Diethylcarbamazine Citrate

We hypothesized that leukotrienes are involved in hypoxic pulmonary vasoconstriction, since they are pulmonary vasoconstrictors and cells capable of producing leukotrienes are located in the lung near resistance vessels. We investigated in isolated perfused rat lungs whether three structurally unrelated blockers [diethylcarbamazine citrate (DEC), U-60257, and FPL 55712] of leukotriene synthesis or action block hypoxic pulmonary vasoconstriction. DEC blocked ongoing and subsequent hypoxic pressor responses while minimally affecting the angiotensin II pressor response. The inhibition of the hypoxic pressor response by DEC was not affected by cyclooxygenase or H1-receptor blockers. Potassium-induced vasoconstriction, which is dependent on calcium entry, was largely blocked by verapamil but not by DEC, suggesting that DEC was not acting primarily as a calcium-entry blocker. U-60257 blocked the hypoxic pressor response without inhibiting the pressor response to angiotensin II or potassium chloride. FPL 55712, a leukotriene end-organ blocker, in a dose which inhibited vasoconstriction caused by exogenous leukotriene C4, inhibited the pressor response to hypoxia but not to angiotensin II. We conclude that leukotriene inhibitors preferentially inhibit hypoxic pulmonary vasoconstriction in isolated perfused adult rat lungs.

Download Full-text

A Study of Prostaglandins and Prostaglandin Antagonists in Relation to Anaphylaxis in Calves

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y74-123 ◽

1974 ◽

Vol 52 (5) ◽

pp. 942-951 ◽

Cited By ~ 16

Author(s):

J. F. Burka ◽

P. Eyre

Keyword(s):

Arterial Pressure ◽

Broad Spectrum ◽

Systemic Arterial Pressure ◽

Protective Effects ◽

Systemic Anaphylaxis ◽

Superfusion System ◽

Transient Rise ◽

Diethylcarbamazine Citrate ◽

Pulmonary Arterial ◽

Prostaglandin Antagonists

Actions of prostaglandins (PG) E1, E2, and F2α on the cardiovascular–respiratory systems of anesthetized calves were studied in conjunction with the effects of a series of prostaglandin antagonists on acute systemic anaphylaxis. Meclofenamate, acetylsalicylic acid (ASA), phenylbutazone, and indomethacin, all inhibitors of PG synthesis, were particularly effective in protecting calves from anaphylactic cardiovascular shock. Meclofenamate showed "broad spectrum" antagonism of the mediators of anaphylaxis. Indomthacin and ASA eliminated the biphasic fall in systemic arterial pressure, suggesting that prostaglandins may be involved, together with biogenic amines, in the early stages of anaphylaxis. SC-19220, polyphloretin phosphate, and diethylcarbamazine citrate (DECC) had little or no inhibitory effects against exogenous prostaglandins and afforded only weak protection against systemic anaphylaxis. "Broad spectrum" inhibition of amine and PG receptors, as well as inhibition of slow-reacting substance of anaphylaxis formation and release, may account for part of the protective effects of DECC. A blood-bathed superfusion system suggested participation by PG F2α in bovine anaphylaxis. Cardiovascular–respiratory changes induced by exogenous prostaglandins in calves suggest that PG F2α may be responsible for the transient rise in systemic arterial pressure and increase in pulmonary arterial pressure in anaphylaxis, whereas PG E1 and E2 may be participating in the primary fall in systemic arterial pressure.

Download Full-text