Somatostatin in paroxysmal supraventricular and junctional tachycardia.
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Biomedical subjects
Publications and source records attributed to G Ghirlanda.
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The effect of secretin on insulin release has been studied in normal subjects after prestimulation with arginine. In order to make a comparison a pulse of glucose with arginine prestimulation was given. A pulse of 1 U/kg b.w. of secretin provokes a secretion of insulin that is weak and brief compared to that provoked by glucose; thus secretin fails to potentiate arginine-induced insulin secretion. Such a result does not support the hypothesis of secretin as the central hormone in the enteroinsular axis.
Glucose, C-peptide and insulin concentrations in amniotic fluid were measured in 63 women, 19 of whom had insulin-dependent diabetes. The amniotic fluid glucose concentration was higher in the diabetic (37.4 +/- 4.1) than in the normal women (19.4 +/- 5.1 mg/dl; P less than 0.01). The amniotic fluid insulin concentration was higher in diabetic than non diabetic women (15.9 +/- 3.1 versus 8.9 +/- 2.1 microU/ml; P less than 0.01). The C-peptide concentration was also higher in the amniotic fluid of diabetic women than normal (1.60 +/- 0.66 vs 0.26 +/- 0.15 nmol/l; P less than 0.001). The lecithin/sphingomyelin (L/S) ratio in the amniotic fluid was greater than 2 in 61 mothers; only two diabetic patients had an L/S ratio lower than 2. Five neonates of diabetic mothers were macrosomic and three of these were also hypoglycaemic. A negative correlation was observed in diabetic women between insulin and C-peptide concentrations in the amniotic fluid and Apgar score of the newborn infants both at 1 and 5 minutes; no correlation was found on the contrary with the amniotic glucose. In the prognostic evaluation of the fetus with a diabetic mother one must consider many parameters. Among these more consideration must be given to the levels of C-peptide and insulin in amniotic fluid than to glucose level.
A case of fibrolamellar carcinoma (FLC) in a noncirrhotic liver of a 20-year-old man is described. Gross features and the presence, among the tumor cells, of bile ducts, of thick-walled blood vessels and nerves, and, ultrastructurally, of myofibroblast-like cells are the most significant findings, suggesting that FLC is the malignant counterpart of focal nodular hyperplasia with oncocytic change. Histochemical and immunohistochemical methods demonstrate the presence inside the oncocytic tumor cells of copper, copper-binding protein, and alpha 1 antitrypsin. The pathogenesis and the significance of these findings then are discussed and related to the restricted capacity of oncocytic cells to fulfill normal cellular function.
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The physiopathology and clinical picture of hyperosmolar diabetic coma are described, and four personal cases are presented. This form of coma is a rare, but particularly serious complication of diabetes mellitus. Since its prognosis is poor, even when suitable treatment is provided, the greatest possible care should be devoted to preventing its main cause, namely dehydration.
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The adult respiratory distress syndrome in major complication of hospitalized patients. The therapeutic role of intravenous albumin, diuretics, corticosteroids and oxygen administration is yet doubtful. The Authors, after a description of pathogenetic, histological and clinical aspects of the syndrome, report a case occurred at their observation; it is showed the important role of intravascular coagulopathy and reversible ECG alterations, and the therapeutic valve of positive end-expiratory pressures (PEEP).
Serum gastrin and lower esophageal sphincter (LES) responses to somatostatin infusion were evaluated in ten normal subjects and in nine achalasic patients in order to determine evidence of hormonal (presumably gastrin)control of LES pressure. After somatostatin infusion, a significant decrease of serum gastrin was observed in normal subjects at 30 min (81.6 +/- 3.2 versus 40.0 +/- 4.7 pg/ml; p less than 0.01) and a rapid increase of LES pressure was also observed (26.0 +/- 1.3 versus 34.1 +/- 1.6 mmHg; p less than 0.01). In achalasia no change was observed in serum gastrin concentration after somatostatin infusion. LES pressure at 20 min however significantly decreased (45.8 +/- 7.6 versus 31.6 +/- 2.3 mmHg; p less than 0.05). Endogenous gastrin is not a major control factor for LES pressure in either normal or achalasic subjects.
Some physiological digestive processes thought to be under the control of VIP-ergic neurones are presented. The etiological role of the Vasoactive Intestinal Polypeptide in the Verner Morrison syndrome is discussed.
Irreversible lactic acidosis occurred in two phenformin-treated diabetics. In the first case, blood creatinine was 3 mg % ml, arterial blood pH was 7,12 and ketostix was negative; in the second case, blood creatinine was 1,3 mg% ml, arterial blood pH was 7,22 and ketostix was negative. Diabetic patients to be treated with phenformin must always be carefully selected and this treatment should be reserved for cases where there is a precise indication. Lactic acidosis may occur even in the presence of almost normal serum creatinine concentrations.
The literature on the possible implications of the Vasoactive Intestinal Polypeptide (VIP) in the digestive processes is widely and critically reviewed. Special attention is directed to the likely function of the polypeptide as a neurotransmitter in the gastroenteropancreatic system.
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Chenodeoxycholic and ursodeoxycholic acids reduce significantly the hepatic synthesis of lipids in rats. The present study has been carried out using (1-14C)acetate and evaluating its incorporation into different lipidic fractions of the liver by thin-layer radiochromatography. Ursodeoxycholic acid proved to be more active than chenodeoxycholic acid: in addition to a significant decrease of the hepatic incorporation of the acetate into cholesterol and triglycerides an increase of the hepatic incorporation of the acetate into phospholipids has been observed. The exogenous administration of bile acids diminishes the hepatic synthesis of cholesterol and therefore its biliary excretion; it enriches the bile acid and phospholipid pool in the liver and bile. By this way the action of bile acids establishes in the liver a condition which induces such an increase of availability of mixed micelles in the bile as to make it unsaturated in cholesterol.
The effect of low-dose insulin infusion (4.8 U/h) in diabetic ketoacidosis was compared to that of low-dose insulin infusion (4.8 U/h) plus somatostatin (500 microgram/h IV). Treatment with insulin only in 20 patients caused normalization of blood glucose levels within 6 hours and resolution of ketoacidosis within 5 hours. During insulin plus somatostatin infusion in 7 patients, blood glucose levels returned to normal within 4 hours and acidosis was reduced within 3 hours. Correction of acidosis is the most important problem in diabetic ketoacidosis: in the severest cases cardiovascular and cerebral complications may ensue. The data presented show that addition of somatostatin to treatment with low doses of insulin reduces and resolves acidosis in a shorter time while plasma levels of glucagon and GH were concomitantly reduced.
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