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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary embolism may cause pulmonary hypertension by mechanical obstruction, which might be amplified by vasoconstriction induced by serotonin released from the emboli. The purpose of the present study was to examine whether 5-HT2-receptors are involved in serotonin-induced pulmonary hypertension. Ketanserin was used as 5-HT2-serotonergic antagonist. In nine anesthetized mongrel dogs, the effect of serotonin infusions (10, 50, 100 micrograms/kg . min) on mean pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), cardiac output (CO), stroke volume (SV), cardiac contractility (dP/dtmax), heart rate (HR), and mean aortic pressure (PAO) was studied with and without treatment by ketanserin (20 and 100 micrograms/kg). Serotonin caused dose-dependent increase in PAP, PVR, CO, SV, and dP/dtmax. A dose of 20 micrograms/kg ketanserin did not affect hemodynamics significantly, whereas 100 micrograms/kg of the compound significantly reduced PAO, TPR, and left ventricular dP/dtmax. The serotonin-induced increases in PAP, PVR, dP/dtmax, CO, and SV were reduced significantly by 100 micrograms/kg ketanserin; the lower dose of ketanserin had only a slight blocking effect. Ketanserin blocks serotonin-induced pulmonary vasoconstriction partly, but it seems also to antagonize the positive inotropic effect of the monoamine.
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PMID:Effects of serotonin on the cardiopulmonary circulatory system with and without 5-HT2-receptor blockade by ketanserin. 241 62

Vasodilators including isoproterenol, nitroprusside, nitroglycerin, and oxygen were administered to 5 patients with chronic pulmonary hypertension secondary to pulmonary embolism. The patients' mean pulmonary artery pressure was 54 +/- 8 mmHg, and their average total pulmonary resistance (TRP) was 17 +/- 11 mmHg/L/min. Each patient experienced a decrease in TRP in response to at least 1 of the vasodilators, and the mean maximal decrease was to 57 +/- 10% of the baseline value. Although these decrements in TRP were accompanied by an increase in cardiac output in all but 1 patient, changes in PAP were variable. Treatment with nitroglycerin was continued in 3 of the 5 patients and all 3 have reported improvement in their exercise tolerance. We conclude that the elevated TPR seen in patients with chronic embolic pulmonary hypertension is due to increased vascular tone in addition to fixed vascular obstruction.
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PMID:Partial reversibility of chronic pulmonary hypertension caused by pulmonary thromboembolic disease. 678 32

The aim of this study was to evaluate the contribution of clinical, angiographic and haemodynamic findings in predicting the cardiorespiratory efficacy of thrombolytic therapy in acute massive pulmonary embolism. Haemodynamic measurements and pulmonary angiography were performed before (H0) and 12 h after (H12) initiating thrombolytic therapy in 23 patients with acute massive pulmonary embolism (Miller index > or =20/34), and free of prior cardiopulmonary disease. Patients were divided into two groups according to the variation in oxygen delivery (deltaDO2) between H0 and H12: deltaDO2 >20% (responders, n=10) and deltaDO2 < or =20% (nonresponders, n=13). Before thrombolysis, clinical and angiographic findings were similar in both groups. Mean right atrial pressure (RAP) and total pulmonary (vascular) resistance (TPR) were higher, while cardiac index (CI), DO2 and mixed venous oxygen saturation (Sv,O2) were lower in responders. DO2 and Sv,O2 were more closely correlated with deltaDO2 than RAP, TPR and CI. Eight out of the 10 responders and two out of the 13 nonresponders had an Sv,O2 <55%, while nine of the responders and two of the nonresponders had a DO2 <350 mL x min(-1) x m(-2). In conclusion, the initial oxygen delivery and mixed venous oxygen saturation may predict the cardiorespiratory efficacy of thrombolytic therapy in acute massive pulmonary embolism. When pulmonary angiography is performed, measurement of mixed venous oxygen saturation may be a simple method by which to select patients for thrombolytic therapy.
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PMID:Cardiorespiratory efficacy of thrombolytic therapy in acute massive pulmonary embolism: identification of predictive factors. 1023 35