Surgical treatment of aortic stenosis by valve replacement.
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Biomedical subjects
Publications and source records attributed to C Cochrane.
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Jaundiced Gunn rats, treated with phenobarbital (60 mg per kg i.p. for 7 to 10 days) showed 25 and 36% decreases in mean plasma bilirubin levels in two experiments (p less than 0.01). Kinetic studies with tracer 14C-bilirubin revealed that there was no change in bilirubin turnover or total pool size due to phenobarbital, but a 49% increase in the hepatic pool and a 27% decrease in the cutaneous pool of bilirubin. The increase in the hepatic pool accounted for over 90% of the bilirubin lost from the plasma. Such pretreatment with phenobarbital did not alter the decline in plasma bilirubin or total bilirubin pool due to subsequent phototherapy. Phenobarbital followed by phototherapy produced a significantly greater reduction in plasma bilirubin levels than either treatment alone. These studies demonstrate that phenobarbital does decrease plasma bilirubin in Gunn rats primarily by shifting the pigment to the liver, and suggests that combined treatment with phenobarbital and phototherapy might be of value in patients with congenital hyperbilirubinemia due to glucuronyl transferase deficiency.
The obese (C57BL/6J ob/ob) mouse is a commonly used animal model of non-insulin-dependent diabetes mellitus. Recent experiments have shown that stress hyperglycemia can be classically conditioned in the obese but not in the lean mouse. In the present study, classical conditioning of insulin secretion was attempted in C57BL/6J obese and lean animals. For 21 days, obese and lean mice were exposed to a conditioned olfactory stimulus prior to and during eating. On the 22nd day, blood was sampled for all animals following presentation of the conditioned stimulus; testing was repeated 2 weeks later following an additional 4 days of conditioning. Results indicated an effect of conditioning, with significantly greater plasma insulin for trained than for untrained obese mice. That insulin secretion can be more easily conditioned in the obese mouse suggests that a cholinergic mechanism may be involved in the hyperinsulinemia characteristic of this animal.
The genetically obese mouse (C57BL/6J ob/ob) is a commonly used animal model of non-insulin-dependent diabetes mellitus. These mice show exaggerated glycemic responses during behavioral stress and adrenergic stimulation, but the precise glucoregulatory mechanisms are not well characterized. The ob/ob mice have multiple endocrine abnormalities, including elevated pituitary and circulating beta-endorphin levels; and a relationship between hyperglycemia and altered opioid function has been suspected. We now report that opiate antagonism with naltrexone potentiates hyperglycemic responses during stress and epinephrine challenge in obese mice. This effect of opioid blockade suggests that endogenous opioids inhibit stress- and epinephrine-induced hyperglycemia in the genetically obese mouse.