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)

Experimental Lassa virus infections of squirrel monkeys, guinea-pigs, and the African multimammate rat, Mastomys natalensis, were studied virologically and pathologically. In the monkeys, early viral lymphoreticulotropism, hepatotropism, nephrotropism, and viraemia were noted. At the time of death, viral titres in nearly all target organs were associated with necrotic changes: splenic lymphoid necrosis, renal tubular necrosis, myocarditis, arteritis, and hepatocytic regeneration. In convalescent monkeys, organ titres diminished slowly, and viraemia persisted at 28 days. At this time, renal and splenic regeneration was occurring and a new lesion, choriomeningitis, was present.Guinea-pigs infected with Lassa virus developed respiratory insufficiency with pulmonary oedema, alveolar hyaline membranes, myocarditis, and focal calcification of myocardial fibres and hepatocytes. Dying animals contained Lassa virus in virtually every organ tested, whereas survivors at 56 days were free of virus and had high complement-fixing antibody titres.Infection of neonatal Mastomys did not cause any clinical disease or pathological lesions despite the presence of virus in the blood, lymph nodes, liver, spleen, lung, brain, urine, and throat secretions throughout the 74-day study. Infected adult Mastomys also remained normal but had virus in many organs. In one animal, virus persisted until the termination of the study at 103 days. Several animals developed a mild meningoencephalitis. The pattern of infection and virus shedding in M. natalensis is ideal for maintenance of the virus in nature; together with the epidemiological field data this emphasizes the incidental nature of the exposure and infection of man.
 ...
PMID:Comparative pathology of Lassa virus infection in monkeys, guinea-pigs, and Mastomys natalensis. 82 25

Renal transplantation in infants has been associated with a high incidence of acute tubular necrosis and of renal artery thrombosis. Since 1978, 24 infants who received an adult kidney transplant at the University of Minnesota have had aggressive administration of intravenous colloids to increase the central venous pressure to 16-20 mm Hg before renal reperfusion. Acute tubular necrosis developed in only two infants, and there were no cases of renal artery thrombosis. Chest radiographic evidence of pulmonary edema was present in the recovery room in seven patients (29%) and within the first four postoperative days in five patients (21%). Yet, only two infants (8.3%) required postoperative mechanical ventilation beyond 24 h to manage fluid overload. With aggressive intravenous colloid administration, infants in renal failure can receive an adult kidney transplant with a low incidence of active tubular necrosis or renal artery thrombosis, but pulmonary edema may develop requiring ventilatory support.
 ...
PMID:Anesthetic management of infants receiving an adult kidney transplant. 195 73

Two cases of fatal hydrogen sulfide poisoning are described which occurred during cleaning of a tank that had transported polysulfides. The most characteristic findings of the autopsy were: a blackish-green pigmentation at macroscopic examination; pulmonary edema, steatosis, intrahepatic cholestasis and renal tubular necrosis at microscopic examination. The blood concentration of sulfide ions exceeded 3.5 mg/l. These cases are compared to others described in the literature. The preventive measures that should be adopted to avoid this type of poisoning are stressed.
 ...
PMID:Fatal hydrogen sulfide poisoning. 279 35

Pyridoxal 5'-phosphate (PLP), the active form of vitamin B6, readily forms complexes with a wide variety of potentially toxic substances, including cyanide (KCN), spermine (SPM), gentamicin (GM), and dopamine (DOP). The role of PLP as an antidote for these toxicants in vivo was studied. Rats were given intraperitoneal injections of the toxicant, followed by injections of either saline or PLP. For KCN, PLP increased the LD50 from 0.088 to 0.188 mmol/kg and extended the survival time at the highest dose employed from a median of 3 min to a median of 60 min. For SPM, PLP increased the LD50 from 0.162 to 0.262 mmol/kg and prevented death from renal failure at all doses employed except the highest. PLP protected against GM-induced neuromuscular paralysis and death. In the case of DOP, results were equivocal, but no deaths were seen in the PLP-treated rats. The combination of individually nontoxic doses of GM, DOP, and SPM caused death with renal tubular necrosis, pulmonary edema and hemorrhages, congestion of the viscera, and a diffuse coagulopathy. Because many seriously ill patients have elevated SPM levels and are given GM and/or DOP, we suggest that further investigation of the potential protective role of PLP in serious illness be undertaken.
 ...
PMID:Pyridoxal 5'-phosphate as an antidote for cyanide, spermine, gentamicin, and dopamine toxicity: an in vivo rat study. 357 25

A report is made of a 44-year-old female who died of malignant hyperthermia during general anesthesia for an operation of left subtrochanteric femoral fracture. Symptoms began with increases in heart rate and blood pressure after the introduction of anesthesia with halothane and were accelerated by the administration of succinylcholine, followed by muscle rigidity and high temperature. The typical wine red urine was observed. The oral temperature of 42 degrees C was recorded within 1 h after succinylcholine. The rectal temperature was 30 degrees C 22 h after death. Severe pulmonary edema and tubular necrosis of the kidney were found by postmortem examination. No latent myopathy was observed. The creatine phosphokinase levels in plasma obtained after the onset of malignant hyperthermia and at the time of autopsy were abnormally high and were 5632 and 34,854 mU/ml, respectively. Plasma myoglobin levels were 130,000 and 2.8 X 10(6) ng/ml, respectively.
 ...
PMID:An autopsy case of malignant hyperthermia. 398 93

Seven of 74 patients with early functioning cadaveric renal homografts developed acute oliguric renal failure after the second but before the ninth day post-transplantation. The syndrome characteristically begins with an abrupt and simultaneous decrease in creatinine clearance, urine volume and urine sodium concentration. After a variable period and despite a reduction in immunosuppressive therapy, a diuretic phase ensues and renal function is restored. Complications associated with the syndrome include groin hematoma, pulmonary edema and renal rupture with shock. Renal rupture does not require nephrectomy: if the hemorrhage is controlled, the transplanted organ will resume function. Angiographic studies show normal nephrograms, stretched arterial vasculature and filling defects in the veins. Percutaneous renal biopsy shows interstitial edema and hemorrhage, venous congestion and tubular necrosis. Evidence is presented to support the hypothesis that this is a form of rejection occurring as the result of injury to the renal venous system.
 ...
PMID:Early acute rejection of renal homografts: a characteristic clinical syndrome. 457 54

Twenty-two patients who had been bitten by a Russell's viper were studied. Neurological manifestations and generalized myalgia were observed, respectively, in 86.4% and 72.7%. Renal failure did not occur in three patients who received antivenin within 5 hours of the bite, and it is suggested that administration of antivenin within the first few hours following the bite could prevent renal failure. Of 19 patients who were in acute renal failure, seven responded to conservative management while 12 needed peritoneal dialysis. Nine patients developed pulmonary edema and four had grand mal seizures. Five patients died. Autopsy revealed massive pulmonary edema, thought to be the immediate cause of death, in four of them and extensive cortical and tubular necrosis in three.
 ...
PMID:Russell's viper bite in Sri Lanka. A study of 22 cases. 673 82

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

Hantaviruses chronically infect rodents without apparent disease, but when they are spread by aerosolized excreta to humans, two major clinical syndromes result: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Both diseases appear to be immunopathologic, and inflammatory mediators are important in causing the clinical manifestations. In HPS, T cells act on heavily infected pulmonary endothelium, and it is suspected that gamma interferon and tumor necrosis factor are major agents of a reversible increase in vascular permeability that leads to severe, noncardiogenic pulmonary edema. HFRS has prominent systemic manifestations. The retroperitoneum is a major site of vascular leak and the kidneys suffer tubular necrosis. Both syndromes are accompanied by myocardial depression and hypotension or shock. HFRS is primarily a Eurasian disease, whereas HPS appears to be confined to the Americas; these geographic distinctions correlate with the phylogenies of the rodent hosts and the viruses that coevolved with them.
 ...
PMID:Spectrum of hantavirus infection: hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome. 1007 92

This study investigated the effect of glycine on hemorrhagic shock in the rat. Rats were bled to maintain mean arterial pressure at 30-35 mm Hg for 1 h and subsequently resuscitated with 60% shed blood and lactated Ringer's solution. Only 20% of rats receiving saline just prior to resuscitation survived 72 h after shock. Survival was increased by glycine (11.2-90.0 mg/kg, i.v.) in a dose-dependent manner (half-maximal effect = 25 mg/kg) and reached maximal values of 78% at 45 mg/kg. Eighteen hours after resuscitation, creatinine phosphokinase increased 23-fold, transaminases increased 33-fold, and creatinine was elevated 2.4-fold, indicating injury to the heart, liver, and kidney, respectively. Pulmonary edema, leukocyte infiltration, and hemorrhage were also observed. In the kidney, proximal tubular necrosis, leukocyte infiltration, and severe hemorrhage in the outer medullary area occurred in rats receiving saline. Glycine reduced these pathological alterations significantly. It has been reported that oxidative stress and tumor necrosis factor(TNF)-alpha-production are involved in the pathophysiology of multiple-organ injury after shock. In this study, free radical production was increased 4-fold during shock, an effect blocked largely by glycine. Increases in intracellular calcium and production of TNF-alpha by isolated Kupffer cells stimulated by endotoxin were elevated significantly by hemorrhagic shock, alterations which were totally prevented by glycine. Taken together, it is concluded that glycine reduces organ injury and mortality caused by hemorrhagic shock by preventing free radical production and TNF-alpha formation.
 ...
PMID:Glycine improves survival after hemorrhagic shock in the rat. 1046 52


1 2 Next >>