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Biomedical subjects

J W Fiolet

Publications and source records attributed to J W Fiolet.

47 records · Page 3Linked to original sources
PubMed1977

Determination of creatine kinase isoenzyme MB (CK-MB): comparison of methods and clinical evaluation.

An ion-exchange chromatography method based on the method of Mercer is advocated for the routine determination of serum CK-MB. This method has some prominent advantages over other methods with which it is compared, and which include electrophoresis and an immunological technique. This method proves to be reliable and highly reproducible, while it allows a rather large number of samples to be analyzed within a relatively short period of time. Some parameters of the release pattern of CK-MB after acute myocardial infarction are characterized: normal values, time of first rise, time of peak value and rate-constant of inactivation. The clinical significance of serum CK-MB determination is evaluated.

Chromatography, Ion Exchange↗
PubMed1975

On the stimulation of the light-induced proton uptake by uncoupling aminoacridine derivatives in spinach chloroplasts.

1. Light-induced proton uptake by spinach chloroplasts is enhanced several-fold by 9-(4-diethylamino-1-methylbutylamino)-6-chloro-2-methoxyacridine (atebrin). This stimulation does not depend on the chlorophyll concentration. The amount of extra protons taken up in the presence of atebrin is determined by the pKa values of atebrin and the pH of the incubation medium. 2. Both the stimulation of the proton uptake and the maximal binding capacity for atebrin is sensitive to uncouplers. However, the ratio of bound to free atebrin does not depend on the presence of uncoupler up to the saturating atebrin concentration. 3. From simultanious kinetic measurements of atebrin fluorescence and proton movement it seems that after binding of the completely protonated atebrin the dye and the protons can move separately. This can also be inferred from the spectral behaviour of atebrin in illuminated chloroplasts. 4. The stimulation of the proton uptake by atebrin does not depend on the presence of salts in the incubation medium. However, the 'saturating' atebrin concentration increases strongly with increasing salt concentration in the medium. 5. It is concluded that the interaction of atebrin and other acridines with energized chloroplasts most likely occurs at the level of the membrane proper. 6. It is proposed that uncoupling by atebrin is a consequence of the creation of a high proton activity at the periphery of the thylakoid membrane, which opposes a proton gradient across the membrane. The uncoupling by atebrin is not of the protonophoric type according to this mechanism.

Anilides↗
PubMedDate not supplied

Osmotic changes and transsarcolemmal ion transport during total ischaemia of isolated rat ventricular myocytes.

Transsarcolemmal water and ion movement during 1, 7.5, 15, and 30 min of total ischaemia was studied in suspensions of isolated rat ventricular myocytes, with a control ratio of about 1 of intracellular volume (ICV) to extracellular volume (ECV). In this preparation, contrary to the intact heart: 1) There is no external exchange of matter, 2) the sum of ICV and ECV remains constant and 3) ECV is homogeneous; no separate interstitial and intravascular compartments are present and no extracellular metabolite or ion gradients develop as may occur in the intact heart. We demonstrate that: 1) It is possible to make an ischaemic preparation of isolated myocytes with a procedure which causes only minimal mechanical damage to intact myocytes. The preparation allows measurement of ECV with the non-cardiac enzyme alpha-amylase as a macromolecular extracellular marker. 2) The time course of change of metabolites relevant to energy metabolism (creatinephosphate (CrP), creatine (Cr), ATP, ADP, inorganic phosphate P(i) and lactate) is similar to that in the intact heart. 3) ECV has decreased and ICV increased by about 20% after 30 min of ischaemia. 4) Extracellular [Na+], [K+], [Cl-], and [P(i)] increase, but not in proportion to the decrease of ECV. There is net efflux of K+, P(i), H+, and lactate-; efflux of K+ and P(i) is quantitatively much less than influx of Na+ and Cl-. 5) Measured extracellular osmolality has increased with up to 70 mOsm/l after 30 min of ischaemia. The increase of extracellular [lactate-], [Na+], [K+], [Cl-], [P(i)] and the decrease of [glucose] account for the change of osmolality measured. 6) Summation of the electrical charges associated with measured increase of extracellular [lactate-], [Na+], [K+], [Cl-], [P(i)] shows a surplus of negative charge, which almost equals extracellular [lactate-], suggesting an equally large increase of osmotically inactive H+ as the compensatory ion. 7) Blockade of anaerobic metabolism with iodoacetic acid (IAA) reduces efflux of lactate and P(i) but greatly amplifies influx of sodium and chloride and efflux of potassium.

Animals↗
PubMedDate not supplied

Transmural inhomogeneity of extracellular [K+] and pH and myocardial energy metabolism in the isolated rat heart during acute global ischemia; dependence on gaseous environment.

We investigated in the isolated rat heart the influence of the gas surrounding the globally ischemic heart on transmural inhomogeneity of energy metabolism, extracellular K+ accumulation, and change of extracellular pH. Hearts were made ischemic in 100% N2 (N2-ischemia), 100% O2 (O2-ischemia) or 100% CO2 (CO2-ischemia). We measured: 1) Midmural, subepicardial, and epicardial changes of extracellular [K+] and pH during successive 6-min periods of global ischemia, and 2) content of creatinephosphate (CrP) in consecutive tissue sections of 100 microns, from the subepicardium after 10 min of ischemia. A) During O2-ischemia both extracellular [K+] and change of pH in the subepicardium are significantly less than in the midmyocardium. During N2-ischemia only minor differences exist in [K+] and pH between the subepicardium and the midmyocardium. During CO2-ischemia midmural and subepicardial [K+] are similar to those during N2-ischemia. The midmural change of pH resembles that during N2-ischemia; subepicardial change of pH, however, was slightly larger. Midmural changes in [K+] and pH were not influenced by the nature of the surrounding gas. B) After 10 min of O2-ischemia a gradient of tissue content of CrP extends from the epicardium (CrP about 30 mumoles/g dry weight) to a distance of about 1000 microns (CrP 1 mumoles/g dry weight). In N2- and CO2-ischemia a CrP gradient is absent; CrP is appreciably less than 1 mumoles/g dry weight at any distances from the epicardium. C) We conclude that diffusion of O2 into the myocardium and of CO2 from the myocardium affects transmural gradients of [K+], pH, and energy metabolism during ischemia. Local availability of O2 increases the capacity of the ischemic tissue to generate high energy phosphates and mitigates ischemia-induced changes of transsarcolemmal ion gradients.

Acid-Base Equilibrium↗
PubMedDate not supplied

Substrate dependence of reoxygenation arrhythmias in the isolated rat heart.

Isolated rat hearts perfused with various substrates were subjected to oxygen restriction followed by sudden reoxygenation. The incidence of ventricular arrhythmias occurring after reoxygenation appeared to be dependent on the substrate present during oxygen restriction; it was low with glucose (11 mM) and significantly higher with oleic acid (FFA to albumin molar ratio 4), with beta-hydroxy butyrate (11 mM), with acetate (11 mM) or without added substrate. When verapamil (1 muM) was also present in the medium, these arrhythmias were largely prevented. When glucose or verapamil were present during the reoxygenation period only, the incidence of reoxygenation arrhythmias was high. Tissue levels of long-chain acyl-CoA increased during oxygen restriction under all substrate conditions tested. At the moment when reoxygenation was started they were most elevated in hearts perfused with oleic acid. Verapamil did not influence levels of long-chain acyl-CoA. The amount of creatine-kinase (CK) released from the heart after reoxygenation did not correlate with the observed arrhythmias and was greatest in hearts perfused with oleic acid. Verapamil protected against CK release in the absence of added substrate, but not when oleic acid was present. It is concluded that ventricular arrhythmias after reoxygenation are not necessarily caused by FFA or long-chain acyl-CoA.

Acyl Coenzyme A↗
PubMedDate not supplied

Tissue osmolality, metabolic response, and reperfusion in myocardial ischemia.

We studied the effect of tonicity of the perfusate during reperfusion after global ischemia, in both the rat and the porcine heart. After 50 min, tissue osmolality increased by about 40 mOsm/kg. Normotonic as well as hypertonic reperfusion resulted in limited areas of "no-reflow". Metabolic restoration after reperfusion was not dependent on the tonicity of the perfusate, nor was recovery of contractility. Hypertonic reperfusion induced a higher coronary flow rate. In porcine hearts, scatter of metabolic data indicated inhomogeneity of reperfused tissue. The results differ substantially from data obtained after reperfusion of regionally ischemic hearts. Reasons for these differences are discussed.

Adenosine Triphosphate↗