: 0.67 +/- 0.82 and 0.07 +/- 0.26; and subendocardial damage: 0.77 and 0.40. LCN and AMD markedly decreased stress-induced myocytolysis (p less than 0.01) (graph 1), but LCN was more effective than AMD (p less than 0.05). Comparison of severity and extension of contraction bands showed that only LCN had a significant effect (p less than 0.01) (graph 2); the same was observed as regards the decrease of damaged zones (p less than 0.05). From our data, LCN and AMD appears to have the capacity of reversing some of the stress-induced myocardial damage in rats.

A routine method for diagnosis of early myocardial infarction.

We compared Barbeito-Lopez Trichrome stain with H-E, the basic fuchsin picric acid and Nitro Blue of Tetrazolium stains. The Barbeito-Lopez Trichrome stain was much more sensitive than the other stains for the diagnosis of early myocardial coagulation necrosis.

An overall review on prenylamine mechanisms of action in experimental models of myocardial damage.

In this review we present the effects of a well-known antianginal drug, prenylamine (PNL), in experimental models of acute myocardial damage induced by a beta-agonistic drug, isoproterenol (ISP), in several trials conducted in our laboratory in both rats (n = 204) and monkeys (n = 26). PNL significantly inhibited ISP-induced lesions, protecting the majority of animals studied. Studies dealing with the site of action of the drug, such as 45Ca, 3H-PNL and 3H-ISP trials, showed a clear membrane effect slowing down Ca transport. Correlation between ECG (inhibition of ST depression after ISP) and pathological findings in monkeys was also obtained in one of our experiments. These series of assays were useful in obtaining a more complete idea of activity and site of action of the drug. It seems that, in acute models, PNL acts as a calcium antagonistic drug rather than an adrenergic moderator.

Normal and pathological electrocardiographic patterns in the Cebus monkey.

The normal electrocardiographic (ECG) pattern was determined for Cebus monkeys and compared with those obtained in animals subjected to experimental heart damage. ECG patterns were related to the anatomopathological findings in both normal and treated animals. The anatomic study revealed a vertical heart in which both ventricles constituted the frontal aspect. The experimental heart injury either through the inoculation of Trypanosoma cruzi or after the treatment with isoproterenol induced ECG changes which were correlated with specific anatomopathological lesions.

Isoproterenol-induced 45ca uptake into myocardium of rats.

Myocardial lesions induced by isoproterenol (ISP) are similar to those of human "coagulative mycocytolysis" or "myofibrillar degeneration". The localization of tritiated ISP in the damaged myocardium of rats has been recently described. Since H3-ISP was noted in "grooves" along the sarcolemma of ischemic and necrotic fibers, an action on the membrane with exaggerated calcium inflow was suggested. For this reason, the quantity of 45Ca in rats treated with ISP was studied. Thirty rats were given 5 mu Ci of 45Ca. Twenty (Group B) of them were also given ISP 10 mg/kg. Animals were killed at 1 h after the injections. The hearts were sectioned transversally and autoradiography was performed. Serial sections were examined to localize the 45Ca, and its topographic distribution. In Group A (injected only with 45Ca) the myocardium showed + of 45Ca (600 dots in a field x 400) inside the fibers. In Group B (injected also with ISP) 45Ca was deposited +++ (more than 1,200 dots) and related to extensive myocytolysis. These findings confirm that the crucial point in the ISP-induced lesions is the increase of calcium inflow, and if the pathogenesis of human myocytolysis is related to catecholamine effects pharmacological measures may be adopted to prevent these myocardial lesions.