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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blockade of the arachidonic acid cascade has been shown to improve survival and hemodynamic alterations in animal models of sepsis and acute respiratory failure (ARF). The effects of intravenous ibuprofen, a cyclooxygenase inhibitor, were observed in 20-30 kg pigs with ARF induced by a continuous LD100 infusion of live Pseudomonas aeruginosa (2 X 10(8)/20 kg/min). Cardiopulmonary parameters were monitored in animals intubated, paralyzed, and ventilated at a 250-ml tidal volume and 0.5 FiO2. Pigs were randomly assigned to three groups: Group I received 2 bolus infusions of ibuprofen (12.5 mg/kg) at 20 and 210 min after baseline; Group II had Ps. aeruginosa (2 X 10(8) CFU/20 kg/min) only; Group III received Ps. aeruginosa and 12.5 mg/kg of ibuprofen at 20 and 210 min of ARF. Ibuprofen alone caused no significant changes in cardiorespiratory parameters. With Ps. aeruginosa infusion, significant pulmonary hypertension, hypoxemia, increased intrapulmonary shunt fraction, and systemic hypotension occurred. In the septic animals treated with ibuprofen, oxygenation was improved by a significant decrease in shunt, pulmonary edema, and pulmonary hypertension.
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PMID:Effects of ibuprofen on a porcine model of acute respiratory failure. 670 94

Acute burn wound sepsis is a common clinical entity resulting from a showering of the circulation with gram-negative organisms which grow abundantly in the burn. We duplicate this state in our laboratory by creating 40%, third degree burns (anesthetic burns) in chronically instrumented sheep. Three days following the thermal insult, the burn wound is infected by injecting gram-negative organisms (3 X 10(10)) into it. Cardiopulmonary variables and pulmonary lymph flux data are monitored two hours prior to the injection of organisms and for three hours following it. Three different organisms were used in this study; Pseudomonas aeruginosa (N = 12), Escherichia coli (N = 9), and Klebsiella pneumoniae (N = 2). The injection of all three organisms resulted in a similar response; an early marked pulmonary hypertension and a late increase in microvascular permeability. These changes occur concomitantly with an elevation in hematocrit and an early marked fall in neutrophils. The cardiac output gradually falls over the period of observation despite vigorous body shivering associated with a febrile response. The data from the sheep were compared to similarly instrumented animals (N = 12) which were not burned, but received a very small dosage of E coli endotoxin (0.75 micrograms/kg). The cardiopulmonary response was qualitatively identical to that seen with live organisms. However, the quantitative changes in several of the cardiopulmonary variables were much more marked with endotoxin. It is concluded that the cardiopulmonary response noted with burn wound sepsis is produced by endotoxin.
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PMID:Is endotoxin responsible for the cardiopulmonary lesions seen during acute burn wound sepsis? 675 41

Infusion of Escherichia coli endotoxin (0.12-1.5 micrograms/kg) into unanesthetized sheep causes transient pulmonary hypertension and several hours of increased lung vascular permeability, after which sheep recover. To produce enough lung injury to result in pulmonary edema with respiratory failure, we infused larger doses of E. coli endotoxin (2.0-5.0 micrograms/kg) into 11 chronically instrumented unanesthetized sheep and continuously measured pulmonary arterial, left atrial and aortic pressures, dynamic lung compliance, lung resistance, and lung lymph flow. We intermittently measured arterial blood gas tensions and pH, made interval chest radiographs, and calculated postmortem extravascular bloodless lung water-to-dry lung weight ratio (EVLW/DLW). Of 11 sheep 8 developed respiratory failure; 7 died spontaneously 6.3 +/- 1.1 h, and one was killed 10 h after endotoxin infusion. All sheep that had a premortem room air alveolar-arterial gradient in partial pressure of O2 (PAo2-Pao2) greater than 42 Torr (58 +/- 5 (SE) Torr) died. Of eight sheep that had radiographs made, six developed radiographically evident interstitial or interstitial and alveolar edema. Pulmonary artery pressure rose from base line 22 +/- 2 to 73 +/- 3 cmH2O and remained elevated above baseline levels until death. There was an initial fourfold decrease in dynamic compliance and sixfold increase in pulmonary resistance; both variables remained abnormal until death. EVLW/DLW increased with increasing survival time after endotoxin infusion, suggesting that pulmonary edema accumulated at the same rate in all fatally injured sheep, regardless of other variables. The best predictor of death was a high PAo2-Pao2. The marked increase in pulmonary resistance and decrease in dynamic compliance occurred too early after endotoxin infusion (15-30 min) to be due to pulmonary edema. The response to high-dose endotoxin in sheep closely resembles acute respiratory failure in humans following gram-negative septicemia. Respiratory failure and death in this model were not due to pulmonary edema alone.
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PMID:Respiratory failure after endotoxin infusion in sheep: lung mechanics and lung fluid balance. 675 92

Adult respiratory distress syndrome is becoming more frequent in pediatric age. There are several factors involved in its' etiology. Sepsis is almost invariably present in all patients. Basic mechanism is an increase of pulmonary capillary permeability with production of acute non cardiogenic oedema. The decrease in compliance and functional residual capacity produce a respiratory failure with hypoxemia non-responsive to the increase in FiO2. Pulmonary hypertension and low cardiac output appear once the syndrome has developed. In its' management, cardiorespiratory monitoring is essential. Prophylaxis is based on early treatment of the essential pathological process. Corticoids are only effective if they are administered before development of pulmonary oedema. The treatment is based on: a) Moderate water restriction. b) Early respiratory assistance using PEEP or CPAP. c) Maintenance of adequate oxygen transport. The extracorporeal oxygenation guarantees the oxygen exchange but it does not affect survival. Mortality is 95%. Patients who survive have minimal pulmonary sequelae.
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PMID:[Adult respiratory distress syndrome in childhood]. 681 14

Some newborn infants with either primary or secondary persistent pulmonary hypertension (PPHN) remain hypoxemic, hypercarbic, and acidotic despite therapeutic efforts. In autopsies of 23 infants who had PPHN, diffuse platelet-fibrin thrombi were present in the pulmonary microcirculation of eight (15.2 +/- 18.1 thrombi/cm2 lung tissue) and absent in 15 (0.2 +/- 0.3 thrombi/cm2 lung tissue), (P less than 0.004). Diagnoses in group A (thrombi) were pneumonia and sepsis (four patients), meconium inhalation (3), and primary PPHN (1); and in group B (no thrombi) pneumonia and sepsis (4), meconium inhalation (4), primary PPHN (4), hyaline membrane disease (2), and diaphragmatic hernia (1). The only significant differences between the two groups were the response to tolazoline infusion as assessed by changes in partial pressure of arterial oxygen (PaO2) and the platelet counts. Group A responded less favorably to tolazoline (14.8 mm Hg vs 83.6 mm Hg; P less than 0.05) and had lower platelet counts (51,000/microliter vs 128,000/microliter) (P less than 0.01) than group B. No significant differences could be detected in Apgar scores, duration or mode of mechanical ventilation, oxygen requirements, arterial blood gas tensions or pH, systemic arterial blood pressure, coagulation profile, amount of blood product transfusions, or intravascular catheter use. Pulmonary microthrombi should be added to the list of mechanisms for PPHN and may explain why some infants do not respond well to therapeutic efforts aimed at vasodilation. Thrombocytopenia and failure to respond to pulmonary vasodilators might suggest the diagnosis.
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PMID:Pulmonary microthrombi syndrome in newborn infants with unresponsive persistent pulmonary hypertension. 682 42

The clinical spectrum of neonatal endocarditis, including bacterial and nonbacterial types, is examined in five case reports that were drawn from nursery experiences over a recent 2-year period. In contrast to previous reports of 100% mortality from neonatal endocarditis, one patient survived. Changing heart murmur and hematuria were most frequently associated with bacterial and nonbacterial endocarditis in four of the five cases. Pulmonary hypertension, thrombocytopenia, and coagulopathy were also associated with nonbacterial endocarditis. Echocardiograms were performed on four of the patients; only one was suggestive of endocarditis. Staphylococcus aureus was isolated from both cases of bacterial endocarditis, including the single survivor. Thus, it is suggested that the initial antibiotic coverage of any neonate with the clinical syndrome of sepsis, hematuria, and a heart murmur include antistaphylococcal coverage for the possibility of bacterial endocarditis.
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PMID:Endocarditis in high-risk neonates. 682 46

The mechanism of respiratory distress in sepsis is unknown. Previous work has shown elevations of prostaglandins during sepsis. This study reveals a correlation between levels of prostaglandins F 2 alpha and E and pulmonary hypertension and other parameters of respiratory distress in oophorectomized ewes subjected to endotoxin. The use of prostaglandin synthetase inhibitors prior to endotoxin prevented the rise in prostaglandins and the development of respiratory distress.
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PMID:The role of prostaglandins in endotoxemia: comparisons in response in the nonpregnant, maternal, and fetal models. I. Prostaglandins and the pulmonary effect of experimental endotoxemia. 698 49

Septicemia was induced in cats by infusion of live E. coli bacteria into the inferior vena cava, the portal vein or the aortic arch. Systemic arterial blood pressure, aortic blood flow, pulmonary arterial blood pressure, intestinal blood flow and portal venous pressure were recorded continuously and arterial platelet and white blood cell counts and acid-base balance measured at intervals. Infusion of E.coli into the inferior vena cava induced an initial response characterized by systemic pressure reduction, unchanged or increased aortic blood flow and pulmonary hypertension. Intestinal blood flow decreased moderately, while portal pressure remained unchanged. The arterial infusion evoked a similar response. After portal infusion there was a more pronounced increase of aortic blood flow, a significantly less elevation of the pulmonary artery pressure, and the intestinal blood flow was maintained. The changes induced in arterial acid-base balance or in platelet and white cell counts were not influenced by the route of administration. It is concluded that the route of administration of bacteria is of importance when considering the relevance of experimental data to clinical septic states.
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PMID:Pulmonary vascular reactions in experimental septicemia, A preliminary report. 700 84

The reactions in the series-coupled vascular sections of the small intestine and the changes in aortic blood flow, systemic arterial, and pulmonary arterial blood pressure were followed continuously in cats made septic by IV infusion of live E coli bacteria for 2 hours. Peripheral venous infusion initially induced systemic hypotension, pulmonary hypertension, and increased aortic blood flow, but decreased intestinal blood flow. These changes were normalized within 5-10 minutes. During the next 110 minutes systemic arterial blood pressure, aortic blood flow, and intestinal blood flow decreased continuously while intestinal blood flow resistance remained in the control range. Portal venous infusion induced a significantly less pronounced initial pulmonary arterial blood pressure increase. No initial intestinal vasoconstriction was noticed and intestinal blood flow resistance decreased during the bacterial infusion. In both series only small and insignificant changes of intestinal tissue volume were seen. The data suggest that the route of infusion is important to the response in experimentally-induced sepsis. The constant intestinal tissue volume argues against intestinal pooling as being of importance to the development of low blood pressure in septic shock.
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PMID:Hemodynamic effects of systemic or portal IV infusion of live E coli bacteria in the cat. A preliminary report. 703 61

The use of prostaglandins is currently undergoing clinical trials in respiratory failure accompanying sepsis. The effect of prostaglandin E1 (PGE1) and prostacyclin (PGI2) infusion on endotoxin-induced lung injury, with attention to interstitial fluid flux (QL), pulmonary vascular pressure (Ppa), leukocytes, platelets, and release of the lysosomal enzyme beta-glucuronidase, was investigated. A chronic lung lymph fistula model in sheep was used. Seven sheep alternately received Escherichia coli endotoxin and endotoxin plus PGE at a dosage of 1 microgram/kg/min. Six sheep received PGI2 (0.2 microgram/kg/min) instead of PGE1. Both PGE1 and PGI2 decreased the pulmonary hypertension and the interstitial edema produced by endotoxin primarily through their vasodilatory properties. Prostacyclin seemed to have an additional membrane-stabilizing effect. A rebound increase in QL, Ppa, and platelets occurred when PGE1 or PGI2 infusion was discontinued.
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PMID:Prostaglandin infusion and endotoxin-induced lung injury. 703 77


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