[Questionable usefulness of the edrophonium test in the diagnosis of non-cardiac retrosternal pain]. / Utilité discutable du test à l'édrophonium dans le diagnostic d'une douleur rétrosternale non cardiaque.

Of 69 patients with non-cardiac chest pain, one third had abnormal esophageal motility as evidenced by basal esophageal manometry. 8 patients (12%) reported chest pain during a provocation test (edrophonium). While this pain seemed similar to the spontaneous chest pain described by 7 patients, it was not associated with manometric changes in 30% of these cases. The causal relationship between disorders of esophageal motility and non-cardiac chest pain has still to be confirmed, and caution must be exercised in interpreting edrophonium tests.

[Endoscopic sclerotherapy and esophageal varices]. / Sclérose endoscopique et varices oesophagiennes.

60 consecutive patients underwent sclerotherapy for hemorrhage from ruptured esophageal varices. Sclerosis was always started within the first 48 hours. 12 patients (20%) died during initial hospitalization, but only 5 from recurrent bleeding. Of 48 survivors, 22 (46%) did not rebleed during a mean 18-month follow-up, whereas 26 (54%) had recurrences, 27 of these bleeding episodes occurred early (within 4 months) and 17 late (mean 16.5 months). Eradication of the varices was achieved in 29 patients (60%) with a mean of 6.2 sessions and within a mean of 6 months. Of these 48 patients 2 have been lost to follow-up, 25 (52%) are alive after a mean follow-up of 29 months, and 21 (44%) died (though only 2 from variceal bleeding). The survival curve (Kaplan-Meier) of these 60 bleeders is 45% and 37% at 2 and 4 years respectively. Sclerotherapy caused no death and only minor adverse effects. These results confirm those in the literature. We advocate endoscopic sclerosis as first choice in the treatment of ruptured esophageal varices.

Dynamic response of PG synthesis to peptide hormones and osmolality in renal tubular cells.

A superfusion technique was adapted to collagenase-dispersed renal medullary and cortical tubular cells to study prostaglandin (PG) synthesis in response to arginine vasopressin (AVP), angiotensin II (ANG II), bradykinin (BK), Ca2+ ionophore A23187, and to changes in osmolality. Medullary and cortical cells promptly responded to the stimuli by an increase in PGE2 and PGF2 alpha production, whereas 6-keto-PGF1 alpha was not detected. AVP and BK were active on medullary cells, and ANG II was active mainly on cortical cells. A23187 stimulated PG synthesis in both cells but predominantly in the medulla. PG synthesis was dependent on the presence of extracellular Ca2+. The Ca2+ entry blocking agents verapamil and lanthanum did not inhibit the PG response to AVP, BK, and ANG II. Thus peptide hormone-stimulated PG synthesis in renal tubular cells did not depend on Ca2+ influx through channels blocked by these agents. Hyperosmolar NaCl or mannitol stimulated PG synthesis in cortical and, more markedly, in medullary cells. Hyperosmolar urea inhibited PGE2 synthesis stimulated by peptide hormones, NaCl, and A23187 in both cell preparations. In conclusion, the superfusion of isolated tubular cells is a useful method to study the dynamic aspects of renal PG release in response to various sequentially applied stimuli.

Effect of noradrenaline, vasopressin and angiotensin II on renal prostaglandins in man.

To examine the response of renal prostaglandins (PG) to systemic and renal vasoconstriction noradrenaline (NA), arginine vasopressin (AVP) and angiotensin II (ANG II) were each infused into eight healthy female subjects for 3 h on different days. Urinary excretion of PGE2, PGF2 alpha and 6-keto-PGF1 alpha was determined hourly. NA and ANG II stimulated excretion of PGF2 alpha significantly, but not of PGE2 or 6-keto-PGF1 alpha. AVP stimulated renal PGF2 alpha and 6-keto-PGF1 alpha significantly, but not PGE2. A weak correlation was found between urinary PGF2 alpha and diastolic blood pressure during NA and ANG II infusions, but not during AVP infusion. The release of renal PG does not appear to constitute an obligatory and concomitant response to the blood pressure rise induced by the pressor agonists. The greater response of PGF2 alpha than of PGE2 may result from a preferential direct effect on PGF2 alpha secretion or from an increased conversion of PGE2 into F2 alpha.