[Hyperventilation syndromes in internal diseases. II. Hyperventilation syndrome (respiratory neurosis)].
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Biomedical subjects
Publications and source records attributed to S Filipecki.
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In order to relate urinary prostaglandin excretion in pheochromocytoma (Ph) to the pattern of noradrenaline (NA), adrenaline (A) and dopamine (D), 14 patients with this disease were investigated during normal sodium intake. 20 healthy volunteers served as controls (C). Urinary PGs were determined by RIA; NA, A and D were measured fluorometrically. In patients with elevated excretion of NA + A (n=3), NA alone (n=6) and D (n=5), urinary PGE2 was significantly (p less than 0.01) diminished respectively 367,4 +/- 143,6; 445 +/- 104; 440,4 +/- 125,2 pmol/24h in comparison to C/1075 +/- 165,4 pmol/24 h. On the other hand urinary excretion of PGF2 alpha was distinctly increased in patients with elevated NA + A, normal NA + A and elevated D respectively 6375 +/- 1697, 1035 +/- 217,8, 5070 + 1225 pmol/24 h and decreased in patients with elevated A 989 +/- 217,5 pmol/24 h in comparison to C/1886 +/- 255,7 pmol/24 h. It is concluded, that in patients with Ph PGs excretion is related to the pattern of catecholamines excretion. Low PGE2 excretion in most patients with Ph suggests that the physiological interrelationship between catecholamines and PGs is disturbed in this disease. High PGF2 alpha excretion may reflect enhanced activity of 9-ketoreductase PGE2 probably caused by an excess of catecholamines.
In view of the possible role of prostaglandins /PG/ in the pathogenesis of hypertension we have determined PGE2 and PGF2 alpha levels simultaneously with plasma renin activity/PRA/ in renal venous and caval venous blood in 13 patients with unilateral renal artery stenosis/RAS/ and in six untreated patients with unilateral parenchymal renal disease/PRD/. Four patients with essential hypertension were the control group. PG levels and PRA were estimated by RIA. In patients with RAS the mean PGE2 level as well as PRA was higher on the side of the stenosis. No such difference was found in the PGF2 alpha level. There was a significant correlation between the renal vein PGE2 ratio and renin ratio /stenotic side versus contralateral side/ r=0.520, 0.02 less than p less than 0.05. In patients with PRD prostaglandin levels in venous blood of the affected kidney were similar to that of venous caval blood, but markedly elevated in the venous blood of the contralateral kidney. PRA was similar on both sides. The data obtained in this study indicate, that prostaglandins in renal venous blood behave differently in hypertensive patients with RAS and PRD. In patients with RAS augmented PGE2 release may serve as a protective mechanism. In patients with PRD, the increased PG level in the non-affected kidney may reflect a compensatory mechanism in spite of the atrophic process in the affected kidney.
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