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C M Jabs

Publications and source records attributed to C M Jabs.

9 recordsLinked to original sources
PubMed1990

Adenosine, inosine, and hypoxanthine/xanthine measured in tissue and plasma by a luminescence method.

This simple method for sequentially quantifying hypoxanthine (HYP), inosine (INO), and adenosine (ADN) concentrations exploits the H2O2 peroxidase-catalyzed chemiluminescence of luminol. Though applied here only to tissue and plasma, this method can be adapted to analyze other body fluids. HYP in human plasma was stable for 30 min in 10 mmol/L EDTA reagent, whereas ADN was slowly converted to INO. Analytical recovery of HYP and INO added to plasma was 102% each; that of ADN was 95%. The within-run mean CVs for determinations of HYP, INO, and ADN at 1 mumol/L were 3.46%, 2.65%, and 3.01%; at 10 mumol/L they were 2.16%, 1.88%, and 1.63%, respectively. Corresponding between-run CVs were 5.34%, 4.09%, and 4.17%; and 3.43%, 2.40%, and 2.88%, respectively. Bilirubin at a concentration greater than 50 mumol/L interferes, but this interference is eliminated by bilirubin oxidase. Results for both tissue and plasma are compared with previously published results based on different analytical methods.

Adenosine↗
PubMed1989

Plasma metabolic disturbances and reperfusion injury following partial limb ischaemia in man.

Despite efficient revascularisation procedures for vascular disease, the limb can occasionally be lost following reperfusion. One contributing factor might be the formation of oxygen free radicals. This study attempts to describe the conditions necessary for oxy-radical formation from adenine nucleotide breakdown products and the role of plasma creatine content as a marker of cellular injury. Twelve patients undergoing aortic reconstructive surgery were studied. Only partial ischaemia of the lower limbs was induced by the aortic clamping, since varying degrees of collateral circulation existed. Radial arterial and external iliac venous blood was obtained simultaneously before, during and after cross-clamping of the aorta, and plasma levels of ATP, ADP, hypoxanthine, phosphocreatine, creatine, creatinine and lactate measured using luminescence and spectrophotometry. Venous creatine content increased during ischaemia and was doubled 30 min after recirculation. This increase was possibly due to leakage following cellular injury agreeing with a previously observed decrease in muscle tissue creatine content. The iliac arterio-venous difference of hypoxanthine and lactate markedly increased immediately post-ischaemia, while the phosphocreatine difference decreased. Plasma hypoxanthine was abundant in the leg on reoxygenation. The existence of a xanthine oxidase system in skeletal muscle could produce favourable conditions for oxy-radical formation through hypoxanthine degradation, which may contribute to the known muscle tissue injury.

Adenosine Diphosphate↗
PubMed1988

Plasma creatine determination using a luminescence method.

A new luminescence procedure based on the creatine kinase reaction was developed for measuring creatine in plasma. The method is highly applicable to small animal work where the amount of blood volume is critical. Only 20 microliter of sample is necessary for creatine analysis. Deproteinizing the plasma sample with ethanol at room temperature is convenient. This extraction method is adaptable to a clinical setting. The ethanol used in the extraction is compatible with the luminescence method but precipitated enzymes in the NADH spectrophotometric method because of the greater sample volume needed for analysis. The creatine concentration is stable in plasma for at least 1 hr in a final anticoagulant concentration of 10 mM EDTA. The correlation between the new luminescence method with the established NADH spectrophotometric method was excellent (r = 0.99). The accuracy of the within-run precision is high, with a mean coefficient of variation, 2-3%. Plasma creatine levels could be an important indicator denoting early cellular damage and of potential prognostic value. Preliminary studies in human muscle ischemia and early shock in rabbits revealed a significant increase in plasma creatine levels. Further investigations are necessary to evaluate its clinical importance.

Creatine↗
PubMed1978

Plasma ADP levels: direct determination with luciferase luminescence using a biometer.

A method is described for the determination of low plasma levels of adenosine-5'-diphosphate (ADP) using a Dupont Biometer to measure luminescence produced by the luciferin-luciferase reaction. Endogenous ATP is removed by incubation with luciferase. The remaining ADP is then quantitated, following its conversion to ATP, after incubation with creatine phosphate and creatine kinase. The mean coefficient of variation for 0.02 and 2.2 micromol/liter ADP standards were 2.1 and 1.8% respectively. The method has been applied to human and rabbit plasma. Human plasma ADP concentrations were found to be 0.13 +/- 0.025 (10) micromol/liter and rabbit plasma concentration were 0.07 +/- 0.05 (5) micromol/liter. Several other possible applications of the method are discussed.

Adenosine Diphosphate↗
PubMed1977

Microdetermination of plasma ATP and creatine phosphate concentrations with a luminescence biometer.

We optimized conditions for determination of adenosine-5'-triphosphate (ATP) and creatine phosphate from plasma extracted with ethanol/water (96/4 by vol). The procedures utilize the firefly luciferin/luciferase reaction, the bioluminescence being measured with a Du Pont Biometer. ATP is quantitated directly and creatine phosphate is quantitated by reaction with creatine kinase and ADP, after plasma ATP is removed by incubation with the enzyme apyrase. The method is applied to plasma from humans, rabbits, and rats, and possible clinical applications are discussed.

Adenosine Triphosphate↗
PubMedDate not supplied

Plasma changes in endotoxin and anaphylactic shock (ATP, ADP and Creatine phosphorus).

Decisive patterns have been demonstrated in plasma adenosine 5' triphosphate (ATP) levels in both endotoxin and anaphylactic shock which correlate with periods of low platelet counts, low arterial pressures and abnormal electrocardiograms. When these irregularities were occurring, the plasma ATP level was low; when improvement occurred, the plasma ATP level rose. Plasma ATP levels appear to be an index to the metabolic state of the animal. The plasma creatine phosphate (CP) level showed a tendency to decrease when the ATP level dropped in anaphylactic shock, although the CP level did not recover to the same extent as the ATP level. In endotoxin shock, the plasma CP level increased on an average of six-fold. It is proposed that this rise resulted from either CP mobilization from tissues, for the purpose of replenishing the energy deficient myocardial muscle, or possible leakage from damaged cells. Adenosine diphosphate (ADP) plasma values were measured in both anaphylactic and endotoxin shock. High initial ADP values were prone towards a more severe anaphylactic reaction and a shorter survival time in the endotoxin shock experiments.

Adenosine Diphosphate↗
PubMedDate not supplied

Comparative study of blood clotting factors in anaphylactic and primary and secondary endotoxin shock.

Cinephotomicrography shows emboli are formed in the lung during stages of anaphylactic and endotoxin shock and platelet counts are decreased. Rabbits in anaphylactic shock had a 50 percent mortality while 100 percent mortality was associated with endotoxin shock. During the terminal phase, the platelet count recovers in anaphylactic shock but not in endotoxin shock. This suggests a difference in the emboli formed during these two forms of shock. This study was directed at determining what might be the difference. Periodic measurement of electrocardiographic tracings, fibrinogen, factor VIII and fibrin degradation products (FDP) were made using standard equipment and test kits. The results of the study showed no changes in any of the measured clotting factors during anaphylactic shock. However, in endotoxin shock FDP appeared after seven to 10 hours, fibrinogen levels decreased from 221 mg per dl to 85 mg per dl and factor VIII time increased significantly. From these results, it is concluded that platelet aggregation in anaphylactic shock does not involve fibrin deposition, whereas in endotoxin shock platelet aggregation and fibrin deposition are both a factor in the formation of the emboli, possibly explaining the irreversible aggregation observed in terminal endotoxin shock.

Adenosine Diphosphate↗