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Biomedical subjects

J A Barcat

Publications and source records attributed to J A Barcat.

At least 37 records · Page 2Linked to original sources
PubMed1989

Severe pulmonary hypertension with diffuse smooth muscle proliferation of the lungs. Pulmonary tuberous sclerosis?

A 49-year-old man with normal intelligence and no cutaneous lesions had symptoms and signs of cor pulmonale. The chest roentgenogram showed an interstitial pattern. Hemodynamic studies revealed increased pulmonary arterial and wedge pressures. The patient died in shock, and the postmortem findings were a diffuse smooth muscle proliferation in the lungs as the cause of the pulmonary hypertension. We presume that this is a form of pulmonary tuberous sclerosis of which few cases are reported with such severe pulmonary hypertension as shown by our measurements.

Humans↗
PubMed1989

[Eclampsia induced by skin allografts in spontaneously hypertensive rats].

In order to develop an experimental model for eclampsia, 22 female inbred Spontaneously Hypertensive Rats (SHR) were grafted with skin from Holtzman males. The implantation of four sequential grafts took place at an interval of ten days. Each SHR was mated with its corresponding skin donor ten days after the last graft. Five non grafted SHR mated with Holtzman males were used as controls. In most of the experimental rats that became pregnant we found changes which consisted in: low number of offspring, stillborn fetuses, abortions and growth delay. Renal function was evaluated before and during pregnancy showing a physiological increase in glomerular filtration of 7.5% (basal = 0.93 +/- 0.12 ml/min, peak = 1.00 +/- 0.12 ml/min) as compared with an increase of 166% (basal = 0.68 +/- 0.22 ml/min, peak = 1.85 +/- 0.33 ml/min) in the control group. Renal histology showed lesions corresponding to disseminated intravascular coagulation. These results indicate that the association of skin grafts and hypertension in these rats affects the normal development of pregnancy and suggest that immunological factors could be involved in experimental eclampsia.

Animals↗
PubMed1986

Relationship between severity of renal damage and erythropoietin production in uranyl nitrate-induced acute renal failure.

Adult female Wistar rats were injected with 1 mg/kg body weight of uranyl nitrate (UN). Evaluation of renal function, histopathology studies, and determination of plasma erythropoietin (Ep) titers after exposure to 456 mb for 16 h were performed at 1, 2, 7, 10, 15, and 21 days after drug injection. Plasma urea and creatinine concentrations markedly increased during the first seven days after injection, reaching maximal values on day 7 and decreasing thereafter. Significant increases in urine volume and significant depressions in urine osmolality also were observed; both alterations were most marked on day 7 after injection. A coagulative necrosis of the epithelium of proximal convoluted tubules, desquamation of the necrotic cells, and dilation or collapse of the tubular lumen were observed; the lesions were more marked on day 7. Plasma Ep levels in UN-treated rats exposed to hypobaria were markedly lower than in noninjected controls similarly exposed. Measurements were performed one, two, and seven days after UN injection, with maximal depression observed on day 7. These observations indicate that there is a correlation between the extent of both tubule damage and degree of renal dysfunction and plasma Ep production during exposure to hypoxia in UN-treated rats. This suggests that the renal Ep component is derived primarily from tubular cells.

Acute Kidney Injury↗
PubMed1983

Alteration of blood coagulation and complement system in neotropical primates infected with Junin virus.

The neotropical primate Callithrix jacchus infected with Junin virus presented an acute disease with hematological and neurological manifestations and died 17 to 24 days after infection. This picture is similar to that of human Argentine hemorrhagic fever (AHF). Blood coagulation and complement studies were performed in ten C jacchus animals inoculated with 10(3) TCID50 of Junin virus, the prototype pathogenic XJ strain. Four monkeys were used as normal controls. Infected monkeys and normal controls were bled to death on days 7, 14, 17, and 21. A progressive decrease in the number of platelets was found after day 7 of infection. On day 21, the last monkey had a value of 24,000/microliters. The levels of blood clotting factors did not change until day 17, when a shortened partial thromboplastin time activated with Kaolin (PTTK) (36 sec) and increased factors VIII (192.2%) and VII-X (266.6%) were found. On day 21, the PTTK was prolonged (50.7 sec) and factors II, V, and VIII, were decreased. Thrombin time was found prolonged from day 14 onward. Fibrinogen and fibrin degradation products (FDPs) were increased on days 17 (754 mg/dl and 9.2 microliters/ml) and 21 (457 mg/dl and 29.4 micrograms/ml). No changes in the levels of alpha 2 macroglobulin were observed. Complement hemolytic levels were found to be low on day 7 (58.3 UCH50, increased on day 14 (165.1), and within normal range at the end of infection (107.2). C3 levels showed a similar pattern. The bone marrow was active and hypercellular, and the number and morphology of megakaryocytes were normal in all but one of infected animals. The results of blood clotting suggest a limited activation. The complement system presented a profile of activation followed by a rebound phenomenon. The activation of complement appeared ten days before the alteration of the clotting system was evident.

Animals↗