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

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.
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PMID:Pathophysiological mechanisms of brain damage from status epilepticus. 838 2

The 1991 American Association of Gynecologic Laparoscopists membership survey on operative hysteroscopy had a total of 630 respondents (almost double the 1988 number) who reported performing 17,298 procedures as compared to 7,293 in 1988. Directed biopsy and endometrial ablation were the procedures reported most commonly. Endometrial ablation increased fivefold since 1988, and myomectomy increased fourfold. The majority of operative hysteroscopies were performed for a complaint of abnormal bleeding (73%). The most frequently reported complication was uterine perforation not requiring transfusion (11 per 1,000 procedures). The rate of water intoxication or pulmonary edema dropped from 3.4/1,000 in 1988 to 1.4/1,000 in 1991. However, some serious complications (eight laparotomies for bowel injury, three CO2 embolisms and three deaths) were reported for 1991.
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PMID:Operative hysteroscopy. American Association of Gynecologic Laparoscopists 1991 membership survey. 841 Aug 57

1. The possible contribution of endogenous endothelin (ET) to the pathogenesis of seizure-associated pulmonary oedema was examined in mechanically ventilated rats after intravenous bolus injection of the gamma-aminobutyric acid (GABA) antagonist, bicuculline (1.2 mg kg-1). 2. Recurrent seizure activity elicited by bicuculline injection led to rapidly developing pulmonary oedema. Within 4 min after bicuculline application (1.2 mg kg-1), arterial O2 partial pressure (PaO2) significantly dropped from 17.49 +/- 1.20 kPa to 7.51 +/- 2.21 kPa (P < 0.01) and arterial CO2 partial pressure (PaCO2) significantly increased from 4.64 +/- 0.56 kPa to 8.15 +/- 0.99 kPa (P < 0.01). Gradually a progressive acidosis developed. Moreover, mean arterial blood pressure (MABP) and end-inspiratory airway pressure (Paw) rapidly increased. 3. Concomitantly there was a time-dependent increase of big ET-1 and ET-1 levels in bronchoalveolar lavage (BAL) as determined by combined reverse phase high performance liquid chromatography (h.p.l.c.) and radioimmunoassay. BAL levels of both peptides increased up to 8 min after bicuculline injection and slowly decreased subsequently. In contrast, BAL from animals injected with vehicle did not contain detectable amounts of ET. 4. Pretreatment with the endothelin-converting enzyme inhibitor, phosphoramidon (5.4 mg kg-1, i.v.) for 5 min significantly (P < 0.001) reduced peak ET-1 levels in BAL fluid by 65.4 +/- 9.9% at 8 min after bicuculline injection. Simultaneously it afforded protection from hypoxia. PaCO2 did not increase and PaO2 decreased only slightly from 14.63 +/- 1.00 kPa to 12.97 +/- 0.61 kPa (P > 0.05) after phosphoramidon pretreatment. In contrast, vehicle-treated animals that received bicuculline showed both significant hypercapnia as well as profound hypoxia. Phosphoramidon significantly diminished the maximum increase in Paw by 76.7 +/- 12.4% (P <0.005), but only slightly affected the MABP. Phosphoramidon pretreatment had no effect on the acidosis.5. Pretreatment with the ETA receptor antagonist, BQ-123 (1 mg kg-1, i.v.), for 5 min did not affect the levels of ET-1 in the BAL fluid at 8 min after bicuculline injection but did ameliorate the development of hypoxia. No hypercapnia developed and Pa02 decreased only moderately from 16.65 +/-0.25 kPa to 14.19 +/-2.15 kPa (P>0.05) in BQ-123-treated animals. In contrast, vehicle-treated animals that received bicuculline exhibited significant hypercapnia as well as profound hypoxia. BQ-123 significantly reduced the increase in Paw by 51.3 +/- 12.8% (P < 0.01). It affected MABP only slightly and had no effect on the acidosis.6. These results suggest that ET peptides play a significant role in this model of neurogenic pulmonary oedema and may act as mediators of respiratory distress. The deleterious effects of endogenous ET in this model are primarily mediated via the ETA receptor, for they were inhibited by the ETA receptor antagonist, BQ-123. ETA receptor antagonists may therefore be of potential therapeutic value in respiratory distress.
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PMID:A role for endothelin in bicuculline-induced neurogenic pulmonary oedema in rats. 854 73

In an effort to increase the donor pool for lung transplantation (LTX), we have demonstrated the feasibility of LTX from circulation-arrested cadavers in a canine LTX model. We hypothesized that ventilation of the cadaver lung with alveolar gas (20% O2, 5% CO2, balance N2) (AG) would be superior to ventilation with 100% oxygen (O2) after circulatory arrest of the donor. Twelve mongrel dogs were intubated, heparinized and euthanized by pentothal injection and ventilated with AG (n=6) or O2 (n=6). Four hours later, donor animals underwent sternotomy, and the lungs were flushed with cold modified Euro-Collins solution, harvested, and stored inflated in ice slush. Left lung allotransplantation was performed, and recipients were made dependent o n the transplanted lung by occlusion of the contralateral bronchus and pulmonary artery. Recipient animals were ventilated with an FiO2 of 0.4 and followed for 8 hr. Total ischemic time was 7.9 hr for both groups. Pulmonary edema developed in all recipients of AG lungs; one recipient survived the 8-hr observation period with poor oxygenation. In contrast, three of six recipients of O2-ventilated lungs survived for 8-hr with excellent gas exchange. Specimens of donor lungs before and after transplant were evaluated histologically utilizing trypan blue exclusion as an indicator of cell viability. At the time of organ retrieval 4 hr after death, 6% of cells were nonviable in the O2-ventilated cadaver lungs. Circulation-arrested cadaver lungs ventilated with 100% O2 prior to organ retrieval have superior pulmonary function after transplant compared with lungs ventilated with AG. Ventilation of cadaver lungs with AG induces pulmonary injury in this model. retrieval of donor lungs from circulation-arrested cadavers has potential for increasing the pulmonary donor pool.
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PMID:Cadaver lungs for transplantation. Effect of ventilation with alveolar gas. 862 77

Our purpose if to develop a survival strategy for man trapped in a confined space. A previous study showed that in the rat there is a critical exposure time beyond which hypoxic survival improves. To evaluate the general applicability of these findings in the rat and the influence of body size, the effect of exposure time on hypoxic survival was studied in immature pigs (26 kg). The pig consumed the oxygen in a sealed chamber until hypoxic collapse. We measured blood pressure, oxygen consumption, inspired O2 and CO2, minute ventilation, ECG, body temperature, and PO2, PCO2 and pH in arterial and venous blood. Five groups of pigs were confined in different initial volumes of air, producing total exposure times of 0.5, 1.3, 2.3, 4.8 and 6.7 h. There was no significant difference between the experimental groups for any of the parameters measured during the exposure. Unlike the rat, in the pig there was no "adjustment time" beyond which the animal could survive to a lower PIO2. Terminal inspired PO2 increased as a function of exposure time. This was related to either hypoventilation or lung edema. There was a correlation between the level of carbon dioxide in the blood at 60-70 torr inspired oxygen and the terminal PO2. Pigs which failed to clear the carbon dioxide succumbed early to hypoxia. In a confined space it is preferable to maintain normoxic conditions for as long as possible.
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PMID:Effect of exposure time on the survival of immature pigs in a confined atmosphere. 887 28

Acute pulmonary edema after a large air embolus occurring during neurosurgery is a recognized phenomenon. The authors describe the course of a 76-year-old man who presented with noncardiogenic pulmonary edema shortly after undergoing resection of a high convexity meningioma. Transthoracic Doppler sonography, however, showed no evidence of a large intraoperative emboli; the evidence for ongoing but low-magnitude air embolus included visualization of bone aspiration of irrigant before bone-edge waxing, transient intraoperative declines in end-tidal CO2 tension, and an increase of the fraction of inspired oxygen to maintain adequate saturation after removal of the craniotomy flap. There was no hemodynamic instability noted. The airspace disease was self-limited and resolved on supportive treatment after approximately 1 week, as would be expected for pulmonary edema caused by a single large intravenous air embolus. The authors present this case as the first report of pulmonary edema resulting from low-level air embolus occurring during craniotomy. This situation may go unrecognized intraoperatively but can cause the same significant postoperative morbidity as larger, more easily identified air emboli.
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PMID:Acute pulmonary edema after low-level air embolism during craniotomy. Case report. 889 35

In an attempt to identify the range of opinions influencing the diagnosis and therapy of patients with the adult respiratory distress syndrome (ARDS), a postal survey was mailed to 3,164 physician members of the American Thoracic Society Critical Care Assembly. The questionnaire asked opinions regarding the factors important in the diagnosis of ARDS and its treatment. Thirty-one percent of physicians surveyed responded within 4 weeks, the vast majority of which were board certified or eligible in Internal Medicine, Pulmonary Disease, and/or Critical Care Medicine. A known predisposing cause, measure of oxygenation efficiency, and a chest radiograph depicting pulmonary edema were reported to be the most important criteria for a clinical and research diagnosis of ARDS. Lung compliance and bronchoalveolar lavage neutrophil or protein content were reportedly less important. The initial treatment of patients with ARDS was reported to be most commonly accomplished using volume-cycled ventilation in the assist/control mode. Nearly half the responders reported using lower tidal volumes (5 to 9 mL/kg) than the traditionally recommended 10 to 15 mL/kg. Most respondents indicated they have intentionally allowed CO2 retention. On average, oxygen toxicity was thought to begin at an FIO2 between 0.5 and 0.6. It was reported that modest levels of positive end-expiratory pressure (PEEP) were used in incremental fashion as FiO2 requirements increased. Perceived indications for insertion of pulmonary artery catheters and compensation of the effects of PEEP on the pulmonary artery occlusion pressure varied widely among the responders. We conclude that reported practice patterns regarding the care of ARDS patients vary widely even within a relatively homogenous group of critical care practitioners.
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PMID:Diagnosis and therapy of acute respiratory distress syndrome in adults: an international survey. 890 79

Isolated lungs of Wistar rats were ventilated by air that was enriched with 5% CO2 and perfused with homologous blood in a closed circuit (9.5 +/- 1 ml/min) using Hugo Sachs apparatus type 829. Lipopolysaccharide from E.coli (LPS, serotype 0127:B8) at a selected sub-toxic concentration of 300 micrograms/ml added to recirculating blood produced a biphasic response. Instant transient increase in pulmonary arterial and venous perfusion pressures, and a decrease in air tidal volume, and fifty minutes later slowly progressing decrease in air tidal volume without changes in pulmonary haemodynamics, were observed. Inhibition of pulmonary nitric oxide synthase by instillation of NG-nitro-L-arginine methyl ester (L-NAME) at a final concentration of 300 microM to recirculating blood dramatically changed the response to LPS. In nitric oxide deficient lungs LPS caused prompt increase in arterial and venous pressures and a fall in air tidal volume with accompanying rise in airway resistance. Within 6.3 +/- 0.5 min a fulminant pulmonary oedema developed and all functions of the lung stopped abruptly. We conclude that pulmonary nitric oxide plays a defensive role in protecting rat lungs against LPS-induced injury.
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PMID:Increased pneumotoxicity of lipopolysaccharide from E.coli in nitric oxide deficient blood-perfused rat lungs. 944 14

At the University of Minnesota, University of Wisconsin (UW), modified Euro-Collins (MEC), and Marshall (M) solutions were compared as agents for pulmonary preservation in an isolated rabbit lung model. Normal saline (NS) was used as a control. The heart-lung blocks of donor rabbits were flushed with, and then preserved in, one of the solutions at 4 degrees C. Five rabbits were studied in each group. After 8 h of cold ischemia, the left lung was ventilated and reperfused with fresh venous blood from donor rabbits for 30 min. Pulmonary function was assessed by serial measurements of oxygen (O2) and carbon dioxide (CO2) tensions in blood obtained from the left atrial appendage. The ratios of wet/dry (W/D) weight of the lungs were calculated to assess the extent of pulmonary edema. After 8 h of preservation followed by 30 min of reperfusion, O2 tension was significantly higher with UW (178.36 + 1.72 mmHg). The calculated P values were UW vs NS, < 0.0001; UW vs MEC, 0.154; and UW vs M, 0.0001. CO2 tension with UW was also lower than the other solutions: UW, 35.8 +/- 0.698 mmHg; NS, 48.5 +/- 0.745 mmHg; MEC, 40.69 +/- 0.749 mmHg; and M, 44.68 +/- 0.697 mmHg. The calculated P value was UW vs NS, 0.0001; UW vs MEC, 0.0003; and UW vs M, 0.0001 using repeated-measures analysis of covariance. The W/D ratio was lower with UW as well; UW, 6.82 +/- 0.19; NS, 8.01 +/- 0.23; MEC, 7.28 +/- 0.10; and M, 7.34 +/- 0.17. The P value was < 0.001 using post-hoc tests. In this model, UW solution preserved the lungs better than the other three solutions tested and therefore warrants further clinical application.
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PMID:Comparative study of solutions for pulmonary preservation using an isolated rabbit lung model. 965 94

During strenuous exercise in sheep, lung lymph flow increases within seconds and rises to levels 7- to 10-fold over baseline. Concomitant with the flow increase, the lymph protein content rapidly decreases to levels consistent with severe capillary hypertension. This pattern of clearance of filtered fluid is quite different than is seen with the passive capillary hypertension that results from mechanical obstruction of the mitral valve. In passive capillary hypertension, the increase in lymph flow and reduction in lymph protein content develop over several hours. The purpose of this study was to discover if these observed differences in edema clearance are related to the hyperpnea that accompanies exercise. Sheep were instrumented for continuous measurement of pulmonary arterial, left atrial, and systemic pressures, cardiac output by ultrasound, lung lymph flow, and ventilation. First, hemodynamics, ventilatory, and lymph clearance variables were measured during moderate exercise at 2.8 mph on a treadmill. Second, on a separate occasion, sheep were induced to hyperventilate to the same minute ventilation as during exercise, using modest CO2 stimulation. Lymph flow and hemodynamics were unaffected by this hyperpnea. The third arm of the experiment was to raise pulmonary microvascular pressure at rest to the level seen with exercise by means of a balloon catheter placed in the mitral valve. Lymph flow rose and protein content decreased slowly and to a lower degree than seen with exercise despite a comparable microvascular pressure. Finally, left atrial hypertension and induced hyperpnea were combined in sheep at rest, and the resulting lymph flow and protein content were the same as seen with exercise at similar pressures and ventilation. We conclude that hyperpnea is a major mechanism of interstitial liquid clearance during exercise, and may be largely responsible for preventing pulmonary edema that might occur at the high microvascular pressures of strenuous exercise.
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PMID:Clearance of filtered fluid from the lung during exercise: role of hyperpnea. 1125 13


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