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J A Balschi

Publications and source records attributed to J A Balschi.

25 records · Page 2Linked to original sources
PubMed1987

Contractile failure and high-energy phosphate turnover during hypoxia: 31P-NMR surface coil studies in living rat.

Cardiac failure appears rapidly during severe hypoxia and precedes a substantial reduction in adenosine triphosphate content. Reduced adenosine triphosphate turnover, in the presence of nearly normal content, may be the metabolic basis for contractile failure during hypoxia. To measure both the myocardial content and the turnover rates of high-energy phosphate compounds during hypoxia, we performed 31P-nuclear magnetic resonance studies by placing a surface coil directly over the left ventricle in intubated rats that were instrumented for hemodynamic measurements and ventilated with either 21, 10, or 8% O2. Normoxia produced a hemodynamic and metabolic steady state for 4 hours and hypoxia for at least 60 minutes. Under normoxic ventilation (n = 10, mean +/- SD), the arterial PO2 was 96 +/- 14, pH 7.38 +/- 0.11, and systolic blood pressure 96 +/- 8 mm Hg; under hypoxic ventilation with 10% O2 (n = 5), the arterial PO2 was 57 +/- 10, pH 7.39 +/- 0.09, and systolic pressure 68 +/- 10; and under hypoxic ventilation with 8% O2 (n = 5), the PO2 was 52 +/- 7, pH 7.37 +/- 0.04, and systolic pressure 51 +/- 4. Hypoxic ventilation with 10 or 8% O2 decreased the creatine phosphate content from 51.4 +/- 5.4 mumol/g dry wt to 39.3 +/- 5.4 and 45.6 +/- 4.1 and depressed adenosine triphosphate slightly from 25.0 mumol/g dry wt to 21.8 +/- 2.1 and 21.9 +/- 1.0, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗
PubMed1987

Effects of norepinephrine infusion on myocardial high-energy phosphate content and turnover in the living rat.

Using 31P-nuclear magnetic resonance, we studied the relationship between myocardial high-energy phosphate content and flux values for the creatine kinase reaction in the living rat under inotropic states achieved during norepinephrine infusion and halothane anesthesia. Under 2% halothane anesthesia (n = 4), 1% halothane anesthesia (n = 5) and norepinephrine infusion (n = 4), rats developed rate-pressure products of 19.5 +/- 1.6, 32.0 +/- 3.5, and 48.5 +/- 2.0 X 1,000 mmHg/min, respectively. Adenosine triphosphate content was not affected by inotropic state, ranging from 24.3 +/- 1.1 to 25.6 +/- 1.1 mumol/g dry weight, but creatine phosphate content varied inversely and reversibly with cardiac performance from 45.6 +/- 6.0 under 2% halothane to 26.0 +/- 6.5 mumol/g dry weight during norepinephrine infusion. The flux values for the creatine kinase reaction were 15.4 +/- 4.6, 20.5 +/- 2.0, and 30.1 +/- 7.9 mumol/g dry weight per s under 2% halothane, 1% halothane, and 1% halothane with norepinephrine, respectively. These results suggest that the turnover of myocardial high-energy phosphate compounds, not their tissue contents, matches cardiac performance during inotropic stimulation.

Adenosine Triphosphate↗
PubMed1982

Direct high-resolution nuclear magnetic resonance studies of cation transport in vivo, Na+ transport in yeast cells.

A new nuclear magnetic resonance (NMR) method for monitoring transmembrane metal cation transport is reported. It is illustrated with a study of Na(+) efflux from Na(+)-rich yeast cells. The technique involves the use of an anionic paramagnetic shift reagent, present only outside the cells, to induce a splitting of the sodium-23 NMR peak, in this case, into components representing intra- and extracellular Na(+). The time course of the efflux is in good agreement with the literature and can be well fitted with a double exponential decay expression. Splitting of the lithium-7 NMR signal from a suspension of Li(+)-rich respiratory-deficient, petite yeasts is also reported.

Biological Transport, Active↗
PubMed1982

High-resolution NMR studies of transmembrane cation transport: use of an aqueous shift reagent for 23Na.

23Na NMR studies of large unilamellar vesicles of egg lecithin in salt solutions are reported. A shift reagent, the dysprosium nitrilotriacetate ion Dy[N(CH2CO2)3]3-2 has been used to distinguish between 23Na+ inside and outside the vesicles. When both are present and the shift reagent is present on only one side, two clearly distinct resonances are observed. Creation of a Na+ concentration gradient and subsequent catalysis of passive transport induced by the introduction of gramicidin can be monitored easily by using the relative intensities of the two resonances. We report the observation of transport both out of and into vesicles.

Biological Transport↗
PubMedDate not supplied

Aqueous shift reagents for high-resolution cation NMR. VI. Titration curves for in vivo 23Na and 1H2O MRS obtained from rat blood.

Frequency shift/concentration calibration curves applicable to the use of shift reagents (SRs) for in vivo 23Na MRS studies can be obtained from experiments with whole blood. Here, they are reported for titrations of rat blood with the SRs DyTTHA3- and TmDOTP5-. There are a number of considerations that must be made in order to derive accurate calibration curves from the experimental data. These include the effects of bulk magnetic susceptibility (BMS, since the SRs are paramagnetic), the effects of water flux (since addition of the SR stock solution to blood renders the plasma hyperosmotic), and the consequences of restricted distribution of the SR anion in the erythrocyte suspension. We give in some detail the BMS shift theory that obtains in this case and show also how it applies to excised perfused organ as well as in vivo studies. Also, we report significant effects of adjuvant Ca2+ additions in the TmDOTP5- titrations. These are very important to the successful use of this SR in vivo. Finally, our considerations of BMS lead naturally to an understanding of its manifestations in the shifts of the 1H2O resonance frequencies of cell suspensions and tissues induced by SRs. Since these are being increasingly reported, and often misinterpreted, we devote an experiment and some discussion to this subject. We show that this phenomenon cannot be used to quantitatively discriminate intra- and extracellular 1H2O signals.

Animals↗
PubMedDate not supplied

Extracellular volume and transsarcolemmal proton movement during ischemia and reperfusion: a 31P NMR spectroscopic study of the isovolumic rat heart.

We have measured, directly and simultaneously, changes in extracellular volume and intra- and extracellular pH during ischemia in the isolated rat heart using 31P NMR spectroscopy. Hearts were perfused with buffer containing 15 mM sodium phenylphosphonate at pH 7.4. Wash in and wash out experiments showed that phenylphosphonate entered only the extracellular (interstitial, vascular and chamber) space of the heart and had no adverse effects on myocardial energetics, contractile function or coronary flow rate. Hearts were subjected to 28 min of total, global ischemia, during which the phenylphosphonate resonance area in the 31P NMR spectra decreased by 83%, indicating that extracellular fluid had moved rapidly from the heart to the bath surrounding the heart, partly as a result of vascular collapse. A separate, morphological study confirmed that 95% of the vasculature had collapsed by 28 min ischemia. Intra- and extracellular pH were determined from the chemical shifts of the P(i) and the phenylphosphonate resonances, respectively. In the pre-ischemic rat heart, intracellular pH was 7.15 +/- 0.03 and extracellular pH was 7.39 +/- 0.03. By 4 min of ischemia, intra- and extracellular pH were the same and decreased concomitantly throughout the remainder of ischemia to final values of 6.09 +/- 0.19 and 6.16 +/- 0.23, respectively. On reperfusion, the extracellular volume and pH returned to pre-ischemic levels within 1 min, but restoration of intracellular pH took > 2.5 min. Thus, a large volume of extracellular fluid moves out of the rat heart to the surrounding bath and the intra- and extracellular pH become the same during total, global ischemia.

Adenosine Triphosphate↗