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J R Neely

Publications and source records attributed to J R Neely.

96 records · Page 6Linked to original sources
PubMedDate not supplied

Factors determining the utilization of glucose in isolated rat hearts.

Glucose utilization by the isolated rat heart is restricted by flux through the membrane transport, phosphofructokinase and glyceraldehyde-3-P dehydrogenase reactions. These reactions can be accelerated by hormones, such as insulin, by mechanical factors, such as the "garden-hose effect", heart rate, and perhaps ventricular pressure development, and by oxygen deprivation. Glucose utilization is restricted by provision of exogenous non-carbohydrate substrates and by utilization of endogenous substrate stores. Isolated hearts perfused as Langendorff preparations with or without a ventricular drain, working hearts, and ischemic preparations are useful in defining rate-limiting steps and mechanisms of regulation. However, when glucose is supplied as the sole exogenous substrate, its rates of utilization do not reflect the more complex in vivo situation where competing substrates such as fatty acids are preferentially utilized.

Adenosine Triphosphate↗
PubMedDate not supplied

Deleterious effects of digitalis on reperfusion-induced arrhythmias and myocardial injury in ischemic rat hearts: possible involvements of myocardial Na+ and Ca2+ imbalance.

Isolated rat hearts were made ischemic for 25 min after an initial recirculating perfusion, followed by 30 min of reperfusion. In some hearts, interventions including administration of ouabain and/or high [K+] in the buffer were performed during the first 10 min of reperfusion. During ischemia, intracellular Na+ (Nai) increased from 15 to 64 mumol/g dry weight (dwt). During reperfusion, Nai declined rapidly (at 10 min of reperfusion: 48 mumol/g dwt, at 30 min: 25 mumol/g dwt) and regular rhythm was recovered within 10 min in hearts without any intervention during reperfusion. 45Ca2+ uptake increased from 0.8 to 7.5 mumol/g dwt after 30 min of reperfusion. Ventricular function recovered by 45%. A 10-min perfusion with 10 or 50 microM of ouabain increased Nai (17 to 21 or 27 mumol/g dwt) with increased left-ventricular (LV) contractile function, but these effects were reversed by combination of high perfusate [K+] (20 mM) in non-ischemic hearts. A 10-min reperfusion with ouabain retarded or stopped the decline in Nai (at 10 min of reperfusion: 54 or 63 mumol/g dwt, at 30 min: 32 or 40 mumol/g dwt). These amounts of ouabain also increased the incidence of ventricular tachyarrhythmias during reperfusion to 30% or 50%, and increased the duration of ventricular fibrillation from 6.5 to 11.5 or 18.0 min. 45Ca2+ uptake reached to 8.8 or 10.0 mumol/g dwt, and function recovered only 35% or 28%. When high perfusate [K+] was combined with ouabain during reperfusion, the retarded decline in Nai, augmented 45Ca2+ uptake, and reduced recovery of function caused by ouabain alone were attenuated. These results suggest that digitalis has toxic effects on reperfused ischemic hearts by inhibition of rapid active outward transport of previously elevated Nai and potentiation of Ca2+ overload.

Animals↗