Sonographic diagnosis of blunt trauma causing delayed hemopericardium and cardiac tamponade.
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Biomedical subjects
Publications and source records attributed to S Vijayalakshmi.
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Systolic time intervals (STI) are sensitive indices of myocardial function. Passive tilting is a rapidly reversible and non-invasive method for inducing cardiovascular stress. The present work was conducted to study the effect of graded head-up tilt (HUT) on STI. 20 male medical students were subjected to 30 degrees, 60 degrees and 80 degrees HUT on a tilting table. ECG, phonocardiogram and carotid pulse were recorded simultaneously on Grass polygraph. Electromechanical systole (QS2), left ventricular ejection time (LVET), pre-ejection period (PEP), PEP/LEVT ratio, heart rate (HR) and corrected STI were determined immediately after and at 1, 2, 3, 4 and 5 min after each angle tilt. HUT produced a decrease in QS2 which was more pronounced at higher angle tilt. LVET decreased after 60 degrees and 80 degrees HUT. PEP and PEP/LVET ratio decreased after each angle tilt. These changes in STI can be explained on the basis of sympathetic stimulation-induced increase in the inotropic state of the heart.
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The effects of both high and low molecular weight inhibin preparations on testicular and pituitary receptors were studied. Both these preparations were able to inhibit the binding of labelled hFSH to testicular receptor in a dose related manner, but were unable to affect the binding of labelled hCG to its receptor, suggesting that the observed inhibition of FSH binding was specific to inhibin. In addition, the binding of LHRH to pituitary receptors was affected by inhibin preparations. Interestingly, the antiserum raised against high molecular weight inhibin was able to neutralize, totally, the biological effect of high molecular weight inhibin, and only, partially, the biological effect of low molecular weight inhibin.
Inhibin can exist in multiple forms. The size heterogeneity of inhibin (low and high molecular weight) is likely to be due to the purification procedures employed. However, irrespective of their size, both inhibin preparations are capable of suppressing circulating FSH levels. Since inhibin is a native hormone, the toxic effects after therapeutic administration are expected to be minimal. Inhibin is able to suppress only 70%-80% of the FSH secretion. Inhibin and the steroid (estrogen or androgen) may be involved in the physiological regulation of FSH. To completely suppress circulating FSH, administration of either a combination of inhibin and a steroid or a potent synthetic analogue of inhibin may be necessary. Inhibin has a very short half life in the adult animal, which may be due to the involvement of other testicular factors. Identification and characterization of these factors may help in prolonging effectiveness of inhibin.
Low-molecular-weight (< 1500 daltons) peptides with inhibin activity have been isolated from sheep testes and ovaries by simple gel filtration. These peptides were capable of inhibiting the ovarian weight increase in hCG-primed immature female mice and also of suppressing the post-castration rise of serum FSH levels in adult male rats, suggesting similarities in their biological properties. Both testicular and ovarian inhibin were typsin sensitive and heat stable at 100 degrees C for 30 min and were shown to act by interfering with the production of a hypothetical FSH-RH.
Both testicular and ovarian inhibin preparations caused a dose-related inhibition of binding of 125I-hFSH to rat testicular receptors. Testicular inhibin also suppressed the FSH-induced production of cAMP by rats testis in vitro. These data demonstrate a direct action of inhibin at the testicular level by interfering with FSH action.
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