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)

If lungs could be retrieved from cadavers after circulatory arrest, the critical shortage of donors for lung transplantation might be alleviated. To assess gas exchange after transplantation of lungs from cadaveric donors, we performed double-lung transplantation through sequential thoracotomies in 12 dogs. Donors were sacrificed by intravenous pentobarbital injection and then ventilated with 100% oxygen. Lungs were harvested 2 hours (n = 6) or 4 hours (n = 6) after death and flushed with 2 L modified Euro-Collins solution. Recipients underwent sequential right and left lung transplantation; they were then monitored while under anesthesia for 8 hours, with adjustments of the fraction of inspired oxygen. Nine of 12 recipients survived the 8-hour study period. Four of six dogs with cadaveric lungs retrieved 2 hours after death survived; deaths were from pulmonary embolism at 6 hours and pulmonary edema at 2 hours. Five of six dogs with cadaveric lungs retrieved 4 hours after death survived; one died of hypoxia during implantation of the left lung, while dependent on the right lung graft. Postoperative hemodynamic and gas exchange parameters were similar in both groups. Alveolar-arterial oxygen gradient rose significantly compared with baseline 1 hour after transplantation in both groups (462 +/- 60 vs 38 +/- 31 mmHg for 2-hour group, p < 0.0001, and 484 +/- 63 vs 38 +/- 14 mmHg for 4-hour group, p < 0.0002). By 8 hours after operation, the gradients had significantly decreased in both groups (105 +/- 37 mm Hg for 2-hour group and 146 +/- 53 mm Hg for 4-hour group) and were similar to baseline values. Extravascular lung water also rose significantly 1 hour after transplantation (15.7 +/- 2.8 vs 7.9 +/- 0.5 ml/kg for 2-hour group, p < 0.02, and 16.9 +/- 1.2 vs 6.6 +/- 0.4 ml/kg for 4-hour group, p < 0.0001) and decreased gradually during the 8-hour study period. Donor lungs retrieved at 2 and 4 hours postmortem afford similar recipient outcomes. Improvement in alveolar-arterial oxygen gradient and reduction in extravascular lung water during the study period imply that the ischemia-reperfusion injury induced by this model is reversible. If this approach could be safely introduced to clinical practice, substantially more transplant procedures could be performed.
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PMID:Canine double-lung transplantation with cadaveric donors. 880 Jan 42

Cystic fibrosis (CF) is a disease characterized mainly by altered exocrine gland function that eventually produces irreversible dysfunction of the pancreas and lungs. The respiratory insufficiency that develops in CF patients in the advanced stages of disease can only be corrected at this time by lung or heart-lung transplantation. We describe our experience with 6 terminal phase CF patients who underwent sequential double lung transplantation (SDLT). Anesthesia was intravenous, with exhaustive hemodynamic and respiratory monitoring. During surgery the most frequently encountered hemodynamic complications were low minute volume, arterial hypotension and irregular heart rate. The main respiratory complications were hypoxemia, hypercapnia and pulmonary edema of the implanted lung, which developed in all cases to varying degrees related to the organ's state of preservation and duration of ischemia. Other complications were the need for extracorporeal circulation in 1 case, oliguria and blood loss requiring multiple transfusions. The most critical moments were at the time of clamping the pulmonary artery, the period after revascularization of the donated lung, and at the start of patient ventilation through the first implanted lung so that the second could be implanted. Although our series is small, it is of interest given the limited Spanish experience with lung transplantation in CF patients, and the good early results obtained, which are similar to those reported for other diseases.
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PMID:[Anesthetic complications in sequential bipulmonary transplantation in patients with cystic fibrosis. Apropos of 6 cases]. 884 34

Not all possible mediators of lung I/R injury that have been studied, such as cyclooxygenase and lipoxygenase products, have been presented in this review, but it is very clear that oxygen free radicals are the primary mediators of the damage, regardless of their origin. Oxygen radicals are generated by neutrophils, which are sequestered and activated in the ischemic-reperfused pulmonary tissue, and by xanthine oxidase, which is upregulated by ischemia and/or activated neutrophils. The contributions to lung injury by different species of oxygen radicals may very depending upon the lung model used to study I/R. Also, nitric oxide may be injurious or protective in lung I/R injury, depending upon some critical alveolar PO2 level present either during ischemia or at reperfusion. I/R-induced lung microvascular injury ultimately depends upon some balance between lung metabolic stress, the extent of the I/R-induced inflammatory response, endogenous antioxidant levels, and the timing, magnitude, and duration of oxygen free radical generation during both periods of ischemia and reperfusion. The final common pathway causing microvascular permeability to increase after lung I/R is the activation of the endothelial cell's contractile machinery. Particularly, endothelial contraction may occur in a MLCK-dependent fashion. Endothelial contraction may also be related to an intracellular Ca++ increase and subsequent calmodulin activation. The initiating event causing increased intracellular Ca++ is not known, but may be due to endothelial cell/leukocyte interactions, oxygen radical-mediated Ca++ transients, mobilization of intracellular Ca++ pools by various second messengers, or stimulation of Ca++ influx secondarily to changes in the activity of membrane ion pumps such as the Na+/H+ antiport. Increasing cAMP levels in the postischemic lung can prevent and actually reverse I/R-induced microvascular injury, by affecting MLCK, the endothelial cell cytoskeleton, and/or the function of sequestered leukocytes. Also, cAMP elevation aids the resolution of pulmonary edema by facilitating capillary fluid reabsorption. Whatever the mechanism, elevation of cAMP in the setting of lung I/R injury represents a potentially useful therapy for improving early lung function following lung transplantation. Finally, additional studies are necessary to elucidate the complete mechanisms responsible for producing microvascular injury during lung I/R. Specifically, a better understanding of the relationships between the many factors required to produce lung damage is needed. Many interventions into the lung I/R process provide protection against microvascular injury, suggesting that regulation of the endothelial barrier permeability to fluid, protein, and leukocytes is accomplished by several redundant systems. This situation may be similar to mechanisms reported to regulate the immune response mediated by T cells (62a), where T cell activation depends upon multiple signal inputs for the full immune response to occur. Thus, multiple signals in a correct sequence delivered to the endothelium may be necessary to produce the microvascular injury associated with lung ischemia and reperfusion.
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PMID:Endothelial damage caused by ischemia and reperfusion and different ventilatory strategies in the lung. 890 6

Oxidant stress plays a major role in the pathophysiologic processes associated with ischemia-reperfusion injury. Xanthine oxidase (XO) is often implicated as a significant source of oxidants and increases in the circulation after hepatoenteric ischemia-reperfusion. We hypothesized that pulmonary injury is associated with hepatic ischemia-reperfusion resulting from descending thoracic aorta occlusion-reperfusion (AoOR). We also proposed that this remote pulmonary injury is attenuated through inactivation of circulating and tissue XO by tungstate, implicating an XO-dependent mechanism. Aortic occlusion was established in rabbits (standard or tungstate diet) for 40 min by 2 h reperfusion. Sham operated rabbits (standard or tungstate diet) served as controls. Hepatic reperfusion injury, as manifested by release of the hepatocellular enzyme alanine aminotransferase (ALT), was markedly increased after AoOR. Suprarenal-infrahepatic occlusion failed to increase ALT release. Tungstate pretreatment significantly (p < 0.05) reduced XO activity and ameliorated liver and intestinal injury (p < 0.05). Lung injury, manifested by increased bronchoalveolar lavage (BAL) protein concentration, BAL lactate dehydrogenase (LDH) activity and increased lung edema was significantly associated with liver injury (p < 0.05) and circulating XO activity (p < 0.001). XO inactivation significantly decreased BAL protein concentration, BAL LDH activity, and lung edema (p < 0.05). We conclude that remote pulmonary injury is significantly influenced by the extent of liver injury and circulating XO activity.
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PMID:Lung injury after hepatoenteric ischemia-reperfusion: role of xanthine oxidase. 891 49

This study examines the hypothesis that intestinal reperfusion (IR)-induced pulmonary thromboxane A2 (TxA2) release increases local microvascular permeability and induces pulmonary vasoconstriction. Sprague-Dawley rats underwent 120 min of intestinal ischemia and 60 min of IR. Sham-operated animals (Sham) served as controls. After IR or Sham, the pulmonary vessels were cannulated, and the lungs were perfused in vitro with Krebs buffer. Microvascular permeability was quantitated by determining the filtration coefficient (Kf), and pulmonary arterial (Ppa), venous (Ppv), and capillary (Ppc) pressures were measured to calculate vascular resistance (Rt). After baseline measurements, imidazole (TxA2 synthase inhibitor) or SQ-29,548 (TxA2-receptor antagonist) was added to the perfusate; then Kf, Ppa, Ppv, and Ppc were again measured. The Kf of lungs from IR animals was four times greater than that of Sham (P = 0.001), and Rt was 63% greater in the injured group (P = 0.01). Pc of IR lungs was twice that of controls (5.4 +/- 1.0 vs. 2.83 +/- 0.3 mmHg. IR vs. Sham, respectively; P < 0.05). Imidazole or SQ-29,548 returned Kf to baseline measurements (P < 0.05) and reduced Rt by 23 and 17%, respectively (P < 0.05). IR-induced increases in Pc were only slightly reduced by 500 micrograms/ml imidazole (14%; P = 0.05) but unaffected by lower doses of imidazole (5 or 50 micrograms/ml) or SQ-29,548. These data suggest that IR-induced pulmonary edema is caused by both increased microvascular permeability and increased hydrostatic pressure and that these changes are due, at least in part, to the ongoing release of TxA2.
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PMID:Thromboxane A2 mediates increased pulmonary microvascular permeability after intestinal reperfusion. 904 42

To test the effects of eicosapentaenoic acid (EPA) infusion on pulmonary edema induced by coronary ligation and reperfusion, extravascular lung water (EVLW) was measured in situ by the thermal-dye double indicator dilution method in dogs. In the control group of five dogs, 30 mL of a 10% soybean oil emulsion was infused through a leg vein. One hour after infusion, the left anterior descending coronary artery below the first diagonal branch was ligated for 15 min and then reperfused for 30 min. In the EPA group, six dogs were similarly treated with an emulsion of a 10% trieicosapentaenoyl-glycerol (90% pure). EVLW, pulmonary capillary wedge pressure, mean pulmonary artery pressure, mean blood pressure, and cardiac index were measured before and 15 min after coronary ligation, and 15 min and 30 min after coronary reperfusion. There were no significant differences in the hemodynamic indices between the two groups. EVLW significantly increased up to two times of baseline during coronary ligation in the control group (P < 0.05) and more during reperfusion (P < 0.01), whereas EVLW did not increase in the EPA group. In conclusion, EPA inhibited EVLW accumulation and may be useful for ameliorating one of the ischemia-reperfusion-induced complications, pulmonary edema.
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PMID:The effects of infusion of trieicosapentaenoyl-glycerol emulsion on extravascular lung water during myocardial ischemia and reperfusion in dogs. 907

A method to reduce ischemia-reperfusion (I/R) injury can be an important criterion to improve the preservation solution. Although University of Wisconsin solution (UW) works as a lung preservation solution, its attenuation effect on I/R injury has not been investigated. We attempted to determine whether, by adding various protective agents, modified UW solutions will enhance the I/R attenuation by UW. We examined the I/R injury in an isolated rat lung model. Various solutions, e.g., physiological salt solution (PSS), UW, and modified UW solutions containing various protective agents such as prostaglandin E1, dexamethasone, U-74389G, or dibutyryl adenosine 3',5'-cyclic monophosphate were perfused individually to evaluate the I/R injury. Isolated rat lung experiments, with ischemia for 45 min, then reperfusion for 60 min, were conducted in a closed circulating system. Hemodynamic changes, lung weight gain (LWG), capillary filtration coefficient (Kfc), protein content of lavage fluid, concentration of cytokines, and lung histopathology were analyzed. Results showed that the acute I/R lung injury with immediate permeability pulmonary edema was associated with an increase in tumor necrosis factor-alpha (TNF-alpha) production. A significant correlation existed between TNF-alpha and Kfc (r = 0.8, P < 0.0001) and TNF-alpha and LWG (r = 0. 9, P < 0.0001), indicating that TNF-alpha is an important cytokine modulating early I/R injury. Significantly lower levels of Kfc, LWG, TNF-alpha, and protein concentration of lung lavage (P < 0.05) were found in the UW-perfused group than in the control group perfused with PSS. Modified UW promoted the protective effect of UW to further decrease Kfc, LWG, and TNF-alpha (P < 0.05). Histopathological observations also substantiated this evidence. In the UW+U-74389G group, bronchial alveolar lavage fluid contained lowest protein concentration. We conclude that the UW solution attenuates I/R injury of rat lung and that the modified UW solutions further enhance the effect of UW in reducing I/R injury. Among modified solutions, UW+U-74389G is the best. Further investigation of the improved effects of the modified UW solutions would be beneficial in lung transplantation.
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PMID:PGE1, dexamethasone, U-74389G, or Bt2-cAMP as an additive to promote protection by UW solution in I/R injury. 926 56

The inhalation of racemic adrenalin is an important part of the treatment of inflammatory airway obstruction in children. In Norway during the last few years there have been several cases of adrenal solutions intended only for inhalation being accidentally administered as intravenous injections. The solution for inhalation contains an adrenalin concentration 110 times greater than the adrenalin intended for emergency use (0.1 mg/ml). The instant consequences of intravenous injections of inhalation adrenalin include arterial hypertension followed by hypotension, cardiac ischemia and cardiac insufficiency, pulmonary oedema, and respiratory failure and the need for artificial ventilation. The clinical picture in the three patients we describe was very dramatic. The injected doses were 0.16-1.1 mg l-adrenalin per kg body weight. All children survived without sequelae. In order to reduce the risk of accidentally administering intravenous injections of adrenalin intended for inhalation a set of guidelines is being proposed.
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PMID:[Accidental administration of racemic adrenaline. Three life-threatening cases after intravenous injection in children]. 953 34

Coronary artery disease (CAD), arterial hypertension, chronic bronchitis and diabetes mellitus are the most frequently encountered diseases complicating the clinical course of the vascular patient. Clinical signs of cardiac or pulmonary disease are often absent in patients with decreased functional capacity due to claudication. For instance, clinical evidence of coronary artery disease was found in 36% of patients scheduled for different vascular surgical procedures, whereas coronary angiography revealed significant stenoses in as many as 53-68%. Patients with chronic hypertensive disease, coronary artery disease and increased impedance to left ventricular ejection due to atherosclerosis frequently develop impairment of left ventricular (LV) function. Even without clinical or radiological evidence, approximately 20-35% of vascular patients have a LV ejection fraction below 50% indicating impaired systolic LV function. The incidence of diabetes mellitus in vascular surgical patients is around 18%. When requiring insulin treatment, diabetes is an independent risk factor for postoperative ischemic events and congestive heart failure. Those with autonomic neuropathy are often asymptomatic as regards coronary artery disease. Coronary artery disease is responsible for over 50% of the immediate, medium- and long-term mortality and morbidity. Unstable myocardial ischemia, acute myocardial infarction which is detected by troponin I and ischemic pulmonary edema are the most common immediate postoperative cardiac complications. A large number of recent studies, using long-term ECG recording techniques, have allowed more accurate estimation of the incidence and time course of perioperative myocardial ischemia in vascular surgical patients. The highest incidence of ischemia when compared to daily life activities has been noted during the first two days after surgery but has been reported to remain elevated even 3-5 days after surgery. Interestingly, the incidence of intraoperative ischemia is lower than that observed during daily life. Knowledge of the etiology of perioperative myocardial infarction is essential if one is to improve cardiac outcome after vascular surgery. Many studies have addressed this important field in patients undergoing vascular surgery. They have documented a relationship between perioperative myocardial ischemia and postoperative myocardial infarction. Although postoperative myocardial infarctions are in most cases limited to endocardium (non Q wave infarction) they significantly reduce life expectancy of the vascular surgical patients. The reduction of cardiac risk following general surgery should focus on methods by which the incidence of myocardial ischemia, particularly during the postoperative period, could be reduced. These methods include intensive intraoperative analgesia or preventive administration of cardiovascular treatment which limit postoperative stress: alpha-2 agonists or betablocking agents. There are, at present, no studies which convincingly confirm an overall decreased mortality if coronary bypass surgery is performed prior to peripheral vascular surgery. Although it has been demonstrated that the mortality of the peripheral procedure is reduced to approximately one half, the mortality of a coronary bypass procedure in vascular surgical patients is five to eight times that recorded in a coronary artery bypass population without peripheral vascular disease. It remains to be shown if the use of coronary angioplasty prior to peripheral vascular surgery can provide a more satisfactory overall outcome. Several non-invasive techniques have been suggested to improve the identification of high-risk patients undergoing vascular surgery. These tests include exercise ECG, ambulatory ECG, dipyridamolethallium scintigraphy and determination of left ventricular ejection fraction by gated radionuclide imaging. (ABSTRACT TRUNCATED)
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PMID:[Physiopathologic introduction to anesthesia and resuscitation of the vascular patient]. 955 51

Intestinal reperfusion (IR)-induced pulmonary edema has been related to endogenous pulmonary thromboxane A2 (TxA2) release. This study examines the hypothesis that alveolar macrophages (aMphis) activated during IR are an important cellular source of TxA2 in this model. Anesthetized Sprague Dawley rats underwent 120 min of intestinal ischemia and 60 min of reperfusion (IR) or sham operation (Sham). aMphis were isolated by bronchoalveolar lavage and incubated in Krebs buffer for 30 min, after which the supernatant was analyzed for TxB2 (metabolite of TxA2) and prostaglandin E2. Other parameters of aMphi activation measured included lysosomal enzyme release (beta-glucuronidase), superoxide (O2-) release, and procoagulant activity. aMphis from animals sustaining IR generated more than twice as much TxA2 and prostaglandin E2 as did those isolated from controls (p < .05). Other evidence of aMphi activation included a nearly 100-fold increase in procoagulant activity, a 7-fold increase in beta-glucuronidase release, and a 2.5-fold increase in O2- release over that of controls (p < .05). These data suggest that TxA2 is a major eicosanoid product of aMphis during IR and that aMphis may be an important cellular participant in IR-induced pulmonary microvascular injury, either directly by releasing O2-, lysosomal enzymes, and pro-coagulant factors, or indirectly by generating TxA2.
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PMID:Alveolar macrophage response to remote organ injury. 956 54


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