Chronic experimental infection by Trypanosoma cruzi in Cebus apella monkeys

Twenty young male Cebus apella monkeys were infected with CAl Trypanosoma cruzi strain and reinfected with CA l or Tulahuen T.cruzi strains, with different doses and parasite source. Subpatent parasitemia was usually demonstrated in acute and chronic phases. Patent parasitemia was evident in one monkey in the acute phase and in four of them in the chronic phase after re-inoculations with high doses of CAl strain. Serological conversion was observed in all monkeys; titers were low, regardless of the methods used to investigate anti-T. cruzi specific antibodies. Higher titers were induced only when re-inoculations were perfomed with the virulent Tulahuén strain or high doses of CAl strain. Clinical electrocardiographic and ajmaline test evaluations did not reveal changes between infected and control monkeys. Histopathologically, cardiac lesions were always characterized by focal or multifocal mononuclear infiltrates and/or isolated fibrosis, as seen during the acute and chronic phases; neither amastigote nests nor active inflammation and fibrogenic processes characteristic of human acute and chronic myocarditis respectively, were observed. These morphological aspects more closely resemble those found in the "indeterminate phase" and contrast with the more diffuse and progressive pattern of the human chagasic myocarditis. All monkeys survived and no mortality was observed.

Chronic experimental infection by Trypanosoma cruzi in Cebus apella monkeys.

Twenty young male Cebus apella monkeys were infected with CA1 Trypanosoma cruzi strain and reinfected with CA1 or Tulahuen T. cruzi strains, with different doses and parasite source. Subpatent parasitemia was usually demonstrated in acute and chronic phases. Patent parasitemia was evident in one monkey in the acute phase and in four of them in the chronic phase after re-inoculations with high doses of CA1 strain. Serological conversion was observed in all monkeys; titers were low, regardless of the methods used to investigate anti-T. cruzi specific antibodies. Higher titers were induced only when re-inoculations were performed with the virulent Tulahuén strain or high doses of CA1 strain. Clinical, electrocardiographic and ajmaline test evaluations did not reveal changes between infected and control monkeys. Histopathologically, cardiac lesions were always characterized by focal or multifocal mononuclear infiltrates and/or isolated fibrosis, as seen during the acute and chronic phases; neither amastigote nests nor active inflammation and fibrogenic processes characteristic of human acute and chronic myocarditis respectively, were observed. These morphological aspects more closely resemble those found in the "indeterminate phase" and contrast with the more diffuse and progressive pattern of the human chagasic chronic myocarditis. All monkeys survived and no mortality was observed.

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.

Experimental myocarditis induced in Swiss mice by homologous heart immunization resembles chronic experimental Chagas' heart disease.

The Swiss mouse is considered a satisfactory model for experimental chronic chagasic myocarditis and there is some evidence of an immunopathologic mechanism in the development of this disease. To further support this conjecture, 45-day-old albino Swiss mice (40 animals) were immunized with homologous heart in complete Freund's adjuvant. As controls, 20 animals were likewise inoculated with allogeneic testis, as "non-related" antigen. Three mice from the former group died suddenly at 19-21 days postinoculation while the survivors were sacrificed at 60 days for serum samples, and histologic analysis of the heart and skeletal muscle. Electrocardiographic records were taken at Days 0, 30, and 60 postinoculation. Of myocardium-inoculated animals and testis-inoculated mice 33/37 (89%) and 1/20 (5%), respectively, exhibited myocarditis (P less than 0.001). Histologic lesions were highly reminiscent of those observed in chronic experimental Chagas' disease of Swiss mice. Antimuscle antibodies were seen, by indirect immunofluorescence employing cryostat sections, in 30/33 (91%) of the former group and in 3/20 (15%) of the latter (P less than 0.001), some of which recognized a surface antigen of primary cultured fetal rat myocardiocytes. Mice inoculated with myocardium also exhibited electrocardiographic abnormalities consisting in QRS interval widening. Results show that following an autoimmune experimental design the main features of chronic chagasic myocarditis may be reproduced in the Swiss mouse. This agrees with the likely role of an immunopathologic mechanism in heart damage due to Trypanosoma cruzi infection.

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.