Refillable point source for motion correction during first-pass radionuclide angiography.

First-pass radionuclide angiography, for the evaluation of ventricular function during peak physiological stress, requires the use of a low-energy point source for correction of motion artifacts. A design for the construction of a refillable 125I point source is presented.

Effects of cardiac denervation on atrioventricular nodal accommodation and hysteresis.

Conduction through the atrioventricular (AV) node is significantly altered by changes in autonomic tone. AV nodal accommodation (time-dependent changes in AV nodal conduction after a sudden change in atrial cycle length) and AV nodal hysteresis (asymmetry of AV nodal accommodation after directionally opposite atrial pacing cycle length changes) have been characterized in humans. Studies in dogs after cardiac transplantation suggest that the rapid phase of AV nodal accommodation is altered following ablation of neural input to the AV node. To determine if cardiac denervation alters AV nodal accommodation and hysteresis in humans, 13 patients after orthotopic cardiac transplantation and 12 control patients with normal AV nodal function were studied. Atrial pacing was performed for 1 minute at different pacing cycle lengths and AH or AV intervals were measured after cycle length changes. The rapid phase of accommodation is defined as the time required for the AV interval to reach 75% of the final AV interval. During abrupt changes from long to short pacing cycle lengths, the rapid phase of accommodation took 3.2 +/- 1.0 and 4.3 +/- 1.0 beats in control subjects and transplant patients, respectively (p = not significant [NS]). When going from short to long pacing cycle lengths, the rapid phase of accommodation took 1.7 +/- 1.2 and 2.1 +/- 1.8 beats in control subjects and transplant patients, respectively (p = NS). Hysteresis of 1.5 +/- 1.3 and 2.1 +/- 1.4 beats was noted in the control and transplant groups, respectively (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Differentiation of reperfused-viable (stunned) from reperfused-infarcted myocardium at 1 to 3 days postreperfusion by in vivo phosphorus-31 nuclear magnetic resonance spectroscopy.

Thrombolytic therapy has increased the need for a technique to assess the viability of recently reperfused myocardium. This study examined the ability of in vivo phosphorus-31 (P-31) nuclear magnetic resonance (NMR) spectroscopy to distinguish reperfused-viable (stunned) from reperfused-infarcted myocardium at 6, 30, and 54 hours following coronary artery occlusion in a canine model. A 15-minute occlusion produced reperfused-viable myocardium in five animals and a 360-minute occlusion produced reperfused-infarcted myocardium in six animals. Postreperfusion risk zone myocardial phosphocreatine (PCr) concentration measured by P-31 NMR spectroscopy was significantly depressed throughout the 3-day study period in infarcted but not in viable myocardium (p less than 0.01 between groups, all time points). The postreperfusion ratio of inorganic phosphate (Pi) to PCr concentration, as determined by NMR spectroscopy, was elevated throughout the study period in infarcted but not in viable reperfused myocardium (p less than 0.01 between groups, all time points). Postreperfusion Pi concentration was elevated at 6 hours but not subsequently in reperfused-infarcted myocardium, and was not elevated in reperfused-viable myocardium. Logistic regression models selected PCr concentration and the Pi/PCr ratio as providing the best discrimination between reperfused-viable and reperfused-infarcted myocardium. The accuracy of P-31 NMR variables selected by logistic regression analysis for determining myocardial viability ranged from 97% to 100%.

Effect of brief regional ischemia followed by reperfusion with or without superoxide dismutase and catalase administration on myocardial sarcoplasmic reticulum and contractile function.

The effect of reperfusion with and without free radical scavengers on sarcoplasmic reticulum and contractile function was examined in a canine model of 15-minute coronary artery occlusion followed by reperfusion. Dogs were reperfused with (n = 13) or without (n = 16) superoxide dismutase and catalase or were killed at 15 minutes of ischemia (n = 17). Superoxide dismutase and catalase were administered as a bolus (20,000 and 12,500 U/kg, respectively) beginning 1.25 minutes before reperfusion followed by infusion of 16,000 and 12,500 U/kg/hr, respectively. Sarcoplasmic reticulum function was evaluated from the rate of calcium uptake of unfractionated subepicardial, subendocardial, and transmural homogenates determined with and without ruthenium red to close the calcium release channel. Mechanical function was evaluated by means of sonomicrometry. Fifteen minutes of ischemia significantly (p less than 0.05) depressed the sarcoplasmic reticulum calcium uptake rate only in the subendocardium (from 25 +/- 2 to 14 +/- 1 nmol/min/mg without ruthenium red and from 60 +/- 3 to 49 +/- 3 nmol/min/mg with ruthenium red). Reperfusion with or without superoxide dismutase and catalase restored homogenate calcium uptake rates to normal, although severe contractile dysfunction persisted. This indicates that damage to the sarcoplasmic reticulum may not be the major cause of postreperfusion contractile dysfunction. Ischemia-reperfusion caused a decrease in systolic shortening from 19 +/- 2% to 1 +/- 2% with and from 18 +/- 1% to 4 +/- 1% without free radical scavengers (p = NS between groups). Thus administration of superoxide dismutase and catalase beginning shortly before reperfusion had no effect on postreperfusion contractile dysfunction or sarcoplasmic reticulum function.