Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present investigation was to evaluate lung toxicity in 15 patients affected by metastatic melanoma of different sites, and treated with recombinant interleukin-2 (rIL-2) plus lymphokine-activated killer (LAK) cells The treatment regimen included a first and a second course of rIL-2, separated by four consecutive daily leukaphereses. Autologous LAK cells were reinfused during the second course. Lung function was monitored before and after each rIL-2 administration. In the 12 patients who could be followed until completion of the therapy, spirometric parameters and transfer factor of the lungs for carbon monoxide (TLCO) decreased significantly during the first rIL-2 course, remained stable during leukapheresis, and declined significantly further during the second rIL-2 course. In the second phase, chest radiography documented some degree of pulmonary oedema, ranging from interstitial oedema to frank pulmonary oedema. A significant dose-dependent correlation was found between the cumulative rIL-2 dose and the decline in TLCO in the first course of therapy. Moreover, patients who developed symptomatic respiratory insufficiency (World Health Organisation grade III or IV) during the second course of therapy received a higher number of LAK cells than those who did not. The data support the hypothesis that LAK cells have an additional toxic effect on the lung.
 ...
PMID:Pulmonary toxicity of recombinant interleukin-2 plus lymphokine-activated killer cell therapy. 833 2

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.
 ...
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.
 ...
PMID:Operative hysteroscopy. American Association of Gynecologic Laparoscopists 1991 membership survey. 841 Aug 57

Continuous positive pressure ventilation (CPPV) is an established therapy for treatment of acute respiratory failure (ARF). However, cardiac performance may be severely disturbed due to elevated intrathoracic pressure, inducing a decrease in cardiac output (CO) and oxygen delivery (DO2). Alternatively, mechanical ventilation with prolonged inspiratory to expiratory duration ratio (inversed ratio ventilation IRV) has been successfully used in ARF. No data are available about IRV in acute haemodynamic oedema. Thus, the cardiopulmonary effects of CPPV (positive end-expiratory pressure [PEEP] = 10 cm H2O) and IRV (inspiration to expiration duration ratio [I:E] = 3.0) were studied in nine dogs (body weight 29.9 +/- 4.3 kg) before and after induction of myocardial ischaemia. METHODS. Continuous intravenous anaesthesia and muscle paralysis were provided by 1.2 mg.kg-1 x h-1 piritramide and 0.08 mg.kg-1 x h-1 pancuronium, and the animals were ventilated with intermittent positive pressure ventilation (IPPV) as reference method. Cardiocirculatory performance was determined by means of heart rate (HR), mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP) and left ventricular end-diastolic pressure (LVEDP). Cardiac output (CO) was determined by thermodilution method. Systemic vascular resistance (SVR) was calculated. Pulmonary function was assessed by arterial and mixed venous blood gas tension for oxygen (PaO2, PvO2) and carbon dioxide (PaCO2). Functional residual lung capacity (FRC) was measured by means of the foreign gas wash-in method using helium as inert gas, and determination of extravascular lung water (EVLW) using the thermal-dye indicator technique. CPPV and IRV were studied in random sequence in the control phase and 60 min after induction of acute left ventricular ischaemia, which was achieved by occlusion of the ramus interventricularis anterior. RESULTS. During the control phase CPPV induced an increase in MPAP (P < 0.05), CVP (P < 0.05) and PAOP (P < 0.05). HR and MAP remained unchanged, whereas CO decreased by 16% (P < 0.05). FRC was elevated by 25 ml.kg-1 (P < 0.01), but not EVLW (9.1 +/- 3.5 ml.kg-1). There was no improvement in oxygenation; instead, oxygen delivery (DO2) decreased (P < 0.05). During inversed ratio ventilation MPAP, CVP, PAOP increased, but less than during CPPV. FRC was elevated mu 7.0 ml.kg-1 (P < 0.05), which was significantly less than during CPPV (P < 0.05). EVLW revealed no differences. During IPPV in the ischaemia phase cardiopulmonary performance deteriorated significantly. CO decreased by 19% (P < 0.05), whereas HR, MPAP, CVP and PAOP increased (P < 0.05). PaO2 was lower (P < 0.05) and alveolo-arterial PO2 gradient (PAaO2) increased (P < 0.05). All animals revealed moderate pulmonary oedema (EVLW = 15.1 +/- 8.4 ml.kg-1) (P < 0.01) and a lower FRC. Mechanical ventilation with PEEP significantly improved oxygenation and FRC; however, DO2 was slightly lower than during IPPV (not significant). IRV elevated PaO2, FRC and DO2, since CO was not depressed when compared with IPPV. CONCLUSIONS. CPPV and IRV may induce a recruitment of collapsed or hypoventilated lung areas, which is more pronounced during CPPV. During both modes of ventilation, oxygenation was improved without apparent changes in EVLW. Haemodynamic performance was more impaired during CPPV, and no improvement of left ventricular function secondary to an elevated intrathoracic pressure was observed. Occlusion of the RIVA coronary artery typically induces an infarction of 35% of left ventricular muscle mass; however, non-ischaemic myocardium reveals an unchanged or increased contractility. Thus, a reduction of left ventricular preload secondary to CPPV mainly contributes to haemodynamic depression, which is less pronounced during IRV due to a lower peak inspiratory airway pressure and mean airway pressure. IRV may be useful for mechanical ventCntCo
 ...
PMID:[Cardiopulmonary effects of CPPV (continuous positive pressure ventilation) and IRV (inverse ratio ventilation) in experimental myocardial ischemia]. 848 92

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.
 ...
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.
 ...
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.
 ...
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.
 ...
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.
 ...
PMID:Diagnosis and therapy of acute respiratory distress syndrome in adults: an international survey. 890 79

This study was conducted to investigate whether the changes in the pulmonary diffusing capacity found in individuals with acute mountain sickness (AMS) reflect the early stage of high-altitude pulmonary edema (HAPE). We measured the pulmonary diffusion capacity for carbon monoxide (DCO) by the single-breath method, arterialized capillary blood gas, and spirometry in a group of 32 healthy subjects (24 men, eight women) at an altitude of 2,260 m and after ascent to 4,700 m. Twelve subjects (10 men, two women) had symptoms of AMS (AMS group) by the second day after arrival at 4,700 m, but none had clinical signs of pulmonary or cerebral edema. In the non-AMS group, almost all subjects exhibited an increase in DCO at 2,260 to 4,700 m (delta DCO, 10.7 +/- 1.25 mL/min/mm Hg), while the degree of increase in DCO in the AMS group (n = 12) was significantly lower (delta DCO, 1.26 +/- 1.74 mL/min/mm Hg) than that of the non-AMS group (p < 0.01). In four of the 12 subjects with AMS who had a high AMS score, DCO decreased from 38.4 +/- 4.5 to 33.2 +/- 5.3 mL/min/mm Hg (delta DCO, -5.84 +/- 1.1 mL/min/mm Hg). The AMS group showed significantly lower vital capacity, forced expiratory flow during the middle half of FVC, PaO2, and a greater alveolar-arterial oxygen pressure difference at 4,700 m compared with the non-AMS group. DCO showed a significant negative correlation with AMS score (r = -0.885) and a positive correlation with PaO2 (r = 0.757) at 4,700 m. These results suggest that the decreased pulmonary diffusing capacity in subjects with AMS reflects the presence of pulmonary gas exchange abnormality, which is probably due to subclinical interstitial edema of the lung.
 ...
PMID:Low pulmonary diffusing capacity in subjects with acute mountain sickness. 899 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>