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Biomedical subjects

P Simard

Publications and source records attributed to P Simard.

At least 55 records · Page 3Linked to original sources
PubMed1976

Rectal biopsy in type 4 glycogenosis. An ultrastructural cytochemical study.

Rectal biopsy material from a patient with type 4 glycogenosis was studied by ultrastructural cytochemical methods. The diagnosis of the disease was made on the basis of the patient's clinical history, the autopsy findings, and the histopathological features. Numerous large macrophages were observed in the rectal mucosa. They contained large vacuoles filled with filamentous material and small granules. This amylopectin was stained by the Thiery method (periodic acid-thiocarbohydrazide-silver proteinate) after 18 hours of exposure to thiocarbohydrazide; only 30 minutes was sufficient to demonstrate seemingly normal beta-glycogen particles in epithelial cells.

Autopsy↗
PubMed1974

On the mechanisms responsible for selection of hepatic veins as target for thrombosis following injection of endotoxin in hyperlipemic rats.

The feeding of a butter-rich diet, to sensitize rats for studying the phenomenon of hepatic vein thrombosis, is shown to produce severe liver steatosis leading to a sinusoidal barrage and portal hypertension. The portal pressure in these animals was 210 +/- 4 mm of saline, as compared to 113 +/- 3 mm in the normal rat. Blood circulation studies using carbon suspensions revealed production of a vascular stasis in the hepatic veins after 60 to 90 minutes, when endotoxin (Salmonella typhosa, 0.3 mg/kg) is introduced into the blood circulation to initiate hepatic vein thrombosis. Similar results were observed after 15 minutes with ellagic acid (1 mg/kg/min). The stasis was found in connection with an additional intrahepatic resistance to blood flow as evidenced by a rise in portal pressure and by a reduction in liver perfusion in relation with development of systemic hypotension. In contrast with this, endotoxin initiated only slight and transient changes in the normal rat. Thrombosis immediately followed production of stasis in the hepatic vein, whether the phenomenon was initiated by endotoxin or ellagic acid. Furthermore, inhibition of the vascular stasis of alpha-adrenergic blockade (phenoxybenzamine, 3 mg/kg) was accompanied by prevention of hepatic vein thrombosis. It is concluded that stasis in the hepatic veins resulting from a mechanical obstruction of the circulation by steatosis and by an additional reduction in blood flow initiated by endotoxin, is responsible for selection of hepatic veins as targets for thrombosis following injection of endotoxin in hyperlipemic rats.

Animals↗