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

ECG, arterial flow and pressure were recorded during external cardiac compression (ECC) in a patient whose heart had ceased beating. The patient was a 68-year-old female who remained comatose for 2 weeks after an emergency laparotomy for perforated diverticulitis of the colon. She developed sepsis, renal failure, and cardiopulmonary failure. During ECC, the pressure on the sternum was maintained for about 0.5 sec (sustained pressure technique), flow and mean arterial pressure were improved by 32 and 20%, respectively, as compared with flow and pressure obtained with a quick and more jerky compression. During spontaneous heart activity with a low blood pressure, a superimposed ECC improved both flow and mean arterial pressure. Calcium chloride and adrenaline injected into the right atrium increased the tone and contractile power of the heart and greatly improved flow and pressure when the heart was subsequently compressed during asystole.
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PMID:On the technique of external cardiac compression. 65 21

Calcium chloride is administered frequently to critically ill patients to improve cardiac output and BP. However, Ca has been implicated in the pathophysiology of shock and ischemic disorders. To test the hypothesis that Ca may be deleterious to shock outcome, we studied the effects of CaCl and Ca chelator (EGTA) infusions on mean arterial pressure (MAP) responses to endotoxin and 24-h survival in rats. Increasing ionized Ca from 4.1 +/- 0.06 to 4.9 +/- 0.20 and 8.5 +/- 0.52 mg/dl progressively increased endotoxin lethality from 20% to 37% and 80%, respectively. This occurred despite slight improvements in MAP in hypercalcemic rats. Conversely, hypocalcemia (3.6 +/- 0.08 mg/dl) lowered endotoxin-induced mortality to 0 without significant effects on MAP. Ca and EGTA infusions alone were not associated with any mortality. Although Ca administration may improve MAP, it significantly increases mortality associated with endotoxic shock in rats. Based on these observations, we advise caution when using Ca in patients with sepsis.
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PMID:Calcium administration increases the mortality of endotoxic shock in rats. 250 40

In 200 albino rats pathomorphological changes of different organs were studied during experimental staphylococcal sepsis (from 3 to 45 days of the disease), caused by intramuscular injection of 0.15-0.20 ml suspension of microbes (10(15) per ml) in 10% CaCl2 solution. Local piemic focus occurred first, followed by bacteremia and generalized sepsis manifest with secondary piemic foci in the viscera. In the cytologic imprints early stages of piemic metastatic focus formation in liver, kidneys and other organs were demonstrated. Microcirculatory, dystrophic changes, as well as lymphoid system suppression were revealed. The authors come to the conclusion that all the signs are similar to general morphologic criteria of sepsis in humans.
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PMID:[Morphological changes in the internal organs in experimental staphylococcal sepsis]. 356 53

Experimental staphylococcal sepsis has been examined in the model suggested by the authors. Staphylococcus aureus culture in a 10% CaCl2 solution was injected intramuscularly to 230 adult albino rats. Fundamental signs of sepsis have been revealed: increased mortality (up to 28% in rats weighing 120-140 g) from day 1 to day 45 after infection, development of local infectious foci, bacteremia, septicemia and septicopyemia. The authors describe severe dystrophic changes in septic emboli and bacterial colonies in different organs.
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PMID:[Experimental staphylococcal sepsis]. 405 26

A 17-year-old male with previously undiagnosed congenital Factor IX deficiency (13%) presented with gastrointestinal bleeding and a hepatic mass. Prolonged thrombin and Reptilase times, which partially corrected with CaCl2 and a discrepancy between thrombin-clottable and immunoreactive plasma fibrinogen, suggested a dysfibrinogenemia. Laparotomy disclosed metastatic hepatoma. Adequate hemostasis was obtained with clotting factor replacement, but wound healing was delayed. Patient fibrinogen purified with 2.1 M glycine migrated normally on immunoelectrophoresis and 7.5% polyacrylamide-SDS gel electrophoresis. However, fibrin monomers prepared from purified patient fibrinogen displayed impaired aggregation at high and low ionic strengths when compared with fibrin monomers from normal and control Factor IX deficient subjects. Aggregation of normal monomers was delayed when mixed 1:1 with patient monomers. Fibrinopeptide release was normal, and total sialic acid content was similar to that of normal and control fibrinogens. Chemotherapy, consisting of 5-FU given via intra-arterial hepatic infusion, was accompanied by significant transient clinical improvement which coincided with correction of thrombin clotting times and fibrin monomer aggregation. Reappearance of fibrinogen dysfunction occurred with clinical deterioration prior to death from metastatic hepatoma and sepsis. This case is the first to corroborate the postulated tumor marker role of dysfibrinogenemia in a patient with hepatoma by documenting a direct relationship with response to chemotherapy.
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PMID:Acquired dysfibrinogenemia in a hemophiliac with hepatoma: resolution of fibrinogen dysfunction following chemotherapy. 626 56

Resistance to activated protein C (APCR) has emerged as the most important hereditary cause of venous thromboembolism. Using an aPTT-based method together with DNA technique we investigated 120 healthy neonates and infants < 12 months of age and 24 infants with septicaemia for the presence of this mutation. In addition, data of 11 neonates with vascular occlusion, heterozygous (+/-) for the Arg 506 Gln mutation were included. Results of an aPTT-based method (clotting time using the APC/CaCl2 solution obtained in an undiluted, 1:5 and 1:11 dilution with factor V deficient plasma divided by clotting time with CaCl2 in the same plasma dilution) are shown: Whereas 7 (5.5%) out of 120 healthy neonates were (+/-) carriers for the factor V Arg 506 Gln mutation, concordance with the aPTT-based method (cut-off defined as ratio < 2) was found only when using the 1:11 plasma dilution. Six (four) out of 24 infants with sepsis, not carrying the factor V mutation, would have been classified as APC resistant when using the 1:1 (1:5) plasma dilution. Four (two) out of 18 patients, (+/-) for the Arg 506 Gln mutation showed APC ratios > 2 in the 1:1(1:5) plasma dilution.
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PMID:APC resistance in neonates and infants: adjustment of the APTT-based method. 886 17

Sepsis is a major cause of death in intensive care units. Clinically, sepsis induces a number of physiologic and metabolic abnormalities, including decreased myocardial contractility and decreased plasma ionized calcium. There is debate about the proper therapy of hypocalcemia in sepsis because calcium administration may worsen cell function by causing intracellular Ca2+ overload. We investigated the effect of Ca2+ administration on myocardial systolic and diastolic function in an extensively utilized rat model of sepsis, i.e., the cecal ligation and puncture model (CLP). Approximately 24 h after CLP or sham surgery, rats were anesthetized and myocardial function assessed in vivo by a left ventricular Millar catheter and simultaneous two-dimensional guided M-mode echocardiography. Septic rats had a 28% decrease in peak left ventricular developed pressure, a 30% decrease in +dP/ dt, and a 23% decrease in -dP/dt (p < 0.05). Plasma ionized Ca2+ was decreased in septic compared with that in sham rats: 4.9 +/- 0.9 and 5.6 +/- 0.01 mg/dl, respectively (p < 0.05). CaCl2 improved both systolic and diastolic function and there was no evidence of adverse effects of Ca2+ even at supraphysiologic levels. Surprisingly, correction of decreased afterload in septic rats, using the pure alpha-agonist phenylephrine, caused normalization of all indices of cardiac contractility, indicating that the presumed decrease in cardiac function was due entirely to an effect of the decreased afterload to "unload" the left ventricle. We conclude that Ca2+ administration is not detrimental to cardiac function in the rat CLP model. Although the rat CLP model is widely utilized and reproduces many of the clinical hallmarks of sepsis, it does not cause intrinsic myocardial depression and, therefore, it may not be an appropriate model to investigate the clinical cardiac dysfunction that occurs in patients with sepsis.
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PMID:Reversal of hypocalcemia and decreased afterload in sepsis. Effect on myocardial systolic and diastolic function. 984 97

Pathologic disseminated intravascular coagulation (PDIC) is a serious complication in sepsis. In an in-vitro system consisting of incubation of fresh citrated blood with lipopolysaccharides (LPS) or glucans and subsequent plasma recalcification plasmatic thrombin was quantified. Five hundred microliters of freshly drawn citrated blood of healthy donors were incubated with up to 800 ng/mL LPS (Escherichia coli) or up to 80 microg/mL Zymosan A (ZyA; Candida albicans) for 30 minutes at room temperature (RT). The samples were centrifuged, and 30 microL plasma were recalcified with 1 volume or less of CaCl(2) (25 micromoles Ca(2+)/mL plasma). After 0 to 12 minutes (37 degrees C), 20 microL 2.5 M arginine, pH 8.6, were added. Thirty microliters 0.9 mM HD-CHG-Ala-Arg-pNA in 2.3 M arginine were added, and the absorbance increase at 405 nm was determined. Fifty microliters plasma were also incubated with 5 microL 250 mM CaCl2 for 5, 10, or 15 minutes (37 degrees C). Fifty microliters 2.5 M arginine stops coagulation, and 50 microL 0.77 mM HD-CHG-Ala-Arg-pNA in 2.3 M arginine starts the thrombin detection. The standard was 1 IU/mL thrombin in 7% human albumin instead of plasma. Arginine was also added in the endotoxin exposure time (EET) or in the plasma coagulation reaction time (CRT). Tissue factor (TF)-antigen and soluble CD14 were determined. LPS at blood concentrations greater than 10 ng/mL or ZyA at greater than 1 microg/mL severalfold enhance thrombin generation, when the respective plasmas are recalcified. After 30 minutes EET at RT, the thrombin activity at 12 minutes CRT generated by the addition of 200 ng/mL LPS or 20 microg/mL ZyA is approximately 200 mIU/mL compared to approximately 20 mIU/mL without addition of endotoxin, or compared to about 7 mIU/mL thrombin at 0 minutes CRT. Arginine added to blood or to plasma inhibits thrombin generation; the inhibitory concentration 50% (IC 50) is approximately 15 mM plasma concentration. Endotoxin incubation of blood increases neither TF nor sCD14. This assay allows the study of the hemostasis alteration in PDIC, particularly in PDIC by sepsis. The thrombin generated by blood plus endotoxin incubation and plasma recalcification suggests that the contact phase of coagulation; e.g., triggered by cell components of (phospholipase-) lysed cells such as monocyte or endothelium DNA or phospholipid-vesicles (microparticles), is of primary pathologic importance in sepsis-PDIC. Arginine at plasma concentrations of 10 to 50 mM might be a new therapeutic for sepsis-PDIC.
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PMID:Thrombin generation by exposure of blood to endotoxin: a simple model to study disseminated intravascular coagulation. 1670 16

An overview of a little-known method, which was discovered by Dr. Alexander S. Samokhotskiy, for treatment of gangrenous, traumatic, and postoperative inflammation, sepsis and some other diseases, was represented. Dr. A. S. Samokhotskiy carried out numerous animal experiments and clinical trials and found that application of wet bandages and/or intravenous injection of solution containing trivalent chromium ions (Cr3+), alum, resorcinol, sodium salicylate, lactate buffer, colloidal sulphur, thioglycolic acid and glutathione with adding KCl, MgCI2, CaCl2 or NaCl solutions can heal inflammation of various etiology. Intravenous injections of particular therapeutic solution containing Na+, K+, Ca2+ or Mg2+ ions were administered in dependence on concentration of these ions in patient's blood plasma. Thousands of patients, many of them with fatal afflictions, where other methods were helpless, were healed by Dr. A. S. Samokhotskiy with the help of his method. Purpose of this publication is to inform the international medical community with the Dr. A. S. Samokhotskiy's discovery and initiate further research in this area.
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PMID:Dr. Samokhotskiy's method of healing inflammation by the analysis and regulation of blood electrolyte balance. 2625 94