Biomedical subjects
Publications and source records attributed to S Rao.
A ganglioneuroblastoma developed in a 35-month-old boy with both the fetal hydantoin and fetal alcohol syndromes. Our case, plus two recent reports in the literature, would very likely establish the relationship between fetal hydantoin syndrome and the development of neural crest tumors. Infants exposed in utero to hydantoins should be closely observed for the development of these tumors.
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Does cerebellar retraction during operations in the posterior fossa contribute to increased morbidity and mortality, and if so, what are the critical factors involved? In order to answer these questions, graded retractor pressures of 10, 20, and 30 mm Hg were applied for one hour to the cerebellar hemispheres of dogs in the sitting position. It was noted that the amount of mechanical pressure and the difference between systemic perfusion pressure and retractor pressure were important determinants of the outcome. The mechanism of damage from retractor pressure is discussed.
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To evaluate the importance of time, temperature, and cardioplegia on the ability of the canine myocardium to maintain functional and ultrastructural integrity following induced arrest, we studied 220 dogs by varying myocardial temperature (34 degrees, 24 degrees, and 11 degrees C.), arrest time (0 to 120 minutes), and cardioplegic agents. Change in left ventricular function (LVF) was defined as the arithmetic difference in the center of mass between prearrest and postarrest LVF curves and was expressed as percent recovery of left ventricular stroke work. Left ventricular biopsies were obtained for semiquantitative electron microscopic analysis. After 90 minutes of cross-clamping, only hearts protected with combined hypothermia (H) and potassium-induced cardioplegia (K) significantly recovered prearrest function (24 degrees C.--80 percent, 11 degrees C.--99 percent). Hypothermia (H) alone for 90 minutes was less protective (24 degrees C.--49 percent, 11 degrees C.--59 percent). H preserved 84 percent of function after 60 minutes and 91 percent after 45 minutes. Normothermic arrest resulted in only 39 percent return of function at 45 minutes but could be extended with potassium-induced cardioplegia(K) to 78 percent at 60 minutes and 54 percent at 90 minutes. The addition of procaine plus HK improved protection over HK alone (95 percent versus 80 percent) but by itself was not effective. Neither hydrocortisone nor pretreatment with glucose-insulin-potassium, branched chain amino acids, or propranolol increased the protective effect of HK plus procaine. Inadequately protected groups (normothermia or H without K) showed more myocytic and capillary endothelial damage than the HK groups. No technique of myocardial protection studied completely preserved LVF, but the combination of HK plus procaine resulted in maximal recovery of LVF following cross-clamping for up to 120 minutes.
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Reversible cerebellar dysfunction is described in a patient with primary hemochromatosis. The electroencephalographic abnormalities initially recorded became normal after repeated phlebotomies. Both cerebellar dysfunction and electroencephalographic changes were present without clinical signs of hepatic failure, but may be related to the altered hepatic function tests.
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A 46-year-old male with bilateral genito-femoral neuralgia is presented. The patient complained of groin and testicular pain, the onset following asynchronous bilateral inguinal herniorrhaphy. Relief was effected by genito-femoral nerve resections. The operative approach is discussed. The differentiation between this syndrome and ilio-inguinal nerve entrapment is tabulated.
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The response patterns of plasma cortisol and plasma free cortisol have been studied in 20 consecutive patients undergoing cardiac surgery involving the use of heart-lung bypass. Sixteen consecutive patients undergoing closed mitral valvotomy have been used as controls. Total plasma cortisol levels fell at the onset of extracorporeal circulation (ECC) and did not rise significantly throughout the period of ECC. The peak cortisol level in the bypass patients occurred at 24 hours postoperatively with elevated levels still present at 48 hours. This pattern was significantly different from the control patients (P less than 0.001) who exhibited the typical cortisol stress response pattern. Synthetic ACTH stimulation of the adrenal cortex during heart-lung bypass produced a positive response (i.e., a rise in plasma cortisol greater than 7.5 mug/100 ml) in all six patients studied while the six mitral valvotomy patients had no response to synthetic ACTH administration during operation (P less than 0.01). Plasma free cortisol estimations indicate that a rapid and significant rise in % free cortisol occurred at the onset of ECC, but that despite the rise in percentage free, the overall plasma free cortisol concentration (i.e., total plasma cortisol X % free) was significantly lower during ECC in the bypass patients when compared with control (P less than 0.01). Twenty-four hours postoperatively these concentrations were significantly higher in the bypass patients (P less than 0.001).
The effects of long-term administration of nafenopin, a potent hypolipidemic drug with marked hepatomegalic and peroxisome-proliferative properties, were studied in wild-type (Csa strain) and acatalasemic (Csb strain) mice. Nafenopin was administered in the diet at a concentration of 0.1% during the first 12 months and then at 0.05% until the termination of the experiment at 20 months. By 56 weeks, 100% mortality occurred in both male and female wild-type mice, whereas the mortality rate in acatalasemic mice was approximately 50%. Between 18 and 20 months of the experiment, 9 of 9 male and 12 of 12 female acatalasemic mice that survived chronic nafenopin treatment developed hepatocellular carcinomas, some of which metastasized to the lungs. None of the 15 male and 15 female acatalasemic controls developed liver cancers. Numerous peroxisomes were seen in the lung metastases of these hepatocellular carcinomas on electron microscopic examination; in contrast the number of peroxisomes in primary liver tumor cells varied considerably. The hepatocarcinogenicity of nafenopin strongly suggests the need for long-term studies with other hypolipidemic drugs that cause hepatomegaly and peroxisome proliferation to clarify the role, if any, of peroxisome proliferation in liver carcinogenesis.
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