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Query: UMLS:C0031154 (peritonitis)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reduced oxygen consumption and lactic acidosis were observed frequently in patients with peritonitis. This study was designed to evaluate whether reduced oxygen consumption is secondary to deficient oxygen delivery or is a function of primary injury to mitochondria. Peritonitis was produced in rats by cecal ligation and perforation. Animals were killed at 2, 4, and 6 hours and agonally. Oxygen utilization was studied polarographically in isolated hepatic mitochondria with glutamate, pyruvate, and succinate substrates. State 3, state 4, respiratory control index (RCI), and ADP:O ratios were determined. Whole tissue and isolated mitochondrial ultrastructure were examined by electron microscopy. Systemic blood pressure and oxygenation were monitored. Hepatic tissue oxygenation was examined using a surface oxygen electrode. Peritonitis resulted in acceleration of state 3 respiratory rates and increased respiratory control indices at all time intervals. Maximal respiratory control was observed at 4 hours with all substrates. Whole tissue mitochondria demonstrated mild swelling and thinning of membranes and matrix. Experimental and control isolates showed similar orthodox-to-condensed conformational changes. Hepatic tissue oxygenation declined to less than 10% of control by 6 hours, while arterial Po2 was unchanged. The conclusions of this study are that lethal peritonitis results in (1) no primary injury to the hepatic mitochondria, (2) increased efficiency of hepatic mitochondrial oxygen utilization, and (3) reduced hepatic tissue oxygenation. The exact mechanisms of defective oxygen delivery require further study.
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PMID:Hepatic cellular hypoxia in murine peritonitis. 45 75

Experience with chronic intermittent peritoneal dialysis is reviewed to focus on automated peritoneal dialysis (APD) regimens, adequacy and indications. From 1969 to 1990, 74 ESRD patients were treated: 59 patients with Intermittent Peritoneal Dialysis (IPD: 30-40 l x 3/week) and fifteen patients with hour Daily Peritoneal Dialysis (DPD: 25 l x 6 nights/week). Fourty-four patients were regularly treated with IPD. Of these 33 were adequately dialysed, maintaining residual renal function, whilst oligo-anuric patients developed underdialysis. DPD patients were adequately dialysed, having satisfactory peritoneal clearances. Peritonitis rate was 1/19.2 pt months in IPD patients and 1/13.4 pt months in DPD patients. Technique survival was 78% at the end of the first year, and 52% the second year. IPD is adequate only for low body weight patients with residual renal function. In-hospital IPD must be taken into account only for patients unable to perform dialysis without partner assistance. Home DPD, like CCPD and NPD, is generally adequate and yields fairly good quality of life, but the cost is high, probably because of limited ADP diffusion. Prescription must be therefore restricted to patients unable to perform dialysis with working partners, workers who cannot cope with CAPD exchanges, and CAPD failures.
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PMID:Indications and adequacy of automated peritoneal dialysis in 74 patients. 168 Apr 56

The effect of feline infectious peritonitis virus (FIPV) on platelet aggregation and 14C-serotonin release induced by threshold levels of four agonists (adenosine diphosphate [ADP], collagen, arachidonic acid, and epinephrine) was examined in vitro in ten specific-pathogen-free cats. Purified suspensions of FIPV added to stirred platelet suspensions (virus to platelet ratio equal to 1:320) 1 minute prior to the addition of agonist potentiated the ADP-induced aggregation response by greater than 100% in seven cats. Platelet 14C-serotonin release was increased by greater than 100% in four cats. Collagen-induced platelet aggregation was enhanced in ten cats while collagen-induced 14C-serotonin release was enhanced in eight cats. Potentiation of arachidonic acid-induced platelet aggregation was observed in three cats, two of which demonstrated enhanced platelet 14C-serotonin release. Although epinephrine-induced platelet aggregation was enhanced in five cats, the samples displayed only fine microaggregates. Enhanced 14C-serotonin release from platelets in response to epinephrine was not demonstrated. Interaction with the outer platelet membrane and internalization of viral particles within the surface-connected open canalicular system were demonstrated by electron microscopy within 5 minutes of the addition of virus to platelet suspensions with or without added agonists. Decreasing the virus concentration by ten- or one hundred-fold abolished the potentiating effect observed previously, while increasing the concentration tenfold resulted in direct platelet activation in the absence of agonist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Potentiation of platelet responses in vitro by feline infectious peritonitis virus. 214 30

Platelet function was evaluated in six specific-pathogen-free cats prior to and following intraperitoneal inoculation with feline infectious peritonitis virus (FIPV). By 4 days post-inoculation, platelet samples from five of six cats responded with irreversible platelet aggregation to threshold concentrations of adenosine diphosphate (ADP). This was accompanied by enhanced platelet 14C-serotonin release (greater than 10%) in two cats. Compared to one of six baseline samples, five of five post-inoculation samples exhibited microaggregate formation in response to 20 microM epinephrine. Enhanced platelet 14C-serotonin release did not accompany these responses. Enhanced platelet responses to ADP and epinephrine were also observed on day 11 post-inoculation and day 16 (when one cat died) or 21 (the end of the study). Platelet 14C-serotonin release in response to 20 microM epinephrine increased markedly in three of five cats on day 21. Enhanced collagen-induced platelet responses were not demonstrated. Although the mechanism for the enhanced platelet responses observed on day 4 was unknown, a direct effect on the virus on platelets, mononuclear inflammatory cells, and endothelial cells must be considered.
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PMID:Enhanced platelet reactivity in cats experimentally infected with feline infectious peritonitis virus. 216 65

The concept of early selective mitochondrial injury has been proposed to explain the global metabolic dysfunction observed in the septic state. A two phase study was undertaken to test the validity of this hypothesis. In the initial phase, an endotoxin shock model was employed in the rat to delineate the function of skeletal muscle mitochondria. Mitochondrial function was determined polarimetrically, comparing state three and state four rates, respiratory control index (RCI) and ADP:O ratios. No significant alteration in these parameters was observed in the endotoxic state. Phase II of the study was designed to investigate mitochondrial function in a bacterial peritonitis rat model. Both liver and skeletal muscle mitochondrial function were determined to control for possible alterations in liver metabolism. Neither muscle nor liver mitochondria exhibited functional impairment during sepsis. We conclude from this study that neither endotoxemia nor peritonitis selectively "kills" mitochondria as previously suggested.
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PMID:Mitochondrial death in sepsis: a failed concept. 352 91

Severe intra-abdominal infection results in significant metabolic dysfunction, multiple systems failure, and mortality. Although the course of peritonitis is particularly rapid and severe in neonates and small children, its physiologic consequences have been poorly studied in these age groups. In order to assess hepatic mitochondrial integrity in a model of fulminant peritonitis in immature animals, the following study was undertaken. Thirty-three immature Sprague-Dawley rats (21 to 28 days of age) and 32 mature rats (weight greater than 250 g) were anesthetized and laparotomies performed. The animals received either cecal ligation and gross perforation (CLP) or cecal manipulation alone (sham). Animals were killed at 2 and 4 hours and livers removed. Mitochondria were isolated by differential centrifugation. Mitochondrial respirations were studied polarographically with glutamate and succinate as substrates in the presence (state 3) and absence (state 4) of adenosine diphosphate (ADP). The Respiratory Control Index (RCI) is the ratio of state 3 to state 4 respiration and is a sensitive indicator of mitochondrial coupling. Results revealed that in mature animals, peritonitis produced a significant increase in RCI with glutamate as substrate (5.2 +/- 0.2) by 4 hours duration as compared with sham operated rats (4.3 +/- 0.1, P less than 0.01). Succinate as substrate revealed no significant alteration in mitochondrial coupling in mature rat hepatic mitochondria in animals subjected to peritonitis. By contrast, peritonitis in immature animals produced a significantly decreased RCI (3.6 +/- 0.2) with glutamate as substrate as compared with sham operated animals (4.8 +/- 0.2, P less than 0.01) by two hours duration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations of hepatic mitochondrial function in a model of peritonitis in immature rats. 372 4

Dissociation of oxidative phosphorylation and the lowering of the respiratory control during oxidation of succinate, alpha-ketoglutarate and pyruvate by hepatocyte mitochondria were observed in rats with experimental fecal peritonitis. The initial increase in the oxidation rate of the substrates enumerated is replaced by inhibition, whose degree is maximal as regards alpha-ketoglutarate, being less manifest as regards succinate. In the absence of the manifestations of the total dehydration, the increased water content in liver, skeletal muscle and renal tissues is coupled with relatively high values of the ADP/O and is in a good agreement with the lowering of the respiratory control during alpha-ketoglutarate oxidation.
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PMID:[Interrelation of the intracellular oxidation-reduction processes and the organic water balance in experimental peritonitis in rats]. 401 52

Insulin-stimulated synthesis of plasma membraneous "signal" ATP (psATP) from ADP and P(i) in oxidation coupled with that of NADH was detected in a preparation of plasma membranes from human erythrocytes; psATP was formed at concentrations of 10(-8)-10(-9) M. Effect of medicinal plasmapheresis on ability of erythrocyte membranes to produce psATP was studied. The rate of psATP biosynthesis was estimated in healthy volunteers and in patients with various diseases: nonspecific aortic arteritis, bronchial asthma, peritonitis, myasthenia before and after plasmapheresis. Distinct values of basal content of ATP (without insulin) and insulin-stimulated biosynthesis of ATP were detected in volunteers. Elevation of ATP biosynthesis, in response to insulin effect, was equal to 8.029 +/- 0.163 nmol/mg of membrane protein per min. Estimation of the psATP biosynthesis rate in patients with various pathological states enabled to detect markedly that psATP content tends to increase after plasmapheresis. Absolute values of psATP content were distinctly lower in these patients than those in healthy volunteers, while after plasmapheresis these parameters approached the normal level. Estimation of the insulin-stimulated synthesis of psATP may serve as a valid criterion of plasmapheresis efficiency.
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PMID:[Synthesis of cell membrane "signal" ATP in human erythrocyte membranes stimulated by insulin as criteria of the efficacy of therapeutic plasmapheresis]. 851 77

Thirty-three children with grave peritonitis were examined 16-24 h after operation. The groups were matched for the hemodynamic status. Group 1 were patients with moderate hyperdynamic status, group 2 those with the extreme hyperdynamic status, and group 3--patients with hypodynamic status. The control group consisted of 36 healthy children subjected to herniotomy. Moderate hyperdynamic status was associated with balanced carbohydrate-energy metabolism. In the second group high levels of ATP+ADP+AMP and G6-PDH+6-PGDH activities and a decrease of ATP/ADP ratio and hypophosphatemia were observed. In the third group, low activity of the direct oxidative pathway and high activity of plasma LDH and hypophosphatemia were observed.
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PMID:[The carbohydrate-energy metabolic and hemodynamic status of children with diffuse suppurative peritonitis in the early postoperative period]. 955 59

Peritonitis generally results from gastrointestinal perforation, with systemic sepsis developing over hours or days from an initially localized nidus of infection. The consecutive inflammatory response induces the widespread generation of oxidants and free radicals, which are potent inducers of breaks and nicks in double-stranded DNA. This genetic damage triggers the activation of the nuclear enzyme poly(ADP-ribose) polymerase 1, which, in turn, cleaves the respiratory coenzyme nicotinamide adenine dinucleotide into nicotinamide and ADP ribose. The consecutive decrease in cellular nicotinamide adenine dinucleotide inhibits glycolysis and mitochondrial respiration, leading to cellular energy collapse and necrotic cell death. In parallel, poly(ADP-ribose) polymerase 1 positively regulates inflammatory signal transduction pathways through a functional association with the transcription factor nuclear factor kappaB, resulting in a progressive amplification of local inflammation. Recent data indicate that these molecular mechanisms are instrumental in the development of cardiovascular collapse and multiple organ dysfunction in sepsis, supporting the view that pharmacologic inhibitors of poly(ADP-ribose) polymerase 1 may represent useful tools for the treatment of this condition.
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PMID:Role of poly(adenosine diphosphate-ribose) polymerase 1 in septic peritonitis. 1265 79


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