Simultaneous measurements of spinal cord blood flow and arterial diameter at areas adjacent to a site of spinal cord injury were carried out to determine changes in CO(2) reactivity and autoregulation. The spinal cord injury was made at T10 level by the epidural clip compression method. A spinal window was drilled at an area either 7 mm caudal or 7 mm rostral to the injury site for the measurement of spinal cord blood flow and arterial diameter at the same time. Spinal cord blood flow was decreased at both spinal windows, especially at the rostral window. Arterial diameter was also decreased significantly at both sites. The ischaemic zone evaluated histologically tended to expand more diffusely in the rostral direction than in the caudal direction. In the pre-injury stage, both CO(2) reactivity and autoregulation were present in the spinal cord. Following the clip injury, CO(2) reactivity and autoregulation were both impaired in the areas 7 mm adjacent to the impact site. Correlation coefficients suggested that the rostral spinal cord tended to sustain more injury than the caudal spinal cord. The histologically proven spinal cord ischaemia following the injury may have resulted from the decreased arterial diameter and impaired CO(2) reactivity and dysautoregulation of the spinal cord.

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To evaluate the effect of transient myocardial ischemia on the transmitral blood flow profile, pulsed Doppler echocardiography was performed in 10 anesthetized dogs during brief occlusion of the coronary artery and in 79 patients with coronary artery disease (CAD) and 19 control subjects who underwent esophageal pacing or dipyridamole stress tests. During coronary artery occlusion, the peak velocity of the rapid filling wave (R) was rapidly reduced and that of atrial contraction (A) augmented. These changes of overall left ventricular diastolic filling variables surprisingly coincided with rapid deterioration of systolic wall thickening at the ischemic segment. In the clinical study, the transmitral flow profile did not change in controls during esophageal pacing. We observed similar changes in the transmitral flow profile in the experimental study in CAD patients. The deceleration time of the early diastolic filling wave was not changed in controls, but was significantly prolonged in CAD patients. Preadministration of sublingual nitroglycerin normalized the postpacing responses of peak velocities and deceleration times induced in CAD patients. With intravenous administration of 0.56 mg/kg of dipyridamole R and A increased, but the A/R ratio was unchanged in both controls and CAD patients. The deceleration halftime, however, was prolonged in CAD patients, as shown during esophageal pacing. These changes of transmitral flow patterns were transient and recovered within a few minutes. Furthermore, they were noted more frequently than the development of chest pain or electrocardiographic ST depression. However, induced changes of transmitral flow profile were not significantly different between patients with multivessel disease and those with single-vessel disease in both stress tests, so that there were limitations in diagnosing the extent of coronary artery disease. These findings suggest that peak velocities or deceleration time responses in transmitral blood flow are early and sensitive markers for evaluating abnormal left ventricular diastolic filling during transient myocardial ischemia. This noninvasive technique may be a reasonable alternative to other imaging examinations for detection and functional assessment of patients with CAD.

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