[Peridural lumbar anesthesia in hypertensives: the effect of immediate preanesthetic treatment with nicardipine].
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Biomedical subjects
Publications and source records attributed to C Landault.
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Animals and humans undergoing treatment with ciclosporin (CS) show a reversible increase in renal vascular resistance and a decrease in glomerular filtration rate. The causes of these abnormalities have not yet been established. We evaluated the effects of a 1-week treatment with CS on creatinine clearance, renal arachidonic acid metabolites, plasma renin activity (PRA), plasma aldosterone levels, urinary excretion and plasma levels of catecholamines in 7 patients with idiopathic uveitis. We show that CS treatment induces a significant (p less than 0.05) decrease in creatinine clearance (from 132 +/- 0.5 to 108 +/- 8 ml/min); urinary 6-keto-PGF1 excretion (from 17.8 +/- 4.9 to 10.9 +/- 3.3 ng/mmol creatinine), urinary thromboxane B2 excretion (from 7.0 +/- 1.0 to 3.6 +/- 0.9 ng/mmol creatinine), upright PRA (from 4.2 +/- 0.9 to 2.3 +/- 0.8) and supine PRA (from 2.0 +/- 0.5 to 1.1 +/- 0.3). We found no change in plasma aldosterone levels and plasma levels and urinary excretion of catecholamines. We suggest that the reversible renal vasoconstriction observed in patients treated with CS may be induced by inhibition of renal prostacyclin synthesis. In this setting inhibition of PRA and angiotensin II formation may impair autoregulation of effective filtration pressure and therefore glomerular filtration rate.
Plasma epinephrine, norepinephrine, and dopamine responses were studied in insulin-dependent diabetic patients at rest, on standing and during insulin-induced hypoglycemia. beta-Adrenergic sensitivity was evaluated by the isoproterenol sensitivity test. Five men who had adrenergic symptoms during hypoglycemia and no severe hypoglycemic accidents (coma, seizures) (group A) and five men who had repeated severe hypoglycemic accidents but lack of adrenergic symptoms of hypoglycemia (group B) were studied. The mean resting plasma epinephrine was lower in group B (147 +/- 22 pmol/L, SEM) than in group A (398 +/- 98 pmol/L, P less than 0.02). On standing plasma epinephrine increased significantly in both groups. During hypoglycemia blood glucose decreased identically in the two groups; plasma epinephrine and norepinephrine increased significantly and to the same extent in both groups; the mean maximal heart rate was significantly greater in group A than in group B. Isoproterenol sensitivity (defined as the dose of isoproterenol required to increase heart rate by 25 beats/min) was lower in group B (5.87 +/- 1.12 micrograms) than in group A (2.37 +/- 0.22 micrograms, P less than 0.01). The group B patients had significantly fewer hypoglycemic symptoms during insulin-induced hypoglycemia than did group A patients. We conclude that decreased beta-adrenergic sensitivity contributes to the lack of adrenergic symptoms of hypoglycemia in insulin-dependent diabetic patients.
Plasma concentrations of atrial natriuretic factor (ANF), catecholamines (adrenaline, noradrenaline, dopamine) and aldosterone, and plasma renin activity (PRA) were measured in a group of 20 patients with moderate to medium heart failure (NYHA class II 7 patients, class III 13 patients), 24 hours after treatment was discontinued. Compared with a control group, plasma concentrations of ANF (p less than 0.01), noradrenaline (p less than 0.05), aldosterone (p less than 0.01) and PRA (p less than 0.01) were significantly increased. There was a significant difference between class II patients and class III patients in plasma ANF (p less than 0.01) and noradrenaline (p less than 0.02) concentrations, but not in PRA and aldosterone levels. A significant correlation was observed between plasma ANF concentration and left ventricular end-diastolic pressure (r = 0.68, p less than 0.001), pulmonary arterial pressure (r = 0.59, p less than 0.01), pulmonary capillary pressure (r = 0.51, p less than 0.02), cardiac index (r = 0.46, p less than 0.05) and left ventricular end-diastolic volume (r = 0.50, p less than 0.05). However, ANF concentration was not correlated with mean right atrial pressure. Plasma adrenaline concentration correlated with systemic arterial resistance (r = 0.80, p less than 0.001), pulmonary arterial pressure (r = 0.57, p less than 0.02), mean pulmonary capillary pressure (r = 0.62, p less than 0.001), cardiac index (r = 0.53, p less than 0.05) and left ventricular end-diastolic pressure (r = 0.58, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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The authors report a series of 11 patients who consulted or were admitted to a hospital medical unit for organic symptomatology, especially hypertensive, diagnosed as panic attacks based on the criteria of the DSM III. Cardiovascular symptoms were dominant in 10 out of the 11 patients. In 7 cases, the symptoms were very suggestive of pheochromocytoma. Treatment based on tricyclic antidepressive drugs associated with behavioural therapy in 5 cases, led to the total regression of acute panic attacks in 9 out of 11 patients with a follow-up period ranging from 1 to 2 years. However, it did not prevent 2 of the patients from developing a chronic anxiety state. After reviewing the principal clinical features of panic attacks, the authors discuss their underlying physiopathological mechanisms. The results of catecholamine metabolic studies in 2 out of 3 patients suggest the possible role of an inhibitor of catecho-o-methyl-transferase, but this requires confirmation by further studies. Panic attacks are very prevalent in the general population (2 to 5 p. 100). The diagnosis must be born in mind to avoid long and costly investigations, and for specific treatment to be instituted. The main risk is the development of chronic severe morbidity with serious socio-familial consequences.
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The biochemical diagnosis of pheochromocytoma is essentially based on the plasma and urinary levels of catecholamines and their derivatives, the metanephrines and vanyl-mandelic acid. The advantages and disadvantages of these investigations are reviewed, especially as regards the specificity and sensitivity of each test. The measurement of urinary metanephrine is the best test as its excretion is relatively higher, and it is rarely normal. The measurement of plasma catecholamines is more difficult but gives satisfactory results, but experience so far is limited.
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