Prostaglandin synthesis inhibition stimulates lithium reabsorption in Henle's loop in rats

Tachyphylaxis to aerosolized histamine was studied in dogs anesthetized with thiamylal after pretreatment with prostaglandin synthesis inhibitors. Three consecutive histamine dose-response curves were obtained in nine dogs pretreated with 5 mg/kg indomethacin; two of these nine were also pretreated with 10 mg/kg indomethacin. Seven of the nine dogs were pretreated with 4 mg/kg sodium meclofenamate; four of these seven were also pretreated with 12 mg/kg. All dogs had tachyphylaxis at high concentrations of histamine regardless of inhibitor used. Pretreatment with indomethacin while the dogs were under alpha-chloralose-urethan anesthesia gave similar results. Histamine tachyphylaxis was also studied both in the presence and in the absence of indomethacin in tracheal smooth muscle strips obtained from seven additional dogs. A decrease in the median effective dose to histamine was observed in the indomethacin-treated strips, but tachyphylaxis to histamine remained. We conclude that prostaglandin synthesis inhibition does not reverse histamine tachyphylaxis either in vivo or in vitro. Thus the mechanism of histamine tachyphylaxis remains unexplained.

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Prostaglandin synthesis inhibition and postprandial intestinal hyperemia

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1982.242.2.g140 ◽

1982 ◽

Vol 242 (2) ◽

pp. G140-G146 ◽

Cited By ~ 1

Author(s):

R. H. Gallavan ◽

C. C. Chou

Keyword(s):

Marked Effect ◽

Metabolic Response ◽

Mean Amplitude ◽

Prostaglandin Synthesis ◽

Cyclooxygenase Inhibitors ◽

Arterial Infusion ◽

Synthesis Inhibition ◽

Anesthetized Dogs ◽

Inhibition Of Prostaglandin Synthesis ◽

The Mean

The effect of prostaglandin synthesis inhibition on the postprandial intestinal hyperemia was examined in the jejunum of anesthetized dogs. Both intravenous and intra-arterial infusion of the cyclooxygenase inhibitors indomethacin and mefenamic acid reduced resting jejunal blood flow and markedly enhanced the food-induced jejunal hyperemia. The jejunal vascular response to food did not change after either intravenous or intra-arterial infusion of the carrier solutions or intra-arterial infusion of angiotensin II. The enhancement of the jejunal hyperemia was associated with an increase in the food-induced increase in jejunal oxygen consumption. Infusion of the cyclooxygenase inhibitors increased the mean amplitude of the monophasic intestinal contractions; however, this did not appear to play a role in the enhancement of the food-induced hyperemia. The study indicates that inhibition of prostaglandin synthesis has a marked effect on the postprandial intestinal hyperemia and that this may be due to its enhancement of the jejunal metabolic response to food. The prostaglandins involved and their mechanism of action are unknown.

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Prevention of Interstitial Pressure Change at Unilateral Nephrectomy by Prostaglandin Synthesis Inhibition

The Journal of Urology ◽

10.1016/s0022-5347(17)49782-5 ◽

1984 ◽

Vol 132 (3) ◽

pp. 623-623

Author(s):

B. Hahne ◽

A.E.G. Persson

Keyword(s):

Pressure Change ◽

Prostaglandin Synthesis ◽

Unilateral Nephrectomy ◽

Interstitial Pressure ◽

Synthesis Inhibition

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Prostaglandin synthesis inhibition restores hypoxic pulmonary vasoconstriction

Journal of Applied Physiology ◽

10.1152/jappl.1977.42.6.903 ◽

1977 ◽

Vol 42 (6) ◽

pp. 903-908 ◽

Cited By ~ 12

Author(s):

J. M. Alexander ◽

M. D. Nyby ◽

K. A. Jasberg

Keyword(s):

Hypoxic Pulmonary Vasoconstriction ◽

Prostaglandin Synthesis ◽

Hypoxic Response ◽

Synthesis Inhibition ◽

Pulmonary Vasoconstriction ◽

Isolated Lungs ◽

The Right

Hypoxic pulmonary vasoconstriction in blood-perfused isolated dog lungs progressively diminishes with repeated hypoxic challenges. We investigated the role of prostaglandins in effecting the decay of the hypoxic response by using a double perfusion preparation that could separately perfuse the right and left lungs of a single dog. Degeneration of this response was reversed by the addition of prostaglandin (PG) synthesis inhibitors, aspirin, or indomethacin. Various PG's known to be produced by the lung (PGE1, PGE2, and PGF2alpha), were infused, and only PGE1 abolished hypoxic pulmonary vasoconstriction. Since other workers have shown that lungs can synthesize and release PG's in response to various stimuli, we postulate that PGE1 synthesis in isolated lungs may increase and thereby cause the degeneration of the hypoxic response. The addition of aspirin or indomethacin could inhibit the synthesis of PGE1 and thereby restore hypoxic pulmonary vasoconstriction.

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