Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine a possible mechanism which could cause arterial hypoxaemia following pulmonary embolism, we collapsed and did not ventilate one lung in each of eleven dogs, to produce hypoxic pulmonary vasoconstriction. In five dogs (Starch Group), PaO2 fell from 10 to 7.7 kPa (76.6 to 58.4 torr) as shunt fraction (Qs/Qt) rose from 19 to 31 per cent. Mean pulmonary artery pressure (ppa), paCO2 and VD/VT remained constant. Starch emboli (63--74 micron) were taken injected. PPA increased significantly and PaO2 dropped further to 5 kPa (37.8 torr) as Qs/Qt rose to 57 per cent. VD/VT increased and PaCO2 remained constant. Microscopic examination of the lungs showed that three times as many emboli went to the ventilated lung compared to the unventilated lung. Six dogs (Blood Clot Group) received 51Cr labelled autologous blood clot. Changes after emboli in PPA, PaO2, Qs/QT, PaCO2 and VD/VT were similar to the results in the Starch group. 125I serum albumin was then injected and the dogs were sacrificed. The lungs were monogenized separately and the 51Cr and 125I counted. The 51Cr counts indicated 66 per cent of the blood clot emboli went to the ventilated lung. Following embolization, the 125I counts suggested a shift in perfusion to the unventilated lung. We conclude from these results that emboli are preferentially distributed to ventilated lung. After embolization PPA increases. At least in this pulmonary embolism model the increased PPA may overcome hypoxic pulmonary vasoconstriction, redistribute blood to non-ventilated lung and create arterial hypoxaemia.
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PMID:Pulmonary embolism distribution to ventilated and unventilated lungs in the dog: a cause of hypoxaemia. 676 66

Seventy-six patients with various forms of pulmonary thromboembolic disease were followed-up for 1 to 15 years. All were free of other cardiopulmonary disease at the time of the first examination which was performed at least two months after the last pulmonary embolism. Catheterization was repeated in all survivors on average 4.8 years later. Severe chronic pulmonary hypertension (mean pulmonary artery pressure (PPA greater than 30 mm Hg) did not occur after a single episode of acute embolism, was infrequent after single subacute or recurrent emboli (8 of 9 patients), and was common after occult emboli (12 of 13 patients). Mortality in all clinical groups correlated with PPA and with the presence of right heart failure. In survivors, no correlation was found between the longterm changes of PPA and age, duration of disease, interval between catheterizations, PaO2, or cardiac output. Pulmonary hypertension progressed further in patients with initial PPA greater than 30 mm Hg. In contrast, none of the patients with normal or borderline PPA at the initial examination developed severe pulmonary hypertension during the follow-up. Since the future course of patients could be predicted from the first examination, repeated hemodynamic investigation proved to be of minor prognostic value.
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PMID:Longterm follow-up of patients with pulmonary thromboembolism. Late prognosis and evolution of hemodynamic and respiratory data. 705 79

CT angiography is now commonly used for the diagnosis of pulmonary embolism, but the contrast media used for imaging produces various hemodynamic changes. In this study, we investigated the bronchovascular and hemodynamic responses to intravenous iopromide, a non-ionic contrast agent used for pulmonary CT angiograms, in anesthetized, mechanically ventilated sheep (n = 6). Bronchial blood flow and cardiac output were measured with ultrasonic flow probes. Systemic and pulmonary arterial pressures were continuously monitored. Injections of 0.9% NaCl (120 ml over 30 s) or iopromide (300 mg/ml, 120 ml over 30 s) were given in random order in a peripheral vein with an angiogram infuser and hemodynamic changes were determined. After these parameters returned to baseline, the left pulmonary artery (LPA) was occluded with a snare and the animals were allowed to stabilize. Injections of NaCl and iopromide were repeated in random order as before. There were no significant hemodynamic effects with infusion of NaCl. With intact pulmonary vasculature, NaCl and iopromide did not cause significant changes in arterial blood gases, however, cardiac output (QT, L/min), mean systemic and pulmonary arterial pressures (PSA and PPA, Torr) increased and bronchovascular resistance (BVR, Torr x min/ml), decreased. Following LPA ligation, pH and PO2 significantly decreased over baseline, whereas PCO2 increased. After LPA ligation, iopromide produced a greater decrease in BVR as compared with preligation intact pulmonary vasculature. In conclusion, iopromide caused rapid hemodynamic changes and decreased BVR, likely secondary to osmolar stress. Bronchovascular effects were more pronounced after pulmonary arterial occlusion.
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PMID:Bronchovascular responses to intravenous contrast media for helical CT pulmonary angiography. 1576 65