Search PubMed⌕ Search

Biomedical subjects

B N Datta

Publications and source records attributed to B N Datta.

At least 91 records · Page 5Linked to original sources

Incomplete rupture of the heart with diverticulum formation.

Two diverticula of the heart that caused no perceptible bulge in the cardiac outline were found at necropsy amongst 197 hearts from patients who had had myocardial infarcts. They lay within the wall of the left ventricle communicating with the left ventricular lumen by a small orifice, had mural thrombus in their lumens, were lined by connective tissue and surrounded by a healing or healed infarct. The lesions resulted from an incomplete rupture of the heart caused by the arrest of a haemorrhagic dissection en route from endocardial to epicardial surfaces through the infarcted ventricular wall. Resorption and organization occurred and a diverticulum formed. The distinct morphology of the diverticulum permits its differentiation from both a left ventricular aneurysm and a pseudoaneurysm.

Aged↗

A key to identify heart valve prostheses.

A system for the identification of heart valve prostheses has been developed. A series of observations is made on the structure of a prosthesis. Following each the most appropriate choice of two or three alternative findings is made. One is then directed to the next observation until a genus of prostheses is found with structural characteristics like the unknown one. Positive identification is aided by a brief description of each prosthesis in the genus.

Heart Valve Diseases↗

Cardiomegaly in chronic anemia in ratsman experimental study including ultrastructural, histometric, and stereologic observations.

Postweanling rats maintained on a milk-sugar diet develop a sideropenic anemia, the hemoglobin values falling to less than 30 per cent within 8 to 10 weeks. In that period the heart weight increases by more than 3 times, both ventricles enlarging proportionately. As in other forms of cardiac hypertrophy, a progressive increase in the numbers of connective tissue cells occurs. Ultrastructural and stereologic studies show an appreciable proliferation of the mitochondrial mass in myocardial cells, the mitochondrial fractional volume increasing from a normal of 0.38 to 0.48 per unit cell volume. This quantitative increase is accompanied by a progressive deterioration of the internal cristal structure and the appearance of abnormal, degenerating, and necrotic forms of mitochondria as congestive cardiac failure develops. Myofibrils remain normal. The heart of an anemic rat subjected to an additional workload produced by subdiaphragmatic aortic constriction shows an earlier deterioration of the mitochondrial ultrastructure and stereologic profiles. However, it does not become as large as the heart of the purely anemic animal. In anemic animals with an increased workload, the myofibrillar fractional volume increases from a normal of 0.52 to 0.57 per unit cell volume initially. The active sarcomerogenesis is achieved by Z-band proliferation, which was not observed in the heart of the purely anemic animal. These findings provide a structural basis for the functional and biochemical cardiac deterioration observed in the cardiomegaly induced by chronic anemia.

Anemia↗