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

Furosemide and morphine reduce pulmonary edema associated with congestive heart failure. It is uncertain whether furosemide or morphine are direct-acting relaxants of arterial and venous smooth muscle. The authors compared the effect of furosemide and morphine on isolated rings of canine pulmonary artery (PA) and vein (PV) and mesenteric, splenic and anterior tibial arteries and their corresponding veins precontracted with norepinephrine or (15S)-hydroxy-11 alpha, 9 alpha-(epoxymethano)prosta-5Z,13E-dienoic acid. Furosemide (10-300 microM) selectively relaxed veins by an endothelium-independent mechanism, with its greatest efficacy on the PV. Morphine (10-1000 microM) relaxed both arteries and veins. The mechanism of relaxation by furosemide and morphine was examined in the PV and PA. Morphine-induced relaxation of the PV and PA was dependent on prostanoid release from endothelium and smooth muscle because it was attenuated in endothelium-rubbed and ibuprofen-treated PV and PA but not in blood vessels treated with inhibitors of nitric oxide system/cyclic GMP system (I-NG-nitroarginine and methylene blue). Furosemide-mediated relaxation of the PV was refractory to each of these interventions. Similarly, furosemide- and morphine-induced relaxation of the PV were unaffected by 4-aminopyridine, tetraethylammonium, glibenclamide, dendrodotoxin and apamin and, thereby, were independent of an action on K+ channels. Reduction of extracellular K+ or Cl- attenuated furosemide-mediated relaxation of, and inhibition of 86Rb+ uptake by, PV even in the presence of ouabain. It was concluded that furosemide relaxes veins by an effect on Na+/K+/Cl- cotransport or chloride-mediated refilling of intracellular calcium stores.
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PMID:Selective pulmonary and venous smooth muscle relaxation by furosemide: a comparison with morphine. 793 55

Two routes by which interstitial pulmonary edema liquid may leave the lung during recovery are reabsorption into the pulmonary circulation and clearance by lung lymphatics. We hypothesized that reabsorption of edema liquid of low protein concentration into the pulmonary circulation would be greater than reabsorption of edema liquid of high protein concentration because of the greater protein osmotic gradient in the former. On the basis of previous studies, lymph flow should contribute minimally to the recovery. In 22 in situ perfused sheep lungs with lymph fistulas, we produced approximately 100 g of osmotic or hydrostatic edema (low protein) or increased leakiness edema by calcium depletion (high protein). To induce reabsorption, we changed the perfusate from low- (1% albumin, osmotic pressure = 4 cmH2O) to high-protein (7% albumin, osmotic pressure = 22 cmH2O) solution in the osmotic group, decreased capillary pressure from 29 +/- 9 to 11 +/- 6 cmH2O in the hydrostatic group, or reversed leakiness by adding CaCl2 to the perfusate in the increased leakiness group. Reabsorption occurred only during recovery from osmotic (40 +/- 22% of filtered liquid) and hydrostatic (15 +/- 11%) edema. Total lung lymph flow during recovery from osmotic, hydrostatic, or increased leakiness edema was 4.9 +/- 3.4, 4.3 +/- 3.4, or 3.5 +/- 1.9 g, respectively. We conclude that during recovery from pulmonary edema interstitial liquid is reabsorbed into the circulation in inverse proportion to its protein concentration. We confirm that only a small fraction of the interstitial edema liquid is cleared by the lymphatics during recovery from any type of edema.
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PMID:Recovery from increased pressure or increased leakiness edema in perfused sheep lungs. 796 Dec 32

A rabbit model with severe smoke inhalation injury was adopted to observe the effect of tetrandrine, a calcium antagonist, on pulmonary dysfunction after smoke inhalation during 24 hours post injury. It was found that tetrandrine could decrease the permeability of pulmonary and tracheal vascular permeability (p < 0.01), reduce lung edema and improve the function of respiration. These results imply that tetrandrine might be used in the treatment of inhalation injury.
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PMID:[An experimental observation of effect of tetrandrine on pulmonary dysfunction in rabbit model of smoke inhalation injury]. 822 5

Pulmonary opacities following orthotopic liver transplantation (OLT) are frequent due to pneumonia, infarction, or pulmonary edema. Metastatic pulmonary calcifications are present as persistent opacities that may mimic these conditions. In a series of 91 patients who underwent OLT, chest radiographs of 77 were reviewed and pulmonary calcinosis was seen in 4 (5.2%). Pulmonary calcinosis may be due to a variety of conditions, including dystrophic calcification in damaged lung and primary or secondary hyperparathyroidism. In this series, patients with pulmonary calcinosis had significantly higher levels of serum phosphate and calcium postoperatively and had received more intraoperative platelets and other blood products containing exogenous calcium than other patients. Pulmonary calcinosis should be considered in patients following OLT when stable, nonspecific pulmonary opacities are present. CT or radionuclide studies will aid in confirming this diagnosis.
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PMID:Pulmonary calcinosis following orthotopic liver transplantation. 824 29

Thirty per cent of patients who started maintenance haemodialysis at our institution between January 1989 and December 1991 had been referred at a very late stage of their renal disease. To assess the causes and consequences of such late referral we retrospectively compared clinical and laboratory features of 65 patients who had been referred less than 1 month prior to first dialysis (late referral, or LR group) and of 153 patients who had been previously followed-up by us for more than 6 months (early referral, or ER group). Age, sex ratio, and socioeconomic status were similar in the two groups. In the LR group, 38 patients had never been referred to a nephrology unit, whereas 27 had discontinued nephrological surveillance. Fluid overload, severe hypertension, and/or pulmonary oedema was present in 57% of LR versus 15% of ER patients (P < 0.001). Mean (+/- 1 SD) systolic and diastolic blood pressure was greater in the LR than the ER group (173 +/- 19/99 +/- 12 versus 147 +/- 15/84 +/- 8 mmHg, P < 0.001). Mean plasma concentration of creatinine, urea and phosphate was significantly greater, whereas bicarbonate, calcium, haematocrit and albumin were less in the LR than the ER group. Most (88%) LR patients started dialysis in emergency conditions through central vein catheterization. Total hospital stay lasted 34.5 +/- 16.3 days in LR versus 5.8 +/- 3.0 days in ER patients (P < 0.0001), resulting in an excess cost of 0.2 million French francs per LR patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Late referral to maintenance dialysis: detrimental consequences. 827 21

Despite broader indications and easier access to renal replacement therapy during the past decades in Western countries, an unduly high number of patients is still referred to maintenance hemodialysis (HD) at a very advanced stage of chronic renal failure (CRF). To assess whether such late referral induces detrimental effects, we retrospectively compared clinical status and laboratory features in 20 patients who had been referred to us less than one month prior to first HD (late referral, or LR group) and in 20 sex- and age-matched controls who had undergone regular follow-up for at least six months prior to HD (early referral, or ER group). Male to female ratio was 12/8 and age averaged 53.5 years in both groups. Mean (+/- 1 SD) systolic and diastolic blood pressure were higher in LR group than in controls (180 +/- 14/102 +/- 10 vs. 153 +/- 15/86 +/- 7 mm Hg, P < 0.001) and fluid overload with pulmonary edema was present in 13/20 versus 3/20 patients (P < 0.001). Plasma concentrations (mmol/liter) of creatinine (1.12 +/- 0.27 vs 0.97 +/- 0.11, P < 0.01) and phosphate (2.58 +/- 0.47 vs. 1.92 +/- 0.31, P < 0.001) were higher, whereas plasma levels of bicarbonate (14.2 +/- 3.9 vs 22.5 +/- 4.2, P < 0.001) and calcium (1.85 +/- 0.24 vs. 2.27 +/- 0.15, P < 0.001) were lower in LR than in ER group, as were hemoglobin (7.1 +/- 1.1 vs. 9.4 +/- 0.9 g/dl, P < 0.001) and serum albumin levels (35.3 +/- 4.8 vs. 39.7 +/- 3.4, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Detrimental effects of late referral in patients with chronic renal failure: a case-control study. 832 Sep 13

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

Rapid ascent to high altitude may be associated with the development of high-altitude pulmonary edema (HAPE) in susceptible individuals. Because lung lavage fluid obtained from such patients can be rich in protein and neutrophils, we considered that an element of lung injury and inflammation contributed to the pathogenesis of some forms of HAPE. On the basis of such a likely contribution of inflammatory mechanisms, we induced pulmonary lung injury and inflammation by priming rats with Salmonella enteritidis endotoxin (ETX) (0.1 or 0.5 mg/kg body wt ip) and examined the influence of added exposure to simulated hypobaric hypoxia (24 h, 4,300 m). The animals that were primed with ETX and exposed to hypoxia, but not those that received either ETX or hypoxia alone, developed lung vascular damage. This vascular damage manifested itself histologically and by increases in the lung vascular permeability-surface area product and the lung bloodless wet weight-to-dry weight ratio. The bronchoalveolar lavage fluid of ETX-primed hypoxia-exposed rats contained a greater number of white blood cells and a higher concentration of protein compared with that of the ETX-primed rats. Hearts of ETX + hypoxia-treated rats showed an increased ratio of right ventricular weight divided by body weight (RV/BW). Neutropenia prevented the development of pulmonary edema and the increase in ETX + hypoxia rats with a Ca2+ entry blocker inhibited lung injury and RV hypertrophy, these results indicate that ETX priming causes pulmonary edema at high altitude and suggest a role for neutrophils and Ca2+ in this rat model of lung injury.
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PMID:Endotoxin priming followed by high altitude causes pulmonary edema in rats. 839 Apr 37

There is evidence supporting the role of active transport of Na+ in the resolution of pulmonary edema, but the exact cellular mechanism(s) underlying this process remain unknown. This study demonstrated the presence of ion channels on adult rat alveolar type II cells that might be associated with this active transport of Na+. Patch-clamp techniques were used to characterize a nonselective cation channel in adult rat alveolar type II epithelial cells held in culture for 24 to 72 h. Single-channel currents were recorded from inside-out, cell-free membrane patches. The most common type of single channel had a linear slope conductance of 20.4 +/- 0.6 pS (n = 22) in symmetrical NaCl (150 mM) solutions. The channel was approximately equally permeable to Na+ and K+ ions (PK/PNa = 1.15) and was highly selective for cations (PCl/PNa < 0.05). Channel activity was Ca(2+)-dependent, and it required at least 10 microM Ca2+ on the cytosolic side of an inside-out patch to activate the channel. Amiloride (1 to 10 microM), a Na+ channel blocker in epithelial tissue, reduced the steady-state open probability of the channel 10-fold but had no significant effect on the magnitude of the single-channel conductance. Single channels with similar properties were not found in cultured rat alveolar macrophages. The possible role of this amiloride-sensitive, nonselective cation channel in Na+ transport and lung liquid clearance is discussed.
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PMID:Identification of nonselective cation channels in cultured adult rat alveolar type II cells. 839 61

In our experience the use of OKT3 as prophylaxis in renal transplantation has been associated with an increased incidence of both delayed graft function and thromboses of graft vessels. OKT3 nephrotoxicity might have been favored by restriction of perioperative fluid infusion to prevent pulmonary edema and by the use of very high dose (30 mg/kg) of methylprednisolone (mPDS) before the first OKT3 injection to reduce the release of cytokines. This led us to modify our perioperative management in three ways: (1) hydration status was optimalized; (2) the calcium-channel blocker diltiazem, considered beneficial for recovery of graft function, was administered on the day of transplantation; and (3) the dose of mPDS given before the first OKT3 injection was fixed at 8 mg/kg. Comparison of two consecutive series of patients (group 1, control patients, N = 172; group 2, managed as described above, N = 173) showed that: (1) the incidence of delayed graft function fell from 52% in group 1 to 22% in group 2 (P < 0.0001): (2) the incidence of pulmonary edema was not significantly increased in group 2 (3.5% vs. 1.7% in group 1, P = 0.5); and (3) the frequency of intragraft thrombosis fell from 7.6% in group 1 to 1.2% in group 2 (P = 0.0034). Multivariate analysis showed that the volemia/diltiazem program and avoidance of high mPDS dose were the most important factors responsible for the reduced occurrence of delayed graft function and graft vessels thrombosis, respectively. We conclude that a combined strategy of appropriate dosage of steroids before the first OKT3 injection, administration of a calcium-channel blocker and optimalization of volemia is safe and efficiently prevents against OKT3 nephrotoxic effects.
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PMID:Prevention of OKT3 nephrotoxicity after kidney transplantation. 877 Sep 89


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