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

Abdominal aortic aneurysmectomy (AAA) results in thromboxane (Tx)A2 generation, a rise in mean pulmonary artery pressure (MPAP), leukopenia, and noncardiogenic pulmonary edema. This study tests whether mannitol, a hydroxyl radical scavenger, modifies these events. Patients received mannitol 0.2 g/kg (n = 14) or saline (n = 12) intravenously before infrarenal aortic clamping. With saline, 30 minutes after clamping, plasma TxB2 levels rose from 124 to 290 pg/mL (p less than 0.01), and MPAP rose from 19 to 27 mmHg (p less than 0.01). Aortic clamp release led to further increases in plasma TxB2 to 378 pg/mL (p less than 0.01) and MPAP to 34 mmHg (p less than 0.01). The white blood count (WBC) fell from 9800 to 4400/mm3 (p less than 0.01). Four to eight hours after surgery, physiologic shunting (Q[sc]S[xsc]/Q[sc]T[xsc]) rose from 9% to 20% (p less than 0.01) and peak inspiratory pressure (PIP) increased from 22 to 32 cmH2O (p less than 0.01). Chest radiography demonstrated pulmonary edema while the pulmonary wedge pressure was 12 mmHg, excluding left ventricular failure. By 24 hours pulmonary edema resolved and the PIP and PaO2 returned to baseline. Mannitol treatment relative to saline, during and after aortic clamping reduced plasma TxB2 levels to 155 and 198 pg/mL, respectively (p less than 0.01); MPAP to 21 and 26 mmHg (p less than 0.01); minimized the decline in WBC to 5850/mm3 (p less than 0.01), and the postoperative rise in Q[sc]S[xsc]/Q[sc]T[xsc] to 12%, and PIP to 28 cmH2O (both p less than 0.01). Chest radiography showed no pulmonary edema. Finally in vitro studies documented that mannitol 1 to 10(-4)M, but not dextrose, in a dose-dependent manner inhibited Tx synthesis by ADP-activated platelets. These data indicate that mannitol maintains pulmonary function after AAA by limiting ischemia-induced thromboxane synthesis.
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PMID:Pulmonary edema after aneurysm surgery is modified by mannitol. 1257 26

This study was undertaken to determine whether lung ventilation during warm ischemia provides a protective effect on lung preservation. The mongrel dogs were made left thoracotomy incision. Following a complete dissection of left pulmonary artery and vein, left lung was subjected to room temperature ischemia for 4 hours or 6 hours by clamping vasculature. Left lung was ventilated with oxygen or collapsed during warm ischemic period. The isolated ventilation of left lung was secured by ligation of left main bronchus over Carlens tube. After the ischemic period, blood supply of the left lung was reestablished by unclamping the pulmonary artery and vein. The contralateral pulmonary artery was ligated 10 min later, and blood gas, pulmonary pressure, and pulmonary shunt were monitored for additional 4 hours while left lungs ventilated with oxygen. In lungs collapsed during 4 hour ischemic period, massive pulmonary edema occurred within 30 minutes after reperfusion. Partial oxygen tension was only 63 mmHg at 1 hour after reperfusion. In contrast, lungs ventilated during 4 hours ischemic period did not manifest pulmonary edema, and PaO2 was 407 mmHg at 4 hours after reperfusion. The lungs collapsed during 6 hour ischemic period showed massive edema. When the lung was ventilated, the lung behaved variably but still better than the collapsed lungs. These results suggest that the ventilation of the lung during warm ischemia provide a protective effect.
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PMID:[Protective effect of ventilation on warm ischemic lungs]. 261 11

Reperfusion following lower-torso ischemia in humans leads to respiratory failure manifest by pulmonary hypertension, hypoxemia, and noncardiogenic pulmonary edema. The mechanism of injury has been studied in the sheep lung lymph preparation, where it has been demonstrated that the reperfusion resulting in pulmonary edema is due to an increase in microvascular permeability of the lung to protein. This respiratory failure caused by reperfusion appears to be an inflammatory reaction associated with intravascular release of the chemoattractants leukotriene B4 and thromboxane. Histological studies of the lung in experimental animals revealed significant accumulation of neutrophils but not platelets in alveolar capillaries. We conclude that thromboxane generated and released from the ischemic tissue is responsible for the transient pulmonary hypertension. Second, it is likely that the chemoattractants are responsible for leukosequestration, and, third, neutrophils, oxygen-derived free radicals, and thromboxane moderate the altered lung permeability.
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PMID:Reperfusion pulmonary edema. 221 74

Left lung autotransplantation was performed in mongrel dogs to examine the limitation of tolerance of the deflated lung against warm ischemia in a warm ischemic time (WIT) range of 60-360 minutes. The animals were divided into the 4 following groups according to the duration of WIT and the use of heparin: Group 1; WIT 60-120 min., heparin (-), Group 2; WIT 120-240 min., heparin (+), Group 3; WIT 240-360 min., heparin (+), and Group 4; WIT 240-360 min., heparin (-). All the Group 1 animals tolerated a right pulmonary artery ligation on the 6th postoperative day, but some of the Group 2 animals died immediately after the reimplantation due to pulmonary edema. All the Groups 3 and 4 animals died. The PaO2 values during the right pulmonary artery occlusion, immediately after the reimplantation, correlated well with the survival of the animals. The maximum tolerable WIT of the deflated dog lung was considered to be 120 minutes.
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PMID:An evaluation of the tolerance of the autotransplanted canine lung against warm ischemia. 267 3

A 27-year-old man was accidentally given 2 mg intravenous epinephrine instead of 2 mg naloxone. He immediately developed chest pain, nausea, and diaphoresis. An ECG taken shortly after the epinephrine administration showed widespread ischemia. Forty-five minutes later the tracing still showed an early repolarization pattern, but ST elevation was less marked and the patient was asymptomatic. Serum potassium was 3.2 mEq/L and serum catecholamines, drawn approximately 20 minutes after the epinephrine administration, were 10 times normal (dopamine, 173 ng/L; epinephrine, 1,628 ng/L; norepinephrine, 1,972 ng/L). There are seven other reports of intravenous epinephrine overdose in the English literature. Two of the previously reported cases had 12-lead ECGs within the first hour. In both there was evidence of transient ischemia similar to that observed in this case. Most of the patients had symptoms consistent with angina, and several developed pulmonary edema. These findings suggest that, in humans, large intravenous doses of epinephrine are likely to produce coronary artery spasm and may decrease coronary artery perfusion.
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PMID:Coronary artery spasm induced by intravenous epinephrine overdose. 275 14

Patients who undergo peripheral vascular surgery are at increased risk for postoperative cardiac events and are difficult to assess preoperatively because of limitations on their activity. We prospectively studied 176 consecutive eligible patients undergoing elective vascular surgery to determine the value in predicting a postoperative cardiac event of preoperative electrocardiographic monitoring to detect myocardial ischemia. Of the 176 patients, 32 (18 percent) had 75 episodes of monitored ischemic ST-segment depression preoperatively (of which 73 were asymptomatic), and 13 (7 percent) met strict criteria for major postoperative cardiac events, including 1 with a fatal myocardial infarction, 3 with nonfatal infarctions, 4 with unstable angina, and 5 with ischemic pulmonary edema. Of the 32 patients with ischemia before their operations, 12 had postoperative events (univariate relative risk, 54; 95 percent confidence interval, 7.2 to 400). Only 1 postoperative event occurred among 144 patients who did not have preoperative ischemia. The sensitivity of preoperative ischemia was 92 percent, the specificity 88 percent, the predictive value of a positive result 38 percent, and the predictive value of a negative result 99 percent. In multivariate analyses, preoperative ischemia was the most significant correlate of postoperative cardiac events and remained a statistically significant independent correlate even after we had controlled for all other preoperative factors (multivariate relative risk, 24.4; 95 percent confidence interval, 6.8 to 88). These preliminary data suggest that preoperative electrocardiographic monitoring to detect episodes of myocardial ischemia is a useful method for assessing cardiac risk in patients who undergo elective vascular surgery. In particular, the absence of ischemia during monitoring indicates a very low risk.
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PMID:Correlation between preoperative ischemia and major cardiac events after peripheral vascular surgery. 279 5

We reviewed the postoperative chest radiographic and CT findings in the first 13 patients who underwent bilateral lung transplantation at our institution. Portable chest radiography was performed daily for about 10 days, after which upright posteroanterior studies were performed daily for about 10 days, and then as clinically required. CT was performed when a complication was suspected. The reimplantation response (noncardiogenic pulmonary edema due to ischemia, trauma, denervation, and lymphatic interruption) occurred in 12 patients and usually consisted of bilateral perihilar and basal consolidation. Twelve episodes of acute rejection, an imprecise clinical diagnosis, occurred in 10 patients. Radiographic changes consisted of bibasal (n = 2), right mid and lower (n = 2), or left basal consolidation (n = 1); there were no changes in seven episodes. Radiographic resolution occurred in four cases after administration of IV steroids. The radiographic findings associated with the reimplantation response and rejection were nonspecific and were mimicked by fluid overload and infection. Bronchial dehiscence and/or stricture formation occurred in seven patients; generally chest radiography was inaccurate and CT was very accurate in the assessment of these complications. Chest radiography was helpful but not definitive in sorting out the problems occurring in the postoperative period after bilateral lung transplantation. CT was excellent for use in demonstrating airway problems.
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PMID:Chest radiographic findings after bilateral lung transplantation. 281 29

We examined the basis of reperfusion-induced pulmonary edema produced by pulmonary artery occlusion and subsequent reperfusion. After a 24-h period of occlusion of a rabbit pulmonary artery followed by a 2-h period of reperfusion, the lungs were removed from the animal and perfused with a 0.5 g% Ringer's-albumin solution. An increase in lung weight was observed within 60 min compared with control lungs (i.e., lungs subjected to pulmonary arterial occlusion but not reperfusion) (p less than 0.05). Shorter periods of occlusion (6 or 12 h) did not result in edema, which suggests that a period of ischemia was required for the reperfusion-induced pulmonary edema. The extravascular lung water content also increased in the contralateral lung (i.e., the lung not subjected to pulmonary arterial occlusion and reperfusion). The capillary filtration coefficient increased in reperfused lungs compared with controls (p less than 0.05), indicating an increase in lung vascular permeability following reperfusion. Infusion of allopurinol (a xanthine oxidase inhibitor) and superoxide dismutase during the reperfusion period prevented the increases in lung weight and vascular permeability; infusion of catalase was ineffective. We conclude that pulmonary reperfusion following pulmonary artery occlusion increases pulmonary vascular permeability, which is mediated by the generation of oxidants.
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PMID:Pulmonary edema after pulmonary artery occlusion and reperfusion. 281 6

We previously demonstrated that in vivo reperfusion of a dog lung after 48 h of pulmonary arterial (PA) ischemia results in pulmonary edema with a significant infiltrate of polymorphonuclear leukocytes. We hypothesized that the injury resulted from production of hydroxyl radical by activated neutrophils. In the current study, we attempted to prevent the injury in both dogs and rabbits with dimethylthiourea (DMTU), a scavenger of hydroxyl radical. After 48 h of left PA occlusion in 18 dogs, DMTU was administered to 9 animals and 9 were not treated. The occlusion was then released, and the dogs were killed 4 h later. Reperfusion resulted in a drop in leukocyte count and left lung edema, but there was no difference between treated and untreated animals. The wet-to-dry ratios of the lungs in the treated group were 5.76 +/- 0.44 (SE) on the reperfused left side and 4.50 +/- 0.06 (P less than 0.05) on the right side. In the untreated groups the comparable ratios were 5.73 +/- 0.31 and 4.92 +/- 0.10 (P less than 0.05 for right vs. left). Histological examination revealed significant differences between the right and left lungs in the extent of intra-alveolar granulocytes and macrophages but did not reveal differences between the treated and untreated animals. To ensure that neither the model nor the lack of response to DMTU was species specific, we then developed a rabbit model of reperfusion edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dimethylthiourea does not ameliorate reperfusion lung injury in dogs or rabbits. 285 Feb 92

Limb ischemia in experimental animals leads to white blood cell (WBC) and thromboxane (Tx)A2 dependent pulmonary dysfunction. This study examines the pulmonary sequelae of lower torso ischemia in 20 consecutive patients aged 63 +/- 5 years (mean +/- SEM) who underwent elective abdominal aortic aneurysm surgery. After 30 minutes of aortic cross-clamping, plasma TxB2 levels had risen from 77 +/- 26 pg/ml to 359 +/- 165 pg/ml (p less than 0.01) and was temporally related to increases in mean pulmonary artery pressure (MPAP) from 18 +/- 1 to 23 +/- 3 mmHg (p less than 0.01), as well as to increases in pulmonary vascular resistance (PVR) from 0.07 +/- 0.02 to 0.12 +/- 0.02 mmHg sec/ml (p less than 0.01). Each time that the aortic clamp was repositioned and with final declamping, after 83 +/- 10 minutes, there were further increases in MPAP to a peak of 32 +/- 2 mmHg (p less than 0.01) and in PVR to 0.26 +/- 0.030 mmHg sec/ml (p less than 0.01), corresponding to a plasma TxB2 level of 406 +/- 177 pg/ml (p less than 0.01). MPAP and PVR returned to baseline values within 30 minutes of declamping. Ten minutes after removal of the aortic clamp, platelet levels had fallen from 180 +/- 41 to 97 +/- 17 X 10(3)/mm3 (p less than 0.01) and WBC levels from 8900 +/- 1100 to 4700 +/- 400/mm3 (p less than 0.01). Both platelets and WBC returned towards normal levels, but at 24 hours, while WBC was elevated at 13000 +/- 900/mm3 (p less than 0.01), platelets were 44% of baseline at 135 +/- 14 X 10(3)/mm3 (p less than 0.01). Four to 8 hours after surgery, pulmonary dysfunction was manifest by increases in physiologic shunt from 9 +/- 2% to 16 +/- 2% (p less than 0.01), and peak inspiratory pressure (PIP) from 23 +/- 2 to 33 +/- 2 cmH2O (p less than 0.01). Chest radiography demonstrated interstitial pulmonary edema in all patients, whereas pulmonary artery wedge pressure was 12 +/- 2 mmHg, excluding the possibility of left ventricular failure. After 24 hours, pulmonary edema had resolved, and the PIP and PaO2 had both returned to baseline. These data indicate that reperfusion of the ischemic lower torso leads to the synthesis of TxA2, an event temporally related to pulmonary hypertension and transient leukopenia with subsequent pulmonary microvascular injury manifest by interstitial edema.
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PMID:Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery. 291 66


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