We studied clearance of acid from the esophagus and esophageal emptying in normal subjects. A 15-ml bolus of 0.1 N hydrochloric acid (pH 1.2) radiolabeled with [99mTc]sulfur colloid was injected into the esophagus, and the subject swallowed every 30 seconds. Concurrent manometry and radionuclide imaging showed nearly complete emptying of acid from the esophagus by an immediate secondary peristaltic sequence, although esophageal pH did not rise until the first swallow 30 seconds later. Esophageal pH then returned to normal by a series of step increases, each associated with a swallow-induced peristaltic sequence. Saliva stimulation by an oral lozenge shortened the time required for acid clearance, whereas aspiration of saliva from the mouth abolished acid clearance. Saliva stimulation or aspiration did not affect the virtually complete emptying of acid volume by the initial peristaltic sequence. We conclude that esophageal acid clearance normally occurs as a two-step process: (1) Virtually all acid volume is emptied from the esophagus by one or two peristaltic sequences, leaving a minimal residual amount that sustains a low pH, and (2) residual acid is neutralized by swallowed saliva.

A method of computing trajectories of objects by using velocity data, particularly as acquired with phase-contrast magnetic resonance (MR) imaging, is presented. Starting from a specified location at one time point, the method recursively estimates the trajectory. The effects of measurement noise and eddy current-induced velocity offsets are analyzed. When the motion is periodic, trajectories can be computed by integrating in both the forward and backward temporal directions, and a linear combination of these trajectories minimizes the effect of velocity offsets and maximizes the precision of the combined trajectory. For representative acquisition parameters and signal-to-noise ratios, the limitations due to measurement noise are acceptable. In a phantom with reciprocal rotation, the measured and true trajectories agreed to within 3.3%. Sample trajectory estimates of human myocardial regions are encouraging.

Quantitative measurements of arterial and venous blood flow were obtained with phase-contrast cine magnetic resonance (MR) imaging and compared with such measurements obtained by means of implanted ultrasound (US) blood flow probes in anesthetized dogs. The US flowmeter was enabled during a portion of each MR imaging sequence to allow virtually simultaneous data acquisition with the two techniques. MR imaging data were gated by means of electrocardiography and divided into 16 phases per cardiac cycle. The rates of portal venous blood flow measured with MR imaging and averaged across the cardiac cycle (710 mL/min +/- 230 [standard deviation]) correlated well with those measured with the flowmeter and averaged in like fashion (751 mL/min +/- 238) (r = .995, slope = 1.053). The correspondence in arterial blood flow was almost as good. No statistically significant difference existed between the paired measurements of blood flow obtained with MR imaging and the implanted probe. It is concluded that, as a noninvasive means of accurate quantification of blood flow, phase-contrast MR imaging may be especially useful in deep blood vessels in humans.

The present results demonstrate that intracoronary infusion of bradykinin produces a preferential increase in blood flow to the subendocardium via stimulation of B2 receptors and the release of an endothelium-dependent relaxing factor that may be nitric oxide.

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The present study was undertaken to characterize regional myocardial alterations of reflected ultrasound during the cardiac cycle in normal, ischemic, and postischemic reperfused myocardium. Time-averaged integrated backscatter (IB) and cardiac cycle-dependent amplitude modulation were measured from subepicardial, midmyocardial, and subendocardial regions of the left ventricular apex and the midportion of the right ventricular free wall under normal conditions (n = 5), after 1 hr of 100% acute left anterior descending (LAD) occlusion (n = 8), and after 15 min LAD occlusion plus 120 min reperfusion (n = 5) in anesthetized, ventilated open-chest dogs. A significant increase in time-averaged IB was observed in the subepicardium, the midmyocardium, and the subendocardium during ischemia and reperfusion, but there was no intramyocardial variability. Cardiac cycle-dependent amplitude modulation of IB was significantly higher in the normal subendocardium than in the subepicardium (4.3 0.6 vs 2.9 0.8 dB, p < .01) and midmyocardium (2.8 ± .05 dB, p < .01). This transmural gradient in amplitude modulation was abolished during ischemia and reperfusion. We conclude that cardiac cycle-dependent amplitude modulation in IB has a transmural dependence in the normal myocardium and this is abolished during acute myocardial ischemia. Circulation 75, No. 2, 436-442, 1987. WHILE ULTRASOUND is widely used to define cardiac anatomy and pathophysiology, quantitative defi- nounced at the left ventricular apex.7 8 Since contractile function in different layers across the left ventricular wall9' 10 has been found to be greater in the subendocardium, it is reasonable to presume that cardiac cycle variability in integrated backscatter would also exhibit transmural dependence, being greater in the subendocardium. Wickline et al." 12 demonstrated a greater magnitude of cardiac cycle-dependent variation in integrated backscatter in the subendocardium than in the subepicardium of the normal myocardium. The present study was undertaken to characterize regional myocardial alterations in reflected ultrasound during the cardiac cycle in ischemic and postischemic reperfused myocardium. MethodsGeneral preparation. Adult mongrel dogs of both sexes (15 to 30 kg) were anesthetized with sodium pentobarbital (30 mg/kg iv) initially, and supplemented with 5 mg/kg/hr. They were ventilated with room air supplemented with 02 (1 to 2 liters/min) with a respirator (Harvard Model 607). Atelectasis was prevented by maintaining an end-expiratory pressure of 5 to 7 cm of water. Throughout the experimental procedure, Po2, Pco2, and pH were maintained at physiologic levels. Body

No abstract

Ultrasonic backscatter is substantially modified by pathologic changes in myocardium. Influence of physiologic changes in heart rate, mean arterial pressure, preload, and inotropic state were studied in 17 anesthetized open-chest dogs. Heart rate was changed with atrial pacing/ULFS'49 (a selective bradycardiac agent). Mean arterial pressure was varied with aortic constriction/nitroprusside, preload was altered with nitroglycerin/volume infusion, and inotropic states were altered with dobutamine (10 lim/kg)/esmolol (100 ,um/kg). IBR5, an optimum weighted frequency average (4 to 6.8 MHz) of the squared envelope of diffraction corrected for absolute backscatter, and the Fourier coefficient of amplitude modulation (FAM), an index of cardiac cycle-dependent variation, were measured from six sequential electrocardiographically gated intervals throughout the cardiac cycle. Heart rate, mean arterial pressure, preload, and inotropic state did not significantly affect IBR5. FAM increased from 3.5 ± 0.3 dB (mean ± SEM) to 7.0 ± 0.4 dB (p < .01) at a heart rate of 120 beats/min, and decreased to 3.9 ± 0.4 at a heart rate of 160 beats/min. No change in FAM was noted with a rise (70 ± 12 to 45 ± 10 mm Hg) in mean arterial pressure or preload (an increase or decrease in diastolic segment length of ± 10% from the baseline). Dobutamine produced a significant increase in left ventricular dP/dt (2600 ± 200 to 3475 275 mm Hg) and FAM (3.4 ± 0.1 to 6.4; p < .01). Esmolol significantly reduced left ventricular dP/dt (2600 ± 200 to 2000 ± 175 mm Hg, p < .05) and FAM (3.4 + 0.01 to 6.4 + 0. 1; p < .01). We conclude that IBR5 is independent of heart rate, mean arterial pressure, preload, and inotropic state. Cardiac changes in cardiac contraction.