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Biomedical subjects

M Ravid

Publications and source records attributed to M Ravid.

At least 127 records · Page 7Linked to original sources

Effects of oxprenolol versus propranolol on myocardial performance and myocardial O2 consumption in hypertensive patients.

The purpose of the study was to compare the effects of oxprenolol, a beta-adrenergic blocking agent with intrinsic sympathomimetic activity, to propranolol, a beta-blocker without intrinsic sympathomimetic activity, on myocardial performance and myocardial O2 consumption (MVO2). Myocardial performance was reflected by the systolic time intervals (STI) and MVO2 by the triple product of heart rate X left ventricular ejection time X systolic blood pressure (HR X LVET X SBP). The trial, a double-blind cross-over study, included 32 hypertensive patients, 17 males and 15 females, with a mean age of 50.9 years. The patients were divided into two groups: group A - 16 patients who were treated with effective antihypertensive doses of oxprenolol and diuretics (Esidrex K) for the first 8 weeks (period I) and with similar doses of propranolol and diuretics for the following 8 weeks (period II); Group B - the same number of patients who received the same drugs in the reverse order. All patients were examined during both periods at 2- and 3-week intervals, blood pressure and heart rate were recorded, and patients were provided with the appropriate study medication. At the end of periods I and II, myocardial function was assessed on the basis of STI, and MVO2 was evaluated on the basis of the triple product of HR X LVET X SBP. Four measurements of STI and MVO2 were carried out for each patient at the end of periods I and II: prior to intake of medication and 1 1/2, 3 and 4 1/2 h after intake of medication.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗

Prolonged dimethylsulphoxide treatment in 13 patients with systemic amyloidosis.

Continuous oral dimethylsulphoxide (DMSO) treatment (7-15 g/day) was given to 3 patients with amyloidosis of familial Mediterranean fever (FMF), 3 patients with idiopathic amyloidosis, and 7 patients with secondary amyloidosis. The nephrotic syndrome and various degrees of renal insufficiency were the major clinical manifestation in all case. Renal function was used as the main parameter for evaluation of therapy. DMSO treatment for 7-16 months produced no effect in the FMF patients and in the patient with idiopathic amyloidosis; they all ran the predictable clinical course of their disease and either died of cardiac failure or have been maintained on chronic haemodialysis. In the 7 patients with secondary amyloidosis an unequivocal improvement of renal function was observed following 3-6 months of DMSO treatment. It was shown by a 30-100% rise of creatinine clearance and a decline in proteinuria. This new equilibrium has been maintained as long as DMSO was administered. No serious side effects of DMSO wee encountered. Mild nausea and an unpleasant breath odour were the patients' main concern. We conclude that a therapeutic trial with oral DMSO is warranted in all patients with secondary amyloidosis. This treatment is unpleasant but bears no exceptional risks. It may significantly prolong life, though its effect on amyloid deposits themselves is doubtful.

Adult↗

Degradation of amyloid by a serum component and inhibition of degradation.

ADA of human serum was demonstrated and investigated with an agar gel diffusion technique using amyloid-impregnated agar plates. Sera of 20 healthy adults, 40 patients with AA-amyloidosis, and 86 nonamyloidotic patients were tested. The presence of an ADF, showing enzymatic properties and strongly bound to albumin, was demonstrated in normals and amyloidotic and nonamyloidotic patients. ADA in the serum of amyloidotic and cirrhotic patients was markedly decreased due to the presence of an inhibitor of ADF. ADA of amyloidotic sera was restored to normal by EDTA, citric acid, and ascorbic acid. The ADA of 16 FMF patients and four of 34 patients with rheumatoid arthritis without amyloidosis was intermediate between normal and amyloidotic values, indicating the presence of lADF at low concentrations in these patients. These findings suggest that amyloid is a normal protein metabolite, possibly with a high metabolic turnover. Accumulation of amyloid may be caused by decrease of the ADA of the serum by its inhibitor, rather than by accelerated production.

Adult↗

Recurrent venous thrombosis: the sole manifestation of an occult myeloproliferative disease.

A myeloproliferative disorder manifested by thrombocytosis, a high leukocyte alkaline phosphatase (LAP) score and an increased red blood cell mass was found in a 64-yr-old woman. During the previous 15 yr, recurrent venous occlusions had taken place, necessitating the resection of ischemic bowel segments and leading to extrahepatic portal venous obstruction. Numerous blood counts obtained during repeated hospitalizations were normal, and these thrombotic events remained unexplained. The sequence of events strongly suggests that the myeloproliferative disorder existed in an occult form during these years and was responsible for the venous occlusions. The possibility of a "smoldering" myeloproliferative disorder should be considered in patients with otherwise inexplicable thrombotic phenomena.

Female↗

Effect of chronic and acute changes in sodium balance on the urinary excretion of prostaglandins E2 and F2 alpha in normal man.

1. The effects of changes in sodium balance on renal prostaglandins have been hitherto studied mainly in experimental animals and the results have been controversial. In this study the 24 h urinary excretion of prostaglandins E2 and F2 alpha was measured by radioimmunoassay in seven normal subjects under basal conditions and after 5 days of a diet containing less than 20 mmol of sodium/day. Subsequently a sodium chloride (150 mmol/l: saline) load (300 mmol of sodium over 4 h) was infused and prostaglandins were again measured in hourly urine collections. Plasma renin activity and aldosterone were also measured under basal conditions, after the low sodium diet and at 2 and 4 h of the saline infusion. 2. Dietary sodium restriction was associated with a marked increase in prostaglandin E2 excretion (from 769.7 +/- 201.6 SEM to 1761.3 +/- 304.9 ng/24 h, P less than 0.0005). Prostaglandin F2 alpha also increased from 1187.0 +/- 390.1 to 1435.6 +/- 344.6 ng/24 h, but this was not statistically significant. The prostaglandin E2/prostaglandin F2 alpha ratio increased from 0.83 +/- 0.2 to 1.52 +/- 0.34 (P less than 0.01). Plasma renin activity and aldosterone rose significantly (P less than 0.05 and less than 0.0025 respectively). 3. During the saline load prostaglandin E2 decreased after 2 h from 142.4 +/- 29.9 to 86.7 +/- 22.9 ng/h (P less than 0.05) and to 36.9 +/- 5.96 ng/h after 4 h. Prostaglandin F2 alpha decreased at a slower rate, from 98.4 +/- 18.7 to 37.5 +/- 8.8 ng/h at 4 h (P less than 0.02). At 4 h the prostaglandin E2/prostaglandin F2 alpha ratio returned to control values (0.90 +/- 0.17). Plasma renin activity and aldosterone decreased significantly after 2 h (P less than 0.02 and less than 0.0025 respectively) and reached control values after 4 h. 4. The present study demonstrates that chronic and acute changes in sodium balance induce changes in the excretion of prostaglandin E2 parallel to changes in plasma renin activity and aldosterone. The similar but quantitatively smaller changes in prostaglandin F2 alpha and the inversion of the ratio between the two prostaglandins during sodium deprivation suggest that at least two factors are involved: increased delivery of substrate for prostaglandin synthase and decreased activity of the prostaglandin E1 9-keto-reductase. Prostaglandins probably play an important role in the adaptation of the kidney to changes in sodium balance.

Adult↗

Alleviation of experimental ischemic acute renal failure by dimethyl sulfoxide.

Acute, ischemic renal failure was induced in rats by clamping of the renal vessels for 1 h. Following the termination of the ischemic period 5 g/kg of dimethyl sulfoxide (DMSO) were administered intravenously as a 20% solution in saline. Control animals received normal saline. There were not deaths among the DMSO-treated animals. Urine flow began within 15 min of DMSO infusion. 24 h after the experiment the mean blood urea was 73 +/- (SEM) 14 mg/100 ml (n = 29). All the control rats died during the week following the experiment. The mean blood urea at 24 h was 276 +/- 18 mg/100 ml (n = 20). In 10 additional animals perfusion of the kidney with DMSO prior to the closure of renal vessels protected the organ from ischemic damage. These experiments have a bearing on the therapeutic approach to ischemic renal failure in man, and on preservation methods of donor kidneys for transplantation.

Acute Kidney Injury↗

The watery diarrhea syndrome with hypercalcemia--a symptomatic response to phosphate buffer.

Two patients with the watery diarrhea, hypokalemia, achlorhydria syndrome are described. Both had hypercalcemia, hypophosphatemia and suppressed parathyroid hormone activity. On repeated occasions the diarrhea was controlled by oral or intravenous phosphate buffer. An exhaustive search by sophisticated non-invasive methods and by celiac arteriography failed to demonstrate a pancreatic tumor. Yet, in both cases fairly large pancreatic non-beta-cell adenomas were found at laparotomy. The removal of these tumors was followed by complete recovery.

Adenoma↗

Recurrent post-partum gastroenteritis with eosinophilia.

A young woman experienced twice in eight years acute, self-limited episodes of gastroenteritis with marked eosinophilia, each one associated with or triggered by a normal delivery. This patient had a normal gastric mucosal biopsy, thus lacking one of the major criteria required by previous authors for the definition of eosinophilic gastroenteritis. Nevertheless, it is our belief that this case does represent a milder and more benign form of the very same syndrome, associated in a dubious way with labour.

Eosinophilia↗

The role of polymorphonuclear leucocytes and T lymphocytes in experimental murine amyloidosis.

Washed cells, from ascitic fluid, which contained predominantly polymorphonuclear leucocytes from casein treated donor mice, induced accelerated amyloid formation in untreated syngeneic recipient animals. A similar transfer model, with lymph node cell suspension, was ineffective. Amyloidogenesis was completely blocked by colchicine treatment of the donors while treatment of the recipients had no effect. A casein induced amyloidogenic stimulus was transferred from nude C3H mice to their normal littermates. When the order was reversed, no amyloidosis occurred in the nude recipients. These experiments indicate the possible involvement of two cells in the biphasic process of casein induced murine amyloid formation: the polymorphonuclear leucocyte in the first phase and the T lymphocyte in the second.

Amyloidosis↗

Bizarre urologic manifestations of pancreas carcinoma.

A 62-year-old patient presented with fever and abdominal pain. Urinary retention and bilateral hydronephrosis were caused by bladder malfunction due to infiltration of the bladder wall by metastases from a carcinoma of the head of the pancreas. Both ureters were free. A previous choledochoduodenostomy prevented the development of jaundice.

Carcinoma↗

Electrocardiographic observations on the termination of supraventricular tachycardia by verapamil.

The effect of intravenous verapamil on the termination of supraventricular tachycardia (SVT) was studied by continuous electrocardiographic monitoring of 27 episodes of SVT. Progressive increase of the cycle length heralded conversion in eight episodes while cycle-length alternation preceded cessation of the arrhythmia in 13 episodes. In five patients the arrhythmia was either stopped or closely followed by a ventricular premature beat (VPB), followed by further VPBs in three. Runs of bizarre ventricular tachycardia followed initial sinus-beats in two patients. Sinus standstill, lasting 30 seconds, was observed in one patient. The first post SVT beats had an aberrant QRS configuration with a normal P-R interval in four cases and an aberrant QRS complex with a short P-R interval, resembling Wolff-Parkinson-White complexes, in a further seven patients. The possible mechanisms causing this variability of pre- and post-conversion period are discussed. It is suggested that some aspects of verapamil action may be explained by a parasympaticomimetic effect on the myocardium.

Adult↗