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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe mitral stenosis of rapid onset and progression was observed in a patient with infective endocarditis superimposed upon mild rheumatic mitral valvular stenosis. This severe stenosis resulted from large vegetations impinging upon the mitral valve orifice. Preoperative studies indicating mitral stenosis with vegetations and pulmonary edema were followed by emergency mitral valve replacement, which was sucessful.
J Thorac Cardiovasc Surg 1979 Jul
PMID:Acute mitral valvular obstruction from infective endocarditis: echocardiographic diagnosis and report of the second successfully treated case. 44 78

In patients with fulminating pulmonary edema not responsive to conventional therapy, venoarterial membrane lung bypass can provide assistance if decreased systemic blood pressure prevents use of high-level positive end-expiratory pressure ventilation. In 10 patients with acute respiratory failure, partial venoarterial bypass provided a rapid and marked improvement of systemic oxygenation. Measurement of pulmonary blood flow (PBF) and intrapulmonary shunting (QS/QP) during bypass via prolonged left heart catheterization showed that left ventricular PaO2 was increased through a rapid and profound reduction of QS/QP. During the first days of bypass, derecruitment of pulmonary vessels is probably the mechanism of improved pulmonary oxygenation. When low pulmonary arterial pressures (PAP) are sustained, resorption of pulmonary edema is favored. Despite the beneficial effects of bypass, death occurred in every case due to diffuse interstitial fibrosis and/or parenchymal damage. The absence of healing, due to prolonged circulatory exclusion, may be detrimental despite immediate improvement. Because of this possibility, venovenous or mixed perfusion should be more extensively explored.
J Thorac Cardiovasc Surg 1978 Jun
PMID:Pulmonary gas exchange during venoarterial bypass with a membrane lung for acute respiratory failure. 66 54

The effects of acute pulmonary hypertension on the fraction of cardiac output shunted through pulmonary arteriovenous communications have been studied in dogs as a possible cause of hypoxia following pulmonary embolization. Pulmonary artery pressure was increased twofold and then fourfold above control values by embolization of the pulmonary vascular bed with polystyrene microspheres. Quantitative measurements of arteriovenous shunt were determined from the fraction of 50 mu radioactively labeled microspheres injected into the inferior vena cava which passed through the pulmonary circulation into systemic vascular beds. There was no increase in the fraction of pulmonary blood flow passing through pulmonary arteriovenous connections, 50 mu in diameter or greater, with pulmonary microembolism when FIo2 was 1. There was a small increase in arteriovenous shunt fraction when pulmonary artery pressure was increased with an FIo2 of 0.21. Physiological shunt measured by the oxygen technique did not increase with pulmonary embolism, but total venous admixture rose significantly. Postmortem gravimetric measurements of lung water indicated pulmonary edema. We conclude that anatomic arteriovenous shunt channels have little physiological significance after pulmonary microembolism in the dog lung. The major cause of hypoxia immediately after pulmonary microembolism is ventilation/perfusion imbalance, probably caused by pulmonary edema.
J Thorac Cardiovasc Surg 1978 Oct
PMID:Effect of pulmonary microembolism on arteriovenous shunt flow. 70 53

Five patients with critical aortic stenosis (aortic valve area 0.6 cm2 or less) died 2 days to 21 days following cardiac catheterization performed in anticipation of cardiac surgery. A sixth patient was successfully resuscitated for spontaneous ventricular fibrillation, and successful aortic valve replacement was accomplished. Two patients had prior history of syncope; one patient, of ventricular tachycardia; three patients, of pulmonary edema; and three patients, of crescendo angina. One patient had severe hypotension during maintenance hemodialysis for chronic renal failure. The mode of death was sudden but not witnessed in two patients. The terminal cardiac rhythms were slow junctional in one patient, idioventricular in one, ventricular tachycardia in one, and ventricular fibrillation in the fourth patient. We conclude that symptomatic patients with critical aortic stenosis should be monitored after cardiac catheterization, and surgery should be performed as soon as possible since sudden death is not unusual.
Cathet Cardiovasc Diagn 1978
PMID:Sudden death in severe aortic stenosis following cardiac catheterization. 75 34

A calf into which a biolized, total artificial heart (TAH) had been implanted survived for 145 days. All measured physiological parameters except central venous pressure (CVP) were back to normal one month after implantation, and thereafter the animal's physiological development was similar to that of a normal calf. The intimal weight, which was 96 kilograms at implantation, reached 190 kilogram at the end of experiment, with a daily gain rate of 0.9 kilogram per day. After the nineteenth postoperative week, signs of congestive heart failure appeared, such as high venous pressure, ascites, and enlarged liver although the calf outwardly appeared well. On postoperative day 146, the animal started foaming at the mouth, and a convulsion occurred; then, the experiment was terminated after 3,494 hours of pumping. At autopsy, there were acute bilateral bronchopneumonia involving mostly both upper lobes, pulmonary edema, slight chronic pneumonitis, and hepatomegaly. There were no serious thrombotic deposits inside the cardiac prosthesis.
J Thorac Cardiovasc Surg 1977 Apr
PMID:Survival for 145 days with a total artificial heart. 83 53

Most previous studies of the efficiency of bypass techniques for respiratory support have been conducted in hypoxic but otherwise normal animals. However, mechanisms of improved oxygenation by partial venoarterial bypass in the presence of acute respiratory insufficiency can be better studied with an appropriate pathophysiologic model; for this purpose, acute hemorrhagic pulmonary edema was induced in sheep by injection of oleic acid into the right atrium. The model presented a 3 hour period of elevated pulmonary shunting with stable hemodynamics. This preparation is being employed to the study of the mechanisms of extracorporeal oxygenation.
J Thorac Cardiovasc Surg 1975 May
PMID:Pulmonary insufficiency induced by oleic acid in the sheep: a model for investigation of extracorporeal oxygenation. 112 78

Thirty-two consecutive preterm infants with birth weights under 1,500 grams and with respiratory distress syndrome (RDS) complicated by a patent ductus arteriosus (PDA) underwent ligation of PDA. The indications for operation were massive left-to-right shunting associated with heart failure (cardiomegaly and pulmonary edema) unresponsive to medical treatment. The clinical manifestations of heart failure were related to the severity of RDS. Infants with mild-to-moderate RDS (21) often recovered and later developed typical findings of PDA (bounding pulses, hyperactive precordium, and murmur). They are now operated upon as soon as respiratory support is required. Infants with severe RDS (11) develop cardiomegaly earlier, and retrograde aortography may show massive left-to-right shunting before the presence of a murmur. Ligation is indicated when blood-gas values deteriorate despite medical treatment. Nineteen (59 per cent) of these extremely preterm infants survived to be discharged and 16 (50 per cent) are developing normally. Three have neurologic impariment. None of the survivors has clinical respiratory disease, and their radiologic findings of bronchopulmonary dysplasia are improving.
J Thorac Cardiovasc Surg 1976 Feb
PMID:Improving the results of ligation of patent ductus arteriosus in small preterm infants. 124 41

Patients with shock lung syndrome were identified as those who developed acute respiratory failure after a profound episode of hypotension secondary to hemorrhagic, gram-negative, or endotoxic shock. In this study, each of the 10 patients with shock lung syndrome received methylprednisolone sodium succinate, 30 mg. per kilogram, intravenously every 6 hours for 48 hours. In addition, all patients were supported with mechanical ventilation, with or without positive end-expiratory pressure (PEEP). Arterial oxygenation improved markedly, and pulmonary edema resolved in all patients. Nine were discharged from the hospital and one died subsequently of disseminated intravascular coagulation. This study demonstrated a significant improvement in mortality rate with repeated pharmacologic doses of methylprednisolone compared to previously reported mortality rates of 60 to 90 per cent in patients with shock lung syndrome treated without repeated pharmacologic doses of steroid therapy.
J Thorac Cardiovasc Surg 1976 May
PMID:Methylprednisolone. Pharmacologic doses in shock lung syndrome. 126 66

Endothelin-1 (ET-1) is a potent vasoactive peptide that has been reported to cause lung edema. This study tested if the edemagenic effect of ET-1 is due to preferential venoconstriction and, if so, whether the site of resistance is similar with salt solution (PSS) and more physiologic blood perfusate. ET-1 caused concentration-dependent contraction of pulmonary arterial and venous rings, with an EC50 of 1.3 nM in artery and 0.6 nM in vein (p less than 0.05). In PSS-perfused lungs, 5 nM ET-1 caused a 7.0 +/- 0.8 torr pressor response that was associated with a 5.0 +/- 0.3 torr increase in microvascular pressure and a 530 +/- 20 mg increase in lung weight within 10 min. In contrast, KCl-treated lungs had an equivalent pressor response (7.4 +/- 1.1 torr), yet the microvascular pressure increased by only 2.5 +/- 0.4 torr (p less than 0.05 from ET-1) and the lung weight was unchanged. Meclofenamate did not prevent the effect of ET-1 on microvascular pressure or lung weight. In blood-perfused lungs, ET-1 caused a 7.3 +/- 0.1 torr pressor response but only a 2.0 +/- 0.5 torr increase in microvascular pressure and no increase in lung weight. ET-1 had no effect on permeability either of cultured endothelial cell monolayers or in the pulmonary microvasculature in vivo. We conclude that the edemagenic effect of ET-1 in PSS-perfused lungs is mediated through venoconstriction and an increase in microvascular pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1992 Oct
PMID:Endothelin-1 increases the pulmonary microvascular pressure and causes pulmonary edema in salt solution but not blood-perfused rat lungs. 128 Jul 24

Effects of single lung transplantation on fatal pulmonary hypertension were evaluated in rats receiving a lethal dose of monocrotaline. Inbred rats treated with monocrotaline (80 mg/kg) received a left lung isograft at 4 weeks (n = 9) and at 6 weeks (n = 6), when moderate and severe pulmonary hypertension, respectively, had developed. Medicated (n = 12) and nonmedicated rats (n = 12) served as control animals. Each rat was tested weekly with treadmill for exercise tolerance and oxygen consumption during a 10-week period after medication and after they were killed. Medicated control rats lost exercise tolerance and highest oxygen consumption per unit time consistently to the range of resting value (or 45% of nonmedicated control rats), and all died from severe pulmonary vascular occlusive disease with right ventricular hypertrophy before 10 weeks (right ventricular/left ventricular weight ratio of 1.16). All rats receiving a left lung isograft at 4 weeks survived and regained highest oxygen consumption per unit time (87% of nonmedicated control rats), with the lung transplant receiving 65% (nonmedicated control rats, 39%) of cardiac output and milder right ventricular hypertrophy (right ventricular/left ventricular weight ratio of 0.46). Except for one, all rats that received a left lung isograft at 6 weeks tolerated single lung transplantation, but they died soon after reperfusion because of pulmonary edema in the graft that received 58% of cardiac output with right ventricular/left ventricular weight ratio of 0.79. Results of single lung transplantation in rats were dependent on severity of pulmonary hypertension. In rats with moderate pulmonary hypertension, single lung transplantation was successful in reversing exercise intolerance and right ventricular hypertrophy. Single lung transplantation was unsuccessful when pulmonary hypertension was severe in the rat model because increased flow toward the lung transplant resulted in graft pulmonary edema.
J Thorac Cardiovasc Surg 1992 Sep
PMID:Single lung transplantation in rats with fatal pulmonary hypertension. 138 40


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