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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Untreated septic shock results in depletion of extracellular fluid, cellular swelling, increased intracellular sodium, and decreased intracellular potassium concentrations in primate skeletal muscle. The Langer rabbit heart interventricular septal preparation was used to determine whether similar changes occur in cardiac muscle during sepsis. Rabbit septa (n = 17) were perfused with control and septic rabbit plasma plus red blood cells. Tissue contractility (developed tension [DT] and rate of tension change [dP/dt]) was followed, plasma cations were measured (Na+, K+, Ca2+, H+), perfusion pressure (PP) was monitored, and 42K efflux was determined. The effect on 42K efflux caused by the addition of potassium chloride to control plasma was determined. During perfusion with septic plasma there was significant decline of septal function (P less than 0.001). In 12/17 experiments DT fell 77.8 +/- 21.4% and dP/dt fell 75.8 +/- 24.8% from control values (means +/- 1 SD). All septa recovered when perfusion with control plasma was resumed. If [K+] was increased in control plasma during 42K washout, the percentage increase of effluent counts per minute per minute correlated with the percentage rise of control plasma [K+] (r = 0.95, P less than 0.001). During perfusion with septic plasma there was no similar correlation (r = 0.277). 42K efflux increased during septic plasma perfusion independent of the differences between control and septic plasma [K+], demonstrating abnormal myocardial K+ efflux. An abnormal efflux of K+ is seen during septic plasma perfusion similar to that described in primate skeletal muscle. It is associated with and may be a mechanism of action for the observed fall of contractility.
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PMID:Altered potassium flux and myocardial dysfunction during sepsis. 638 64

Cell lines Lu-65 and SK-Luci-6 were established from two patients with anaplastic (non-oat cell) lung cancers. These cell lines showed in vivo and in vitro functional activities that could explain the paraneoplastic syndromes which were clinically manifested. In both patients, elevated white blood cell counts occurred in the absence of any evidence of sepsis. Tumor fragments taken directly from one patient and transplanted to nude mice produced a progressive leukocytosis in the mice. Tissue culture-derived cells from both cell lines enhanced white blood cell numbers following heterotransplantation to nude mice. Cell-free extracts from both cell lines were found to enhance granulocyte-macrophage colony formation in soft agar. Greater colony formation was consistently found with the cell line (SK-Luci-6) that was derived from the patient manifesting the more marked leukocytosis. These data suggest that the tumor cells release colony-stimulating activities. Coincidently, one cell line (Lu-65) synthesized and released large amounts of prostaglandin E2 with little or no other prostaglandin product; the other cell line produced no prostaglandins. When the tumor cell lines were cocultured with explanted fetal rat bones, enhanced bone resorption with excessive calcium release occurred. Bone-resorbing activity correlated with tumor prostaglandin synthesis for the cell line releasing prostaglandin E2. An osteolytic factor that was neither prostaglandin nor parathyroid hormone was released by the SK-Luci-6 cell line. Hypercalcemia was a persistent feature only in the patient from whom the latter tumor line was derived.
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PMID:In vivo and in vitro biological activities of two human cell lines derived from anaplastic lung cancers. 640 6

Moderate hypercalcaemia occurred in a 17-year-old male who was immobilized with abdominal and right hip sepsis for 9 months after a motor vehicle accident. The hypercalcaemia was due to bone resorption, with a urine hydroxyproline:creatinine ratio of 0.203 (normal less than 0.017) and a urine calcium loss of 22.9 mmol/24 hr, associated with impaired renal function. There was radiological evidence of severe bone demineralization in the pelvis over 42 weeks. Radiocalcium absorption, using 47Ca, was decreased (0.17, normal range 0.35-1.30), renal tubular maximum for calcium reabsorption was decreased (1.61 mmol/1 glomerular filtrate, normal range 1.8-2.2), the serum parathyroid hormone concentration was in the low normal range (3.2, 3.6 u/l, normal range 2-6) and the plasma 1,25-dihydroxy-vitamin D concentration was decreased despite a normal 25-hydroxy-vitamin D concentration, indicating suppression of the parathyroid, 1,25-dihydroxy-vitamin D axis. The patient was found to be hypogonadal at 41 weeks after admission and testosterone therapy was begun, with associated improvement in mobilization and a reduction of the hypercalcaemia.
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PMID:Immobilization hypercalcaemia with severe bone mineral loss and hypogonadism. 646 82

Studies utilizing animal models of circulatory shock have revealed mitochondrial structural and functional damage in the liver, kidney, and brain. Adenosine triphosphate (ATP) synthesis and calcium transport rates of these mitochondria decline significantly during circulatory shock. The specific enzyme functions affected deleteriously by low flow states are the ATP synthetase, adenine nucleotide translocase, and carrier-mediated calcium transport. Other cellular alterations that possibly are responsible for, or are related to, the shock-induced mitochondrial deterioration are discussed. Differences in the mitochondrial responses to endotoxemia and hyperdynamic sepsis are described. Data are presented on the beneficial effects of early glucocorticoid treatment in prevention of mitochondrial functional deterioration during endotoxemia.
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PMID:Mitochondrial function in shock. 651 84

Mechanisms of subcellular dysfunction of the liver in sepsis are still obscure. The present study investigates changes in oxidative phosphorylative activity and calcium-induced respiration of rat liver mitochondria following live Escherichia coli injection (E coli, Serotype: 0--18. A 1.25--1.5 X 10(9)/100 gm body wt inoculum of E coli bacteria was injected via the tail vein, causing a 100% mortality rate within 24 hours after injection. In order to determine alteration of liver mitochondrial membrane permeability, serum ornithine carbamoyltransferase activity was measured following E coli injection. This activity increased ten to 100-fold over that of controls with time following injection. However, the yield of liver mitochondria from treated rats, estimated by the amount of collected mitochondrial protein and the recovery rate of succinate dehydrogenase activity in the final mitochondrial suspensions, was not significantly different from that of controls. Mitochondrial oxidative phosphorylative activity measured using glutamate as a substrate was enhanced throughout all period to death (P less than 0.01 at three and six hours, P less than 0.05 in the fatal stage) and was associated with concomitant increases in respiratory control ratios. Similar results were obtained using beta-hydroxybutyrate as a substrate. This enhancement was accompanied by an increase in 2-4-dinitrophenol-stimulated ATPase activity (160% at three hours and 130% in the fatal stage). Calcium-induced stimulation of mitochondrial respiration as well as initial calcium uptake rate linked to respiration, using glutamate as a substrate, were higher in liver mitochondria from rats with E coli treatment than in those of controls throughout all periods (P less than 0.01 or less). These results suggest the coexistence of hyperfunctioning as well as deteriorated mitochondria following lethal treatment with E coli.
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PMID:A study of oxidative phosphorylative activity and calcium-induced respiration of rat liver mitochondria following living Escherichia coli injection. 675 40

Twelve dogs with lymphosarcoma and hypercalcemia were treated over a period of 36 months. Signs and laboratory findings were referable to hypercalcemia and azotemia. All dogs were staged, classified histologically, and given cytoreductive chemotherapy, using 5 drugs (vincristine sulfate, cytosine arabinoside, cyclophosphamide, L-asparaginase and prednisone). For azotemia, symptomatic therapy (0.9% NaCl solution and furosemide) was given. Seven dogs responded completely, with marked reduction of lymphadenopathy and return of serum calcium concentration to normal. Median duration of remission in this group was 48 days (range, 14 to 93), and median survival time was 112 days (range, 85 to 153). Five nonresponding dogs had less than 50% reduction in measurable tumor mass, although serum calcium concentration returned to normal. The median survival time for this group was 34 days (range, 23 to 68). Two of the nonresponders died from sepsis and another from disseminated intravascular coagulation. Response to therapy did not appear to be influenced by age, breed, sex, initial calcium concentration, degree of azotemia, or histologic classification.
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PMID:Chemotherapeutic responses in dogs with lymphosarcoma and hypercalcemia. 689 39

The majority of evidence suggests that there is myocardial dysfunction resulting from sepsis. Clinical observations seem to suggest that the dysfunction is not on the basis of decreased venous return of increased afterload. Reduced myocardial compliance and isolated right ventricular failure also do not account for what is seen clinically. The explanation appears to be decreased myocardial contractility. Several factors may be responsible for reducing contractility, including altered response to catecholamines; metabolic acidosis; altered distribution of blood flow within the myocardial wall resulting in hypoxic regions; the elaboration of substances that act directly to reduce contractility, including intestinal shock factors and endorphins; and alterations of excitation-contraction coupling resulting from changes in calcium concentrations or reduced responsiveness to the calcium ion. Further work is needed to determine which of these factors predominate.
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PMID:Myocardial failure. 706 58

Hypocalcemia is an important metabolic problem in critical care medicine. To determine the frequency of this problem and the patient subsets at risk, a retrospective study of a large series of ICU patients was performed. During the study period, 259 patients were admitted to the ICU, of whom 210 (81%) had a serum calcium (Ca++) measured. Of these 210 patients, 135 (64%) were hypocalcemic (serum Ca++ less than 8.5 mg/dl) and 75 (36%) were normocalcemic. Serum albumin concentration was less than 3.5 g/dl in 70% of the hypocalcemic patients who hd albumin measured, suggesting that the ionized Ca++ concentration may have been normal in many of these patients. On the other hand, 32% of the hypocalcemic patients were alkalotic (pH greater than or equal to 7.45) which indicates that ionized Ca++ levels may have been low because Ca++ binding to protein increases with alkalosis. Gastrointestinal bleeders and postabdominal surgery patients were more likely to have low total serum Ca++ whereas cardiac and neurosurgical patients were more likely to have a normal total serum Ca++ (p less than 0.05). Ionized Ca++ was calculated in 36 of the normocalcemic and 80 of the hypocalcemic patients. The hypocalcemic group had significantly lower ionized Ca++ levels when compared to those of the normocalcemic group (p less than 0.001). Patients with low serum Ca++ values spent a longer time in the ICU (p less than 0.01), had an increased incidence of renal failure and sepsis (p less than 0.01), had an increased mortality rate (p less than 0.001), and received a greater number of blood transfusions (p less than 0.001) than patients in the normocalcemic group. It is concluded that: (1) hypocalcemia is a frequent finding in critically ill patients; (2) determining ionized Ca++ levels is useful because many ICU patients have alterations in both arterial pH and serum albumin levels; (3) hypoalbuminemia, sepsis, red cell transfusions, and renal failure are predisposing factors for hypocalcemia; and (4) hypocalcemic patients do less well clinically than normocalcepatientsmic patients.
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PMID:Hypocalcemia in critically ill patients. 714 Mar 32

A commercially available polyvinyl chloride intravenous catheter was studied in 9 horses for 3 to 10 days to evaluate the catheter's suitability for use in the horse, to develop a new insertion technique, and to establish a protocol for catheter care. Seven of the animals were clinically normal horses receiving parenteral nutrition; one was a horse with hypocalcemia receiving frequent intravenous injections of calcium gluconate, and one was a clinically normal horse receiving no infusions. The catheter dressings were changed every 48 hours, and an aspirate from the catheter and the catheter tip was cultured at the time of catheter removal. One catheter became infected following a break in the protocol. It was concluded that the polyvinyl catheter is suitable for use in the horse and that the proposed protocol for catheter insertion and maintenance may reduce the likelihood of complications such as catheter sepsis, thrombophlebitis, and embolism.
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PMID:Evaluation of an intravenous catheter for use in the horse. 722 84

This is a very brief, superficial and biased discussion of the pathophysiologic changes in shock. It was designed to provide some insight into the very complex changes that occur, with particular attention to a few examples of the impaired cell metabolism, including changes in ATP, cAMP, and calcium. Although inadequate tissue perfusion through nutrietn capillaries is the main etiologic factor in most types of shock, it is not the primary problem in many patients, particularly those with early or hyperdynamic sepsis. The importantance of oxygen consumption and the possible benefits of higher hemoglobin levels are discussed to some extent because of their possible clinical application.
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PMID:The pathophysiology of shock. 736 11


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