Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severe falciparum malaria complicated by acute renal failure resulted in very high mortality. Ten patients with acute renal failure from falciparum malaria (infected rbc up to 80%) were continuously dialysed using Tenckhoff peritoneal catheter. Five were oliguric and BUN was maintained between 60 to 80 mg/dl (21.4 to 28.6 mmol/l) by hourly 1 to 1.5 liter dialysate exchange during the acute phase. The peritoneal urea clearance (mean +/- SD) was 12.1 +/- 1.2 ml/min with urea nitrogen removal of 13.4 +/- 2.3 g/day. In nonoliguric cases dialysis was also needed for additional removal of waste products since the remaining renal function could not cope with the hypercatabolic state. Peritoneal glucose absorption (135 to 565 g/day) gave considerable caloric supply without volume load and also contributed to the prevention of hypoglycemia. Varying degree of acute respiratory failure developed in all patients with 5 cases (2 oliguric and 3 nonoliguric) progressing to pulmonary edema. Swan-Ganz catheterization and hemodynamic study suggested the role of increased capillary permeability and volume overload from endogenous water formation in the development of pulmonary complication. Continuous removal of fluid and waste products minimized these problems and may prevent the progression of respiratory failure. One patient died of severe sepsis and the other nine survived. This study showed the beneficial contribution of continuous peritoneal dialysis in the management of acute renal failure from severe falciparum malaria.
 ...
PMID:Continuous peritoneal dialysis in acute renal failure from severe falciparum malaria. 312 24

Endotoxin injected intraperitoneally caused leucopenia and pulmonary oedema in rats. These effects were spontaneously reversed over the 28 h after the single dose of endotoxin. The pharmacokinetics of three substrates, 14C-sucrose, 3H-prostaglandin E2 (PGE2) and 3H-adenosine, were measured in perfused lungs isolated from rats at different times after treatment with endotoxin. The efflux kinetics of radiolabel derived from sucrose and adenosine were little affected, but that from PGE2 was markedly changed. The metabolism of PGE2 was also decreased. The change in PGE2 pharmacokinetics preceded the pulmonary oedema, but both pharmacokinetics and oedema returned to normal at the same time (28 h after endotoxin). It may be feasible to use PGE2 pharmacokinetics as a biochemical index for early warning of acute lung injury caused by sepsis.
 ...
PMID:Effects of endotoxin-induced lung injury on the pharmacokinetics of prostaglandin E2 and adenosine in rat isolated lung. 314 94

Live Pseudomonas aeruginosa (2.5.10(9).kg-1.h-1) were administered to awake (Group A, n = 10) and anesthetized piglets, which were given intravenous ketamine (Group K, 10 mg.kg-1.h-1, n = 8) or pentobarbital (Group P, 15 mg.kg-1.h-1, n = 8). The anesthetized animals were mechanically ventilated. In addition, a pentobarbital group (Group CP, n = 6) and a ketamine control group (Group CK, n = 6) were studied. The mean survival time was 10.5 +/- 3.0 h in Group A, 10.6 +/- 2.8 h in Group K, and 1.8 +/- 1.3 h in Group P. In Group P the arterial pressure, the cardiac output and the systemic vascular resistance declined soon after start of the bacterial infusion, whereas the pulmonary artery pressure increased. The animals died of irreversible circulatory failure. In Group K pronounced pulmonary hypertension and lethal pulmonary edema developed. There was no circulatory failure in Group A, but the animals also died of marked pulmonary edema. Groups CP and CK exhibited stable hemodynamics for a period of 8 h. The results of this study suggest a deleterious effect of pentobarbital on hemodynamics and survival time, and a minor suppressive action of ketamine on the circulation in septicemia. Therefore, data obtained from septic shock studies applying pentobarbital have to be evaluated carefully. Investigation of the effects of gram-negative bacteria or endotoxin should be performed in unanesthetized or, if anesthesia is necessary, in ketamine-anesthetized animals.
 ...
PMID:Comparison of ketamine and pentobarbital anesthesia with the conscious state in a porcine model of Pseudomonas aeruginosa septicemia. 318 20

Neutrophils have been implicated in the pathogenesis of acute lung injury associated with clinical and experimental sepsis. Data from in vitro systems and experimental animals have suggested that neutrophil-derived oxidants, particularly H2O2, may be primarily responsible for endothelial damage, vasoconstriction, and lung edema. With the use of endotoxin infusion as an in vivo model of sepsis we tested the hypothesis that pretreatment with catalase, a peroxide scavenger, would ameliorate the resultant changes in pulmonary vasoconstriction and lung fluid balance. Paired experiments were performed in 16 goats with chronic lung lymph fistulas. One group of animals (n = 7) received endotoxin first alone and then again, several days later, after pretreatment with Ficoll-linked catalase. As a control, identical experiments were performed in a separate group (n = 6) with Ficoll-linked albumin substituted for Ficoll-catalase. A third group (n = 3) was given endotoxin alone and then again during a continuous infusion of catalase. Plasma and lymph levels of catalase were comparable to or exceeded those previously shown to be completely protective in isolated perfused lung preparations and in vitro systems. Endotoxin caused neutropenia, pulmonary arterial hypertension, decreased cardiac output, and increases in lymph flow to approximately three times base line, with a return of all variables toward control values by 6 h. Catalase pretreatment produced no significant differences in any of these variables. These experiments do not support a role for H2O2 as a mediator of acute lung injury due to endotoxemia.
 ...
PMID:Effect of intravenous catalase on the pulmonary vascular response to endotoxemia in goats. 328 99

We prospectively evaluated a protocol that included extravascular thermal volume (ETV) as a measure of extravascular lung water (EVLW) instead of pulmonary artery wedge pressure (Ppaw) measurements to guide the hemodynamic management of 48 critically ill patients. Patients were randomized to either a protocol management (PM), or to a routine management (RM) group. In the RM group, EVLW measurements were unknown to the primary care physicians. The 2 groups were similar with respect to age, gender, and severity of illness. In patients with initially high EVLW, EVLW fell to a greater extent in PM than in RM patients (18 +/- 5 versus 4 +/- 8% decrease, p less than 0.05). This difference was even greater in patients with heart failure. No adverse effects on oxygenation or renal function occurred in following the protocol. Mortality for the groups as a whole was similar, but was significantly better (p less than 0.05) for PM patients with initially high EVLW and normal Ppaw (predominantly patients with sepsis or the adult respiratory distress syndrome). For both groups, patients with an initial EVLW greater than 14 ml/kg had a significantly greater mortality than did those with a lesser amount of EVLW: 13 of 15 (87%) versus 13 of 32 (41%), p less than 0.05. We conclude that management based on a protocol using EVLW measurements is safe, may hasten the resolution of pulmonary edema, and may lead to improved outcome in some critically ill patients.
 ...
PMID:A prospective study of lung water measurements during patient management in an intensive care unit. 330 70

Clinical studies of ARDS have been successful in determining the most common predisposing clinical disorders and the natural history of this syndrome. Sepsis, gastric aspiration, and major trauma are the most frequently associated high-risk factors. Overall mortality is in the range of 60% to 70%, but is even higher if ARDS is associated with sepsis, severe acidemia, or decreased renal function. It is evident that multisystem failure is responsible for death in many patients, as well as secondary pulmonary and extrapulmonary infections. Pathologic studies have provided descriptive information regarding the acute, subacute, and chronic phases of the syndrome, but little insight into the precise pathogenesis of the initial lung injury or the progressive fibrosing alveolitis and lung destruction that develops in some patients. There has been considerable circumstantial evidence from clinical studies implicating the neutrophil as a potentially important mediator of the early changes in lung endothelial and epithelial permeability. However, not all investigators have found the same alterations in neutrophil function in the circulation or in the lavage from the lungs of patients with ARDS. Also, the heterogeneous etiologies of ARDS make it difficult to be sure that there is a final common pathway for acute lung injury in all ARDS patients. In addition, there are a host of mediators, including products of complement activation and arachidonic acid metabolism, that may be important in amplifying the inflammatory response. Also, abnormalities of surfactant production and collagen turnover, as well as impaired host defenses in the lung, may contribute to the progressive respiratory failure that occurs in some ARDS patients, even though the acute, exudative phase of lung injury has resolved. Future human studies may provide useful information about the mechanisms of the acute lung injury through studies of circulating plasma markers, blood elements, and lavage fluids from high-risk patients. On the other hand, samples of cells and mediators from the airspaces with lavage still may not reflect the critical interactions of mediators and cells with the lung endothelium that lead to the protein-rich pulmonary edema that characterizes the first phase of ARDS. Thus, experimental studies must continue to study the details of the early phases of acute lung injury (see article by Flick, page 455). Finally, it is clear that treatment designed to reduce the severity and the incidence of ARDS must be started early, since the syndrome develops so rapidly in high-risk patients.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Pathophysiology of the adult respiratory distress syndrome. What have we learned from human studies? 333 57

Acute renal failure and pulmonary edema developed in a 1-month-old baby with necrotizing enterocolitis and hypovolemic shock. Following resection of 93% of her small intestine and mesentery, peritoneal dialysis was started; it was terminated 96 h later with complete recovery of renal and pulmonary functions. Two weeks later, while on total parenteral nutrition, the infant developed fulminant septicemia and died. Postmortem examination showed normal kidneys. Surface measurement of the abdominal wall and viscera revealed that the actual peritoneal surface area of the patient was 671 cm2, only 44% of her calculated normal peritoneal surface area. We conclude that effective peritoneal dialysis is feasible in infants with acute renal failure even after marked reduction of the peritoneal surface area.
 ...
PMID:Effective peritoneal dialysis in an infant with extensive resection of the small intestine. 336 76

We present a case of adult respiratory distress syndrome (ARDS) after extensive liposuction. On the basis of fever, tachypnea, hypoxia, and ARDS occurring within 48 hours after surgery without evidence of cardiogenic pulmonary edema or sepsis, the etiology is believed to be fat embolism. Although liposuction is generally an effective and safe procedure, awareness of this life-threatening complication is important in order to institute prompt and appropriate treatment. Fat embolism must be differentiated from thromboembolism, as the treatment is different, and heparin is not indicated. It is recommended that training standards and guidelines be devised in order to reduce morbidity and mortality associated with this procedure.
 ...
PMID:Fat embolism after liposuction. 337 Nov 9

We evaluated the development of pulmonary edema early in the course of peritonitis and shock in rats. Peritonitis was established by cecal ligation and perforation. In a preliminary experiment, sepsis was induced in five animals and five animals served as sham-operated controls. Lungs harvested for gravimetric analysis at 6 hours revealed no significant difference in wet-dry/dry (W-D/D) ratios. In a second experiment, 15 rats were randomized to three groups: septic animals, septic animals infused with 5% albumin, and sham-operated animals. Thermodilution cardiac output and arterial blood gases were sequentially measured over a 6-hour interval. At 6 hours, the lungs were harvested for gravimetric analysis. Lung W-D/D and arterial oxygenation were not significantly different between the three groups. The W-D/D was 3.46 +/- 0.10 in sham-operated rats, 3.37 +/- 0.12 in septic rats, and 3.88 +/- 0.27 in albumin-infused septic rats. The alveolar-arterial oxygen difference at 6 hours was 10 +/- 2 mm Hg in sham-operated rats, 7 +/- 1 mm Hg in septic rats, and 13 +/- 6 mm Hg in albumin-infused septic rats. These data suggest that overt pulmonary edema and arterial hypoxemia may not occur early in septic shock when fluid infusion is not excessive.
 ...
PMID:Absence of pulmonary edema during peritonitis and shock in rats. 339 28

Degradation of structural elements and excessive consumption of humoral factors, especially of plasma proteinase inhibitors, by proteolysis and/or oxidation is a major cause of multiple organ failure in sepsis or septic shock. Such pathobiochemical reactions seem to be induced primarily by extracellularly liberated lysosomal proteins from PMN granulocytes (e.g. elastase, cathepsin G, myeloperoxidase, lactoferrin) as well as oxygen radicals produced during extensive phagocytosis. In clinical studies on septicemia and septic shock the consumption of plasma proteins including proteinase inhibitors was inversely correlated to the liberation of lysosomal factors, especially the granulocytic elastase. Administration of relatively specific elastase-cathepsin G-inhibitors (Bowman-Birk inhibitor, eglin) in experimental septicemia proved to be a promising therapeutic approach to reduce consumption of plasma proteinase inhibitors and development of interstitial lung edema in severe inflammation.
 ...
PMID:Pathobiochemistry of sepsis: role of proteinases, proteinase inhibitors and oxidizing agents. 352 75


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