Background-Discrepant reports have been published recently regarding the relationship of contrast-enhanced magnetic resonance image intensities to reversible and irreversible ischemic injury. Unlike image intensities, contrast agent concentrations provide data independent of the MRI technique. We used electron probe x-ray microanalysis (EPXMA) to simultaneously examine concentrations of Gd, Na, P, S, Cl, K, and Ca over a range of myocardial injuries. Methods and Results-Reversible and irreversible injury were studied in 38 rabbits divided into 4 groups defined by occlusion and reperfusion time, as well as time the animals were euthanized. Gd-DTPA was administered, and the hearts were excised and rapidly frozen, cryosectioned, freeze-dried, and examined by EPXMA in up to 3 regions: remote, infarcted, and at risk but not infarcted. Infarcted regions were defined by anti-myoglobin antibody or triphenyltetrazolium chloride staining. Regions at risk were defined by fluorescent microparticles administered during occlusion. Compared with remote regions, in acutely infarcted regions, Gd was increased (235Ϯ24%, PϽ0.005) in the same 50ϫ100-m areas in which Na was increased (154Ϯ5%, PϽ0.001) and K was decreased (52Ϯ8%, PϽ0.001).Similarly, in chronically infarcted regions, Gd was increased (472Ϯ78%, PϽ0.001) in areas in which Na was increased (332Ϯ28%, PϽ0.001) and K was decreased (47Ϯ5%, PϽ0.001). Also compared with remote regions, however, concentrations of Gd, Na, and K were not elevated after reperfusion in regions that were at risk but not infarcted (PϭNS). Conclusions-Regional

Concurrent directionally opposite changes in infarcted and noninfarcted myocardium can be defined serially, noninvasively, and with high spatial resolution and full ventricular coverage following myocardial infarction.

No abstract

Effects of sodium-coupled transport on intracellular electrolytes and electrical properties of proximal renal tubule cells are described in this review. Simultaneous with addition of substrate for sodium-coupled transport to luminal perfusates, both cell membranes depolarize. The luminal cell membrane depolarizes due to opening of sodium-cotransport pathways. The depolarization of the peritubular cell membrane during sodium-coupled transport is primarily due to a circular current reentering the lumen via the paracellular pathway. The depolarization leads to a transient decrease of basolateral potassium conductance that in turn amplifies the depolarization. However, within 5-10 min of continued exposure to substrate, potassium conductance increases again, and peritubular cell membrane repolarizes. During depolarization the driving force of peritubular bicarbonate exit is reduced. As a result net alkalinization of the cell prevails despite an increase of intracellular sodium activity, which reduces the driving force for the sodium-hydrogen ion exchanger and would thus have been expected to acidify the cell. No evidence is obtained for regulatory inhibition of sodium-coupled transport by intracellular sodium or calcium. Rather, luminal cotransport is altered by the change of driving forces.

The AMI size can be measured with MRI using a contrast dose between 0.1 and 0.2 mmol/kg and a time window of 5 to 30 min after contrast administration, provided that the TI is adjusted.