Experimental coronary artery occlusion. II. Spatial and temporal evolution of infarcts in the dog heart.
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Biomedical subjects
Publications and source records attributed to H Frenzel.
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The influence of a non-ketonic, chronically diabetic state (60 mg/kg streptozotocin) on cardiac function and metabolism was studied under in vivo conditions by inserting a Millar-tip catheter into the left ventricle and in the model of the isolated perfused heart. In vivo heart rate and maximal left ventricular systolic pressure were reduced after a diabetes duration of 4 and 12 weeks. The maximal rise and fall in left ventricular pressure progressively declined with the duration of diabetes. The reduced myocardial function was associated with a loss in ATP and adenine nucleotides. In the perfused heart of chronically diabetic rats, heart function was also impaired and could not be restored in vitro by perfusion with glucose and insulin. In the presence of octanoate--a substrate which can be metabolized independently from insulin--heart function of diabetic rats was improved, but remained lowered as compared to controls. Since the content of myocardial creatine phosphate was reduced in diabetic hearts perfused with octanoate, these findings indicate that the suppression of cardiac performance is not only a result of an impaired glucose metabolism, but of a more general defect in energy provision and utilization. In contrast to hearts of acutely diabetic, ketotic rats most often used, the rate of lipolysis of endogenous triglycerides and the contribution of fatty acids to energy production was low in the chronically diabetic state. Inhibition of fatty acid oxidation by an inhibitor of carnitine palmitoyltransferase (CPTI) did not restore the reduced responsiveness of diabetic hearts to insulin. Analysis of intracardiac metabolites revealed that in the perfused heart of chronically diabetic rats glucose-6-phosphate and citrate do not accumulate as in hearts of ketotic, diabetic rats. Therefore, the impaired glucose metabolism presumably reflects a reduced uptake of glucose rather than in inhibition of glycolysis as in hearts of ketotic, diabetic rats.
The effect of long-term GSH administration on aflatoxin B1 (AFB1)-induced carcinogenesis in the livers of male Wistar II rats was evaluated. No significant effect of an 11 months period of reduced glutathione (GSH) administration was observed concerning both the survival curve and the incidence of liver tumors. Liver tissues of all animals were bearing tumors or nodular lesions 24 months after AFB1 treatment, regardless of GSH treatment. The capacity of the GSH conjugation system was elevated in the liver tissue of AFB1-treated animals both by an increase of GSH content and an increase of the specific activities of several GSH S-transferase isoenzymes. Likewise the specific activities of GSH related enzymes as GSSG reductase and gamma-glutamyltransferase (gamma-GT) and the activity of the GSH independent detoxication system NAD(P)H:quinone oxidoreductase were increased in the AFB1-treated livers, there was no significant effect of GSH treatment. These results demonstrate that long-term GSH treatment has no effect on the survival of AFB1-pretreated male rats on the incidence of liver tumors and on the activities of drug metabolizing systems. The hepatic detoxication capacity 24 months after AFB1 treatment is elevated.
Face, mouth and jaws represent seldom localisations of metastatic lesions. 5-20% of these lesions are reported with localisation in the maxilla, whereas 90% are found in the mandibula. Metastatic tumours in the oral soft tissue are very rare. The most common primary tumour seems to be the renal cell carcinoma. Only histological examination can give a differentiation against benign tumours. The diagnostic and therapeutic management of a 46 years old woman with a metastatic intraoral lesion of a renal cell carcinoma is presented.
In 67 patients with giant cell arteritis (GCA) and 133 control patients, the value of eight clinical parameters and five laboratory findings for the diagnosis of GCA was analyzed. Out of the clinical parameters characteristic for GCA, headaches, visual disturbance, pains of the shoulder or hip regions and fever were of diagnostic value. Of the laboratory findings, only the BSR was of diagnostic value. Inappetence, exhaustion and fatigue, although characteristic of GCA, as well as blood count, alpha-globulins, CRP and alkaline serum phosphatase were of no value in differentiating between GCA and other diseases. Each of the valuable parameters increased the probability of diagnosing GCA from 33% (incidence of GCA in our patients) up to between 48% and 52%. The simultaneous evaluation of several parameters elevated the probability of diagnosing GCA to up to 88%. These results provide a basis for a rational decision in favor of or against biopsy of the temporal artery. In the case of a negative histology, they help to decide in favor of or against long term corticoid therapy.
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