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Biomedical subjects

P Lindberg

Publications and source records attributed to P Lindberg.

At least 109 records · Page 6Linked to original sources
PubMed1977

Effects on rat liver acetaldehyde dehydrogenases in vitro and in vivo by coprine, the disulfiram-like constituent of Coprinus atramentarius.

Coprine, the disulfiram-like constituent of the mushroom Coprinus atramentarius was found to inhibit the low-Km dehydrogenase in rat liver and to increase the acetaldehyde level in blood during ethanol metabolism in vivo. Coprine did not inhibit the low-Km enzyme in vitro, but the hydrolytic product of coprine, 1-aminocyclo-propanol, was a potent inhibitor both in vitro and in vivo. A rapid onset of inhibition was observed after administration of coprine and the inhibition was long-lasting. It is suggested that 1-aminocyclopropanol is responsible for the inhibition caused by coprine in vivo.

Acetaldehyde↗
PubMed1975

Histochemical and electron microscopic studies of acute cardiomyopathy induced by restraint stress in pigs.

In 23 healthy crossbred pigs of Yorkshire and Swedish Landrace (body weight 85 to 90 kg), stress was produced by pharmacological restraint. Cardiac lesions were observed in all the experimental animals, but no alterations were seen in the 9 controls. The lesions consisted of focal myocardial necrosis with infiltration of mononuclear inflammatory cells. Histochemical stains for two dehydrogenases, cytochrome oxidase and unspecific esterase, were applied to fresh-frozen sections of heart muscle. The damaged muscle fibers exhibited initially an increase in formazan deposits, and then a decrease and total loss of enzymatic activity. A reduction or total loss of glycogen and accumulation of lipids were demonstrated in the damaged myocardium ultrastructurally. The mitochondria were swollen with focal loss of the cristae. They often exhibited electron-dense of diverse appearance. In degenerating cells, the myofilaments usually lacked the normal cross-striations whereas, in necrotic foci, the changes ranged from clumping to complete lysis of the myofilaments. The sarcoplasmic reticulum and the T system contained numerous dilated vesicles in cells with mitochondrial and myofibrillar damage. It was concluded that the myocardial alterations, following restraint stress, were caused by a reflex liberation of cardiotoxic catecholamines.

Animals↗