Takayasu arteritis in Israel.
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Biomedical subjects
Publications and source records attributed to T Rosenthal.
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OBJECTIVE: The purpose of this study was to measure the circulatory levels of endothelin-1 in the serum of pregnant women with hypertension. STUDY DESIGN: Endothelin-1 levels were measured by means of radioimmunoassay in the serum of 26 pregnant women with hypertension (14 with pregnancy-induced preeclamptic toxemia, 12 with chronic hypertension) and in the serum of 17 control pregnant women and 18 control nonpregnant women. The mean levels in the different groups were subject to statistical analysis with the analysis of variance. RESULTS: The mean level among the women with preeclampsia (29.9 +/- 13.2 fmol/ml) was significantly higher than those of the chronically hypertensive women (16.1 +/- 7.3 fmol/ml, p = 0.002) and of the control pregnant women (19.7 +/- 9.2 fmol/ml, p = 0.011). The mean level of the control nonpregnant women (26.9 +/- 9.3) was significantly higher than that of the control pregnant women (p = 0.029). Among the patients with preeclampsia there was no correlation between endothelin-1 levels and the mean arterial blood pressure. Six to 10 weeks after delivery the mean levels of 15 studied patients (7 with preeclampsia, 8 with chronic hypertension) were similar to the levels of the nonpregnant control women. CONCLUSION: We conclude that increased endothelin-1 production may play a role in the pathogenesis of preeclampsia.
The insulin sensitivity of five essential hypertensive patients was compared to five patients with renovascular hypertension, five patients with primary hyperaldosteronism, and five normotensive subjects, using the euglycemic hyperinsulinemic clamp technique. Essential hypertensive patients had significantly lower insulin sensitivity than patients with hyperaldosteronism and renovascular hypertensive patients (P = .0066, P = .004, respectively). Hyperaldosteronism patients also had less insulin sensitivity than renovascular hypertensive patients (P = .016). A significant negative correlation was found between body mass index and insulin sensitivity index for essential hypertension patients only (r = -0.87, P less than .003). No such correlation was found in the secondary hypertension patients. The findings suggest a causal relationship between insulin resistance and the development of essential hypertension. Secondary hypertension, on the other hand, is not such an insulin resistant state.
Adrenalectomized, spontaneously hypertensive rats (SHR) were used to test the hypertensinogenic property of recently synthesized 18,19-dihydroxycorticosterone (18,19-Di-OH-B). The steroid was given via Alzet miniosmotic pump, with and without aldosterone. Neither 18,19-Di-OH-B (5 micrograms) nor aldosterone (5 micrograms) increased blood pressure in SHR when given alone; when administered together they resulted in a significant rise in blood pressure. Results indicate a high probability that certain mineralocorticoids, which are inactive by themselves, might play a role in the etiology of hypertension when acting together under physiological conditions.
BACKGROUND AND METHODS: Emergency endotracheal drug administration has become an acceptable route for drug delivery during cardiopulmonary resuscitation. The purpose of the present study was to determine whether the site of endotracheal epinephrine injection is an important factor in its absorption. Epinephrine (1:1000), in a dose of 0.02 mg/kg diluted in 2 mL of saline, was given to ten anesthetized mongrel dogs. Each dog was studied twice: once when the epinephrine was injected into the endotracheal tube, and on another day, through the endotracheal tube via a flexible catheter wedged into a peripheral bronchus. Arterial blood samples for plasma epinephrine concentration determinations were collected, before and at 1, 2, 5, 10, 15, and 30 mins after each intratracheal drug administration. RESULTS: Both routes of epinephrine administration significantly increased plasma concentrations within 1 min of injection. Higher plasma epinephrine concentrations were achieved after peripheral bronchial epinephrine administration (maximal concentration 8.9 +/- 3.2 vs. 2.0 +/- 0.4 ng/mL), and the total dose absorbed was significantly (76.5 +/- 13.5 vs. 36.7 +/- 6.5 ng/min/mL, p < .05) higher. The time interval to reach maximal concentration was significantly shorter with the peripheral bronchial dosing than with the endotracheal route (1.3 +/- 0.2 vs. 2.7 +/- 0.5 min, p < .05). Neither group demonstrated a significant change in heart rate, and both had similar, minor decreases in BP for > 2 to 5 mins. There were no significant differences between the arterial blood gases of the two groups at various stages of the experiment. CONCLUSIONS: In dogs, epinephrine administered via the peripheral bronchial route has a clear pharmacologic advantage over the endotracheal route. This advantage may be more important during cardiopulmonary resuscitation conditions and other low flow states, and may account for the failure observed with the endotracheal route in recently published clinical reports.
OBJECTIVE: To examine the relation between plasma atrial natriuretic peptide (ANP) and the natriuresis of fasting. DESIGN: ANP, aldosterone and renin were examined during natriuresis of fasting in 25 obese essential hypertensive patients and nine overweight normotensive subjects placed on a supervised 500-KCal diet composed of 50% carbohydrates, 30% fat and 20% protein, and unlimited salt. Twenty-four-hour urinary electrolytes were measured on days 0, 4, 7 and 10 of the diet. RESULTS: Urinary sodium concentration nearly doubled in the patients on day 4, and increased 1.4-fold in the normotensive controls. Plasma ANP rose nearly threefold in the hypertensives on day 4 and nearly doubled in the normotensives. Patients and controls showed similar patterns of natriuresis and ANP secretion during the diet. CONCLUSIONS: We conclude that there is a clear association between ANP levels and natriuresis of fasting.
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A patient with epilepsy controlled by carbamazepine developed a carbamazepine neurotoxic reaction after being given an increased dosage of diltiazem hydrochloride as adjunctive therapy. Abrupt withdrawal of diltiazem reduced the circulating carbamazepine concentration and resulted in an epileptic attack. Awareness of the interaction between diltiazem and carbamazepine and careful monitoring of carbamazepine blood levels is recommended to prevent the dangerous neurotoxic effect associated with this combination.
BACKGROUND: This study was undertaken to identify whether diabetes mellitus (DM) accelerates the development of left ventricular hypertrophy (LVH) in hypertensive patients. METHODS: Cardiac structure, systolic function, and hemodynamics were evaluated by two-dimensional M-mode echocardiography in diabetic and nondiabetic patients with essential hypertension. RESULTS: Patients with hypertension with and without DM had the same end-systolic and end-diastolic dimensions, cardiac output, total peripheral resistance, and ejection fraction. Diabetic hypertensive patients had greater interventricular septum (1.32 +/- 0.20 vs 1.07 +/- 0.20 cm) and posterior wall (1.20 +/- 0.20 vs 1.00 +/- 0.10 cm) thickness than did nondiabetic hypertensive patients. Consequently, left ventricular mass index was greater in patients with hypertension and DM than in those without DM (158 +/- 45 vs 113 +/- 20 g/m2). With the use of Devereux criteria for recognition of LVH (left ventricular mass index above 134 g/m2 in men and above 110 g/m2 in women), 72% of the diabetic patients had LVH, whereas only 32% of the nondiabetic patients had LVH. Left ventricular contractility, as reflected by the ratio of end-systolic wall stress to end-systolic volume index, was decreased in diabetic compared with nondiabetic hypertensive patients. CONCLUSIONS: The data suggest that DM accelerates the development of LVH in patients with essential hypertension independent of arterial pressure and, therefore, may contribute to the increased cardiovascular morbidity and mortality in patients with hypertension.
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Fine-needle aspiration biopsy (FNAB) was performed in 41 renal transplant patients to assess its value in the diagnosis of the cause of graft dysfunction. The procedure was used on 71 occasions, and in each case a clinical diagnosis was made and compared with the cytological diagnosis made independently by a pathologist. When available, core biopsy histopathology was used to confirm the final diagnosis. Fifty-seven (80%) of the aspirates yielded adequate material. A clinical diagnosis of acute cellular rejection (ACR) was made in 21 patients, 18 (78%) of whom showed confirmatory immune activation on FNAB. The clinical diagnosis of either acute tubular necrosis (ATN) or cyclosporine toxicity was confirmed in 31 (91%) of 34 aspirates. In eight aspirates, the cytological diagnosis was different than that made clinically. Humorally mediated vascular rejection, and lymphocytosis secondary to causes other than rejection, such as viral infection, were considered as possible causes of this discrepancy. Provided that adequate samples are obtained. FNAB is valuable in the clinical management of renal transplant patients. Its accuracy should not be overestimated and the results obtained should be evaluated in the light of the overall clinical picture.
Atrial natriuretic peptide (ANP) was examined in 20 diabetic patients: 10 patients referred from the emergency room with severe hyperglycemia, (Group A), and 10 patients with uncontrolled diabetes referred by the outpatient clinic (Group B). Seven patients from Group A reached the nadir of less than 10 pg/ml, and three reached 12-16 pg/ml; following equilibration of sugar level, mean ANP level rose to 51.4 pg/ml (SD +/- 5.6). In Group B mean ANP level before treatment was 19.2 pg/ml +/- 11.4, and after diabetes control reached 40.4 pg/ml (SD +/- 10.04). Findings demonstrate a significant decrease in ANP in the acute hypoglycemic state, and a return to normal levels when sugar is controlled and hypovolemia corrected. Patients with chronic hyperglycemia exhibit compensation of intravascular volume. It seems that the equilibration system functioning via ANP is highly sensitive as a result of acute changes in total body fluid, and becomes desensitized during chronic disequilibrium.
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