Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the role of serotonin at the 5-HT2 receptor site after pulmonary embolization for changes in hemodynamics, gas exchange, and lung water. Pulmonary embolization was induced using 0.75 gm/kg autologous clot in anesthetized artificially ventilated dogs. Pulmonary vascular resistance rose by 5 min from 3.4 +/- 1.5 to 14.2 +/- 2.1 mm Hg/liter/min (p less than 0.001), arterial oxygenation decreased from 91 +/- 5 to 68 +/- 5 mm Hg (p less than 0.01), platelet count decreased from 201 +/- 64 to 141 +/- 32 ml X 10(3), and the wet to dry weight lung ratio increased from 2.59 +/- 0.34 to 4.21 +/- 0.21 (p less than 0.001). Inhibition by ketanserin, a selective serotonergic inhibitor at the 5-HT2 receptor site substantially attenuated the increase in pulmonary vascular resistance from 3.6 +/- 1.4 to 8.0 +/- 2.5 mm Hg/liter/min, ablated the hypoxemia and platelet reduction and inhibited the formation of pulmonary edema. Infusion of serotonin simulated only some of the above changes as the pulmonary vascular resistance increased from 3.16 +/- 1.6 to 13.5 +/- 4.1 mm Hg/liter/min (P less than 0.01) and the oxygenation decreased from 96 +/- 5 to 57 +/- 4 mm Hg (P less than 0.01). Serotonin infusion, however, did not cause pulmonary edema. The administration of ketanserin ablated the increase in pulmonary vascular resistance and the hypoxemia following serotonin infusion. We conclude that following pulmonary embolization, serotonin at the 5-HT2 receptor is responsible for the fall in PaO2 and partially responsible for the increased pulmonary vascular resistance. Although ketanserin inhibits the formation of pulmonary edema following pulmonary embolization, serotonin does not seem to be directly responsible.
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PMID:Role of 5-HT2 receptor inhibition in pulmonary embolization. 379 78

alpha-Naphthylthiourea (ANTU) damages the pulmonary capillary endothelium producing a marked pulmonary edema. Since the pulmonary microvasculature regulates the circulating levels of serotonin (5-HT), the role of 5-HT in the pathophysiology of ANTU-induced pulmonary edema was examined. Mice treated with ANTU (10 mg/kg, ip) rapidly developed pulmonary edema which was maximal at 3 hr and was resolved by 12 hr. The lung content of both endogenous 5-HT and a tracer dose of 5-[3H]HT paralleled the time course of the development and resolution of the pulmonary edema. ANTU produced a significant thrombocytopenia (58 to 72%) at all time points, and an elevated platelet content of 5-HT and 5-[3H]HT during the resolution phase (6 to 12 hr). Drugs possessing select effects on 5-HT were shown to alter the edematogenic response to ANTU. Fluoxetine, a selective inhibitor of 5-HT uptake, potentiated the pulmonary edema, while clorgyline, an irreversible inhibitor of type A monoamine oxidase, was without effect. Reserpine which depletes 5-HT stores prevented both thrombocytopenia and pulmonary edema in response to ANTU. Reloading the lung and platelet 5-HT stores of reserpinized animals reestablished the normal response to ANTU. Pretreatment with the selective 5-HT2 receptor antagonist, ketanserin, prevented the thrombocytopenia, the increase in lung content of 5-HT and 5-[3H]HT, and prevented the edematogenic response to ANTU by 70%. These data indicate a major role for 5-HT in the pathophysiology of acute lung microvascular injury produced by ANTU.
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PMID:A role for serotonin in alpha-naphthylthiourea-induced pulmonary edema. 642 98

1. The modulatory role of neuropeptide Y (NPY) on pulmonary oedema induced by acetylcholine and capsaicin was investigated. The effects of NPY on the haemodynamic response to acetylcholine, phenylephrine and substance P were also investigated. 2. Isolated, ventilated, exsanguinated lungs of the rabbit were perfused with a constant flow of recirculating blood-free perfusate. The double/arterial/venous occlusion method was used to partition the total pressure gradient (delta Pt) into four components: the arterial gradient (delta Pa), the pre- and post-capillary gradients (respectively delta Pa' and delta Pv') and the venous pressure gradient (delta Pv). Endothelial permeability was evaluated by measuring the capillary filtration coefficient (Kf,c). 3. Acetylcholine (10(-8) M to 10(-4) M) and substance P (SP, 10(-10) M to 10(-6) M) induced a concentration-dependent increase in the Kf,c. Capsaicin (10(-4) M) and 5-hydroxytryptamine (5-HT) (10(-4) M) also increased this parameter. NPY (10(-8) M) completely inhibited the effects of acetylcholine and capsaicin on the Kf,c, without preventing the effects of substance P and 5-HT. 4. Acetylcholine induced concentration-dependent vasoconstriction in the precapillary segment. The effect was inhibited by NPY and aspirin, an inhibitor of cyclo-oxygenase, while ketanserin, a 5-HT2 receptor antagonist, and SR140333, a new NK1 antagonist, had no protective effect. Phenylephrine increased delta Pa at high concentration, an effect also inhibited by NPY and aspirin. Substance P had no significant haemodynamic effect. When injected together with NPY, substance P (10(-6) M) induced a significant increase in the total pressure gradient. 5. It was concluded that NPY can protect the lung against acetylcholine- and capsaicin-induced oedemavia a prejunctional modulatory effect on the C-fibres. NPY also inhibits acetylcholine-evoked precapillary and phenylephrine-induced arterial vasoconstriction, probably by interfering with cyclo-oxygenase products synthesis.
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PMID:Modulatory effect of neuropeptide Y on acetylcholine-induced oedema and vasoconstriction in isolated perfused lungs of rabbit. 753 83