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 studied the role of O2 supply and demand factors for producing diaphragmatic failure in a canine model of cardiogenic shock with pulmonary edema. We produced pulmonary edema with oleic acid and then hypotension with cardiac tamponade and followed the animals until respiratory failure began, which was defined by a 50% fall in frequency of breathing and diaphragmatic pressure-time index (PTI; cmH2O.s-1.min-1) with no decrease in the diaphragmatic electromyogram. Regional blood flows were measured with radiolabeled microspheres. Diaphragmatic O2 consumption (VO2 di) (ml.min-1.100 g-1) was determined from the diaphragmatic blood flow (Qdi) and the arterial and phrenic venous O2 contents. With oleic acid-induced pulmonary edema, PTI Qdi, and VO2 di increased from control of 101.7 +/- 31.7, 17 +/- 1.8, and 0.81 +/- 0.11, respectively, to 187.2 +/- 27.6, 42.2 +/- 7.2, and 3.32 +/- 0.35 (P less than 0.05). With tamponade, PTI did not change (186.7 +/- 60.0), whereas VO2 di increased further to 3.98 +/- 0.98 (P less than 0.05) due to increased O2 extraction and no significant change in Qdi (32.8 +/- 4.0). As fatigue developed, VO2 di decreased to 2.30 +/- 0.23 due to the combined effects of small declines in Qdi and the arterial O2 content but remained higher than control even though the energy demands returned to control values. In conclusion, when cardiogenic shock is added to pulmonary edema VO2 di and energy output do not increase further and eventually fall.
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PMID:Diaphragmatic energetics and blood flow during pulmonary edema and hypotension. 339 91

If respiratory muscle blood flow (RMBF) demands in pulmonary edema are large enough, an imbalance between supply and demand could lead to respiratory muscle failure. Therefore, to determine the magnitude of RMBF in this condition we produced pulmonary edema by injecting oleic acid into the pulmonary circulation and measured RMBF with radiolabeled microspheres injected into the left atrium. We then related changes in muscle blood flow to changes in respiratory variables including frequency of breathing (fb, breaths/min), tidal volume (VT, ml), ventilation (VE, ml . kg-1 . min-1), pleural pressure-time index (PTI, cmH2O), and dynamic compliance (Cdyn, 1/cmH2O) at 0 (control), 30, 60, and 120 min. Cardiac output and blood pressure did not change throughout the experiment, but hypoxia became progressively more severe with a final PO2 of 37 +/- 10 Torr. With pulmonary edema, fb rose from a control value of 32 +/- 13 to 111 +/- 33 at peak, VE rose from 237 +/- 90 to 806 +/- 188, but VT did not change. PTI rose from 54 +/- 16 to 180 +/- 48, and Cdyn decreased from 0.06 +/- 0.02 to 2.02 +/- 0.01. Diaphragmatic blood flow (Qdi) rose from 16.0 +/- 6.26 to 120.1 +/- 54.5 ml . min-1 X 100 g-1 and accounted for 55% of the total RMBF of 217 +/- 100 ml/min. The RMBF accounted for 11.4 +/- 4.7% of the cardiac output at peak affect. The rise in Qdi was best predicted by PTI and to a smaller extent by PO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Respiratory muscle blood flow in oleic acid-induced pulmonary edema. 372 54