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R G Weiss

Publications and source records attributed to R G Weiss.

At least 37 records · Page 2Linked to original sources
PubMed1999

Inactivation determinant in the I-II loop of the Ca2+ channel alpha1-subunit and beta-subunit interaction affect sensitivity for the phenylalkylamine (-)gallopamil.

1. The role of calcium (Ca2+) channel inactivation in the molecular mechanism of channel block by phenylalkylamines (PAAs) was analysed in a PAA-sensitive rabbit brain class A Ca2+ channel mutant (alpha1A-PAA). Use-dependent barium current (IBa) inhibition of alpha1A-PAA by (-)gallopamil and Ca2+ channel recovery from inactivation and block were studied with two-microlectrode voltage clamp after expression of alpha1A-PAA and auxiliary alpha2-delta- and beta1a- or beta2a-subunits in Xenopus oocytes. 2. Mutation Arg387Glu (alpha1A numbering) in the intracellular loop connecting domains I and II of alpha1A-PAA slowed the inactivation kinetics and reduced use-dependent inhibition (100 ms test pulses at 0.2 Hz from -80 to 20 mV) of the resulting mutant alpha1A-PAA/R-E/beta1a channels by 100 microM (-)gallopamil (53 +/- 2 %, alpha1A-PAA/beta1a vs. 31 +/- 2 %, alpha1A-PAA/R-E/beta1a, n >= 4). This amino acid substitution simultaneously accelerated the recovery of channels from inactivation and from block by (-)gallopamil. 3. Coexpression of alpha1A-PAA with the beta2a-subunit reduced fast IBa inactivation and induced a substantial reduction in use-dependent IBa inhibition by (-)gallopamil (25 +/- 4 %, alpha1A-PAA/beta2a; 13 +/- 1 %, alpha1A-PAA/R-E/beta2a). The time constant of recovery from block at rest was not significantly affected. 4. These results demonstrate that changes in channel inactivation induced by Arg387Glu or beta2a-alpha1-subunit interaction affect the drug-channel interaction.

Algorithms↗
PubMed1999

High extracellular K+ during hypoxic preconditioning episodes attenuates the post-ischemic contractile and ionic benefits of preconditioning.

Hypoxic preconditioning improves contractile recovery and decreases calcium loading following ischemia and reperfusion. To test whether changing the trans-sarcolemmal K+ gradient during the preconditioning period changes preconditioning's benefits, isolated rat hearts were subjected to two, 5 min hypoxic intervals in the presence of normal K+ (5mM, NmlK-PC) or high K+ (10.3 mM, HiK-PC), separated by 5 min of normoxic reflow. Preconditioning with 5 mM K+ significantly improved developed pressure (DP) after 30 min of ischemia as compared to non-preconditioned control hearts (55.9+/-4.41% v 12.4+/-2.01% of baseline, P<0.05). DP recovery was diminished with 10.3 mM K+ (25.1+/-4.20% of baseline, P<0.05). At the end of reperfusion, cell Ca2+ trended lower in hypoxic preconditioned hearts compared with control hearts (12.9+/-1.9 v 19.4+/-2.6 micromol/g dry wt, P=0.09) and was significantly lower than high K+ hearts (22.9+/-1.4 micromol/g dry wt, P<0.006). Intracellular K+ during reperfusion was significantly higher in preconditioned compared with control hearts (P<0.02) and high K+ hearts (P<0.002) (231+/-10 v 166+/-17 v 155+/-14 micromol/g dry wt, respectively). Thus, the trans-sarcolemmal K+ gradient during the preconditioning period influences preconditioning effects; decreasing the gradient attenuates preconditioning's favorable influences on contractile recovery, cellular K+ loss, and calcium loading during reperfusion.

Animals↗
PubMed1999

Preservation of canine myocardial high-energy phosphates during low-flow ischemia with modification of hemoglobin-oxygen affinity.

Conventional approaches for the treatment of myocardial ischemia increase coronary blood flow or reduce myocardial demand. To determine whether a rightward shift in the hemoglobin-oxygen saturation curve would reduce the metabolic and contractile effects of a myocardial oxygen-supply imbalance, we studied the impact of a potent synthetic allosteric modifier of hemoglobin-oxygen affinity, a 2-[4-[[(3,5-disubstituted anilino)carbonyl]methyl] phenoxy] -2-methylproprionic acid derivative (RSR13), during low-flow ischemia. Changes in myocardial high-energy phosphate levels and pH were studied by 31P nuclear magnetic resonance (NMR) spectroscopy in 12 open-chest dogs randomized to receive RSR13 or vehicle control during a reversible reduction of left anterior descending (LAD) coronary artery blood flow. Changes in cardiac metabolites and regional ventricular function studied by pressure segment-length relations were also investigated in additional animals before and after RSR13 administration during low-flow LAD ischemia. The intravenous administration of RSR13 before ischemia resulted in a substantial increase in the mean hemoglobin p50 and attenuated the decline in cardiac creatine phosphate/adenosine triphosphate (PCr/ATP), percent PCr, and pH during ischemia without a change in regional myocardial blood flow, heart rate, or systolic blood pressure. RSR13 given after the onset of low-flow ischemia also improved cardiac PCr/ATP ratios and regional function as measured by fractional shortening and regional work. Thus, synthetic allosteric reduction in hemoglobin-oxygen affinity may be a new and important therapeutic strategy to ameliorate the metabolic and functional consequences of cardiac ischemia.

Aniline Compounds↗
PubMed1998

Pertussis toxin-sensitive G proteins influence nitric oxide synthase III activity and protein levels in rat heart.

Inhibitory G protein activity (Gi) and nitric oxide (NO) modulate muscarinic-cholinergic (MC) inhibition of cardiac beta-adrenergic inotropic responses. We hypothesized that Gi mediates MC-NO synthase (NOS) signal transduction. Isoproterenol (0.2-0.8 microg/min) and acetylcholine (1 microM) were administered to isolated perfused rat hearts pretreated with saline (controls; n = 8) or pertussis toxin (PT; 30 microg/kg intraperitoneally 3 d before study; n = 20). PT abrogated in vitro ADP-ribosylation of Gi protein alpha subunit(s) indicating near-total decrease in Gi protein function. Isoproterenol increased peak +dP/dt in both control (peak isoproterenol effect: +2, 589+/-293 mmHg/s, P < 0.0001) and PT hearts (+3,879+/-474 mmHg/s, P < 0.0001). Acetylcholine reversed isoproterenol inotropy in controls (108+/-21% reduction of +dP/dt response, P = 0.001), but had no effect in PT hearts. In controls, NG-monomethyl-L-arginine (100 microM) reduced basal +dP/dt, augmented isoproterenol +dP/dt (peak effect: +4,634+/-690 mmHg/s, P < 0.0001), and reduced the MC inhibitory effect to 69+/-8% (P < 0.03 vs. baseline). L-arginine (100 M) had no effect in controls but in PT hearts decreased basal +dP/dt by 1, 426+/-456 mmHg/s (P < 0.005), downward-shifted the isoproterenol concentration-effect curve, and produced a small MC inhibitory effect (27+/-4% reduction, P < 0.05). This enhanced response to NO substrate was associated with increased NOS III protein abundance, and a three- to fivefold increase in in vitro calcium-dependent NOS activity. Neomycin (1 microM) inhibition of phospholipase C did not reverse L-arginine enhancement of MC inhibitory effects. These data support a primary role for Gi in MC receptor signal transduction with NOS in rat heart, and demonstrate regulatory linkage between Gi and NOS III protein levels.

Acetylcholine↗
PubMed1998

Non-invasive magnetic-resonance detection of creatine depletion in non-viable infarcted myocardium.

BACKGROUND: Preserved energy metabolism is essential for myocardial viability and the creatine kinase reaction is central to energy production and reserve. Although the appearance of myocardial creatine kinase enzyme in the blood is widely used to diagnose cardiac necrosis, there are no non-invasive ways to measure local creatine concentrations in the healthy and diseased human heart. METHODS: We measured total myocardial creatine by spatially-localised, water-suppressed hydrogen magnetic-resonance spectroscopy (1H-MRS) on a clinical (1.5 T) magnetic-resonance-imaging system in ten healthy volunteers (controls) and ten patients with a history of myocardial infarction. We validated this technique by comparison of 1H-MRS values of creatine with biopsy assays in an animal model of infarction. FINDINGS: Total creatine was measured in the posterior and anterior left ventricle and septum, and was significantly lower in regions of infarction (10 [9] SD micromol/g wet weight) than in non-infarcted regions (26 [11] micromol/g, p=0.001) of myocardium in patients or in the myocardium of healthy controls (28 [6] micromol/g, p<0.0001). INTERPRETATION: Spatially localised 1H-MRS can be used to measure total creatine non-invasively throughout the human heart. The detection of regional creatine depletion may provide a metabolic means to distinguish healthy from infarcted non-viable myocardium.

Adult↗
PubMed1997

Normal high energy phosphate ratios in "stunned" human myocardium.

OBJECTIVES: We sought to investigate whether alterations in cardiac high energy phosphates occur in postischemic "stunned" human myocardium. BACKGROUND: Transient postischemic myocardial dysfunction is a common phenomenon that occurs in a variety of clinical settings in the absence of necrosis, and its pathogenesis is still unclear. Cardiac high energy phosphates are reduced during ischemia, and persistently altered myocardial high energy phosphate metabolism has been suggested as a mechanism contributing to stunning. METHODS: We studied 29 patients with a first anterior myocardial infarction (MI) who underwent successful reperfusion within 6 h of the onset of chest pain. These patients underwent 31P magnetic resonance spectroscopy (MRS) a mean of 4 days after MI for measurement of left ventricular contractility and relative high energy phosphate metabolites. Twenty-one patients underwent a second 31P MRS study a mean of 39 days after MI. Eight volunteers served as control subjects. RESULTS: Global and infarct area wall motion scores improved significantly between the early and late studies. No difference was found between early cardiac phosphocreatine (PCr)/beta-adenosine triphosphate (beta-ATP) ratios in patients and control subjects ([mean +/- SD] 1.51 +/- 0.17 vs. 1.61 +/- 0.18, respectively, p = 0.17) or between early and late study results in patients (1.51 +/- 0.17 vs. 1.53 +/- 0.17, respectively, p = 0.6). For alpha of 0.05, the study had a 90% power to detect a 9% difference. CONCLUSIONS: The results of this study demonstrate normal myocardial PCr/ATP ratios in patients with myocardial stunning after reperfusion and suggest that relative cardiac high energy phosphates are not depleted in stunned human myocardium.

Adenosine Triphosphate↗
PubMed1997

Role of preischemic glycogen depletion in the improvement of postischemic metabolic and contractile recovery of ischemia-preconditioned rat hearts.

BACKGROUND: Ischemic preconditioning (IPC) attenuates acidosis during prolonged ischemia and improves contractile and metabolic parameters during subsequent reperfusion. Glycogen depletion induced by IPC is proposed as a potential mechanism. METHODS AND RESULTS: We studied the influence of manipulations of preischemic glycogen levels (Pre-G, micromol glucose/g wet wt) on contractile and metabolic (via 31P-nuclear magnetic resonance) parameters during 30 minutes of ischemia and recovery in four groups of isovolumic rat hearts: First, control (Con, n=18, mean Pre-G, 21.5+/-0.8); second, after two 5-minute IPC periods (IPC, n=12, Pre-G, 11.3+/-0.7); third, a control group in which Pre-G was depleted by glucose-free, acetate perfusion (Con-LowG, n=9, Pre-G, 7.9+/-1.2); and fourth, an IPC group in which Pre-G was raised by glucose and lactate perfusion such that Pre-G was similar to Con (IPC-HiG, n=11, Pre-G, 20+/-1.4). Manipulation of Pre-G significantly altered the pH fall during 30 minutes of ischemia (Con, 5.76+/-.03, Con-LowG, 6.26+/-.07; IPC-HiG, 5.91+/-.02, IPC, 6.05+/-.09). IPC-HiG hearts had significantly worse metabolic recovery (PCr, 70+/-7 versus 91+/-3% initial; IPC-HiG versus IPC, P<.05) and contractile recovery (end-diastolic pressure, 52+/-5 versus 29+/-5 mm Hg, P<.05) than IPC hearts but better recovery than Con (%PCr, 56+/-6% and end-diastolic pressure, 72+/-6 mm Hg). An ischemic rise in intracellular magnesium occurred and was atttenuated in preconditioned hearts. CONCLUSIONS: Pre-G levels before ischemia influence but are not the sole determinants of the extent of acidosis during prolonged ischemia and of metabolic and contractile recovery during reperfusion in control and preconditioned hearts.

Animals↗
PubMed1997

Total creatine in muscle: imaging and quantification with proton MR spectroscopy.

PURPOSE: To provide a noninvasive method of imaging and quantifying total creatine (phosphorylated plus unphosphorylated) in human muscle with proton magnetic resonance (MR) spectroscopy. MATERIALS AND METHODS: Water-suppressed, long echo time, stimulated-echo hydrogen-1 chemical shift imaging and short echo time unsuppressed chemical shift imaging were performed on the lower legs of 10 healthy volunteers at rest. Spatial resolution was 4.5-8.0 cm3. Water signals in unsuppressed data sets were quantified and used as chemical shift and concentration references. Images of the integrated N-CH3 resonance assigned to total creatine were extracted from the water-suppressed chemical shift image data. Correlations between the total creatine, lipid, and water signals from the same voxels were tested. The concentration of total creatine in skeletal muscle was calculated from the ratio of the relaxation-corrected N-CH3 and water signals from the same voxels. RESULTS: Total creatine was localized to muscle bundles. Lipid signals contributed less than 6% to the variance of total creatine signal on images and in measurements and did not correlate with total creatine in the same voxels (P > .1). Total creatine and unsuppressed water signals were positively correlated (P < .0001). MR spectroscopy yielded a total creatine value of 36.2 mmol/kg wet weight +/- 5.0, consistent with prior biopsy data. CONCLUSION: H-1 MR spectroscopy can be used to image and noninvasively quantify total creatine in human muscle. Its use could improve the understanding of the role of altered creatine metabolism in muscle disease and aid quantification of the response to creatine therapies.

Adult↗
PubMed1996

Human cardiac high-energy phosphate metabolite concentrations by 1D-resolved NMR spectroscopy.

We have developed a method that can measure high-energy phosphate metabolite concentrations in humans with 1D resolved surface-coil NMR spectroscopy. The metabolites are measured by phosphorus (31P) NMR spectroscopy, and the tissue water proton (1H) resonance from the same volume serves as an internal concentration reference. The method requires only the additional acquisition of a 1H data set, and a simple calibration, performed separately, to determine the ratio of the signal per proton to the signal per phosphorus nucleus. The quantification method is particularly useful for human cardiac spectroscopy, where it eliminates image-based tissue volumetry and the corrections for signal sensitivity and phase nonuniformity necessary in prior approaches. Corrections are introduced to account for blood and fat contributions to the spectra. The method was validated on phantoms of phosphate of varying concentrations and on the human calf muscle. In calf, the adenosine triphosphate (ATP) and phosphocreatine (PCr) concentrations were 5.6 +/- 1.6 (mean +/- SD) and 26 +/- 4 mmol/kg wet wt, respectively. In normal heart, [ATP] was 5.8 +/- 1.6 and [PCr] was 10 +/- 2 mmol/kg wet wt. These values are in excellent agreement with prior NMR studies and biopsy data. The protocol is easily accommodated within existing 1D cardiac patient protocols, and the same approach is advantageous for eliminating tissue volumetry and sensitivity corrections when measuring concentrations by 2D and 3D resolved spectroscopy.

Adenosine Triphosphate↗
PubMed1996

Attenuated glycogenolysis reduces glycolytic catabolite accumulation during ischemia in preconditioned rat hearts.

Prior transient episodes of ischemia ("ischemic preconditioning") reduce lactate accumulation and attenuate acidosis during a subsequent prolonged ischemic insult. The mechanisms responsible for attenuated glycolytic catabolite accumulation have not been established but may include earlier exhaustion of glycogen stores, slowed glycogenolysis before complete glycogen depletion, and/or inhibition of glycolysis. Simultaneous repeated measures of myocardial glycogen and the rates of glycolysis, glycogenolysis, glucose utilization, and glycolytic ATP production were obtained during total ischemia by 13C nuclear magnetic resonance spectroscopy in control and ischemia-preconditioned isolated rat hearts. Both [13C]glycolytic and [13C]glycogenolytic rates were significantly lower during total ischemia in preconditioned compared with control hearts (0.77 +/- 0.04 versus 1.06 +/- 0.06 mumol/min per gram wet weight [P < .01] for glycolysis and 0.15 +/- 0.07 versus 0.78 +/- 0.12 mumol/ min per gram wet weight [P < .001] for glycogenolysis, respectively, at 2.5 minutes of ischemia). Slowed glycolysis was present even during the early minutes of ischemia, when significant amounts of available [13C]glycogen were still present. Importantly, the reduction in the rate of glycogenolysis was larger and out of proportion to the reduction in glycolysis and occurred despite an increase in glucose utilization in preconditioned hearts (2.23 +/- 0.15 versus 1.5 +/- 0.10 mumol/min per gram wet weight at 1.25 minutes, P < .01). During early ischemia, conversion of glycogen phosphorylase to the a or "active" form was less in preconditioned than in control hearts (29.1 +/- 2.6% versus 41.2 +/- 9.8%, respectively; P < .05). Taken together, these findings demonstrate that ischemic preconditioning significantly depresses glycolytic catabolite accumulation during sustained ischemia not by more severe glycolytic inhibition or exhaustion of glycogen stores but by depressed glycogenolysis from the onset of ischemia.

Animals↗
PubMed1995

Consequences of altered aspartate aminotransferase activity on 13C-glutamate labelling by the tricarboxylic acid cycle in intact rat hearts.

The appearance of 13C label in glutamate has been used to quantify cellular tricarboxylic acid (TCA) cycle activity using 13C-NMR spectroscopy. Glutamate is linked to the TCA cycle by the amino-transferase reactions, however the consequences of alterations in amino-transferase activity on glutamate labelling kinetics, at a constant total tricarboxylic acid cycle activity, have not been investigated. Aspartate amino-transferase activity in [2-13C]acetate-perfused beating rat hearts was found to be similar to total TCA cycle flux in the presence of normal perfusion conditions and was reduced by more than 50% with the subsequent administration of amino-oxyacetic acid (AOA). AOA did not reduce contractile or kinetic measures of total TCA cycle flux, but did slow the 13C labelling of glutamate, in accord with current mathematical predictions. The impact of similar reductions in amino-transferase activity on estimates of total TCA cycle flux derived from several previously reported methods was also evaluated. Because total TCA cycle and the amino-transferase activities both affect the kinetics of 13C-glutamate labelling and because the amino-transferase activities are often unknown under physiologic conditions and can be reduced under pathologic conditions, the calculation of total TCA cycle flux from 13C-NMR data in the future is probably best accomplished either with a sufficiently sophisticated mathematical model that assesses amino-transferase activity or with an empiric model that is relatively insensitive to variations in amino-transferase activity.

Aminooxyacetic Acid↗
PubMed1994

Importance of metabolic inhibition and cellular pH in mediating preconditioning contractile and metabolic effects in rat hearts.

The pathophysiological mechanisms by which brief periods of flow interruption before a prolonged ischemic period, ischemic preconditioning (IPC), increase myocardial tolerance to ischemia and improve myocardial function during reperfusion are not completely understood. To test whether short periods of metabolic inhibition in the absence of a flow reduction induce similar protective effects, we studied cardiac function and metabolism using 31P nuclear magnetic resonance spectroscopy in isolated isovolumic rat hearts. Fifteen hearts underwent IPC, consisting of two 5-minute ischemia-reperfusion cycles (IPC group); 18 hearts underwent brief metabolic inhibition by exposure to two 5-minute infusions of 10 mmol/L sodium cyanide (CN group); and 15 hearts served as controls. Subsequently all hearts were subjected to 30 minutes of total global ischemia at 37 degrees C followed by reperfusion. At the end of the ischemic period, creatine phosphate and ATP levels did not differ among the groups. Cellular pH, however, plateaued at a higher level in the CN group (6.51 +/- 0.03) and IPC group (6.12 +/- 0.06) than in the control group (5.84 +/- 0.01, P < .001). IPC and CN hearts had better functional and metabolic recovery than the control hearts. Improved contractile recovery correlated with coronary flow rates at reperfusion (r = .7, P < .001) and with pHi values at 30 minutes of ischemia (r = .8, P < .001) but not with increased ATP levels during ischemia. Additional control hearts were reperfused at 15 mL/min so as to match the flow rates of IPC and CN groups, but this did not result in improved performance. To test the hypothesis that the preconditioning effect was related to pHi during ischemia, additional IPC and CN hearts underwent the same preconditioning protocol, except that the cellular pH at the end of the ischemic period was lowered by the use of hypercarbic superfusion during ischemia or by the use of bicarbonate-free perfusate just before sustained ischemia. Both of these interventions resulted in significantly lower contractile and metabolic recoveries than those observed in other IPC and CN hearts. Therefore, the preconditioning effect does not require reduced coronary flow but can be effectively elicited by metabolic inhibition per se in this model. The protective effect is not dependent on preservation of global myocardial energy stores but, rather, on reduced acidosis during the prolonged ischemic period.

Acidosis↗
PubMed1994

Magnetic resonance imaging evaluation of chronic changes in latissimus dorsi cardiomyoplasty.

BACKGROUND: Long-term clinical and hemodynamic benefits of dynamic cardiomyoplasty (DC) have been reported. However, no information is available about long-term morphological changes in the wrapped latissimus dorsi (LD) muscle in humans. METHODS AND RESULTS: The LD muscle flap was evaluated by magnetic resonance imaging (MRI) in 13 patients submitted to dynamic cardiomyoplasty for treatment of severe dilated cardiomyopathy. Eight patients were studied 15 days after the surgery (group 1) and 5 patients were studied from 24 to 52 months after the surgical procedure at the time of the cardiomyostimulator replacement (group 2). In the interim, LD was stimulated with burst of 6 pulses (duration, 185 milliseconds; burst frequency, 30 Hz) synchronized to every cardiac contraction, with a maximum of 100 LD contractions per minute. Images were acquired on a GE Sigma 1.5-T system (echo time, 25 milliseconds; repetition time, R-R x 2; slice thickness, 8 mm). The thickness of the LD decreased from 19.6 +/- 7.3 mm for group 1 to 7.6 +/- 0.8 mm for group 2 (P < .01). In addition, the signal intensity of the LD was compared with that of thoracic skeletal muscle and was found to be significantly increased in group 2 (2.19 +/- 0.42) compared with group 1 (1.04 +/- 0.07, P < .001). The signal intensity for group 2 on the T1-weighted images was similar to that of subcutaneous fat in those images. CONCLUSIONS: Morphological changes in the wrapped LD muscle consistent with fatty degeneration occur after DC and can be detected by MRI. Further studies will be necessary to demonstrate the clinical significance of such LD muscle flap changes.

Adipose Tissue↗
PubMed1993

Direct evidence that coronary perfusion affects diastolic myocardial mechanical properties in canine heart.

OBJECTIVE: The effect of coronary perfusion on left ventricular chamber distensibility is only indirect evidence that perfusion alters the mechanical properties of the myocardium. The aim of this study was to demonstrate explicitly the effects of coronary perfusion on these mechanical properties. METHODS: The effects of different levels of coronary perfusion were studied both on in-plane stress-strain relations and on transverse stiffness in an isolated, perfused canine interventricular septal preparation. Additionally, to determine the vascular compartment responsible for the mechanical effects of perfusion on tissue properties, we examined the in-plane stress-strain responses and transverse stiffness after embolisation of the vasculature with 15 microns microspheres. RESULTS: The data show a clear dependence of tissue stress-strain properties on perfusion. The in-plane stress-strain relations were shifted to the left and transverse stiffness increased linearly as septal artery perfusion pressure increased. The dependence of both the in-plane stress-strain relations and transverse stiffness on perfusion was significantly decreased following embolisation. CONCLUSIONS: Myocardial tissue stiffness is directly related to perfusion. The linear relationship between transverse stiffness and perfusion makes it easier to assess the effects of perfusion on tissue stiffness than with in-plane stress-strain relations. Perfusion of capillaries and/or venules is largely responsible for these alterations in myocardial stiffness.

Animals↗
PubMed1993

Intracellular pH determination by 13C-NMR spectroscopy.

A noninvasive method for the determination of pH by the 13C-nuclear magnetic resonance (NMR) chemical shift of the C-3 carbon of sn-glycerol 3-phosphate is described. Nonlinear least-squares analysis of the chemical shift variation of the C-3 resonance of sn-glycerol 3-phosphate with pH at 37 degrees C in solutions and in perchloric acid extracts of tissue yielded a pKa of 6.2, making it a very sensitive indicator of pH in the approximate range of 5-7. Intracellular pH determined by the present 13C-NMR method correlated well with simultaneous measurements of pH by 31P-NMR spectroscopy over a wide range during normal perfusion and ischemic conditions in intact rat hearts. These findings indicate that this approach is particularly suited for quantification of intracellular pH over the physiological range in intact tissues and that observed in ischemic myocardium.

Animals↗