The purpose of this study was (1) to monitor the dynamic effects of T1-enhancing and magnetic susceptibility contrast material on normal canine myocardium using inversion recovery (IR)- and driven equilibrium (DE)-prepared fast gradient-recalled echo (GRE) sequences and (2) to determine the relative value of T1-enhancing and magnetic susceptibility contrast material in detecting regions of ischemia in the same animal. Normal dogs (n = 5) and dogs with acute occlusion of the left anterior descending (LAD) coronary artery (n = 11) were studied using a 1.5-T MR imager. ECG-gated fast IR-prepared GRE images were acquired using TI/TR/TE of 700/7.0/2.9 msec and a flip angle of 7 degrees. Fast DE-prepared GRE images were obtained using a flip angle of 12 degrees and a DE delay/TR/TE of 60/10.2/4.2 msec. Sequential images were acquired to monitor transit of 0.05 mmol/kg gadodiamide injection and 0.2 and 0.4 mmol/kg sprodiamide injection. On slice-nonselective IR fast GRE images, gadodiamide caused significant enhancement of the normal myocardium and the left ventricular (LV) chamber blood. In dogs with LAD occlusion, the ischemic region was defined as an area of low signal intensity (SI). On DE-prepared GRE sequences, administration of sprodiamide resulted in a substantial decrease in signal from normal myocardium and LV chamber blood in normal dogs. In animals subjected to LAD occlusion, this contrast medium produced a transient decrease in SI from normal myocardium (P < .05) and no significant change in SI from ischemic myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMedDate not supplied

Hyperglycemia augments ischemic brain injury: in vivo MR imaging/spectroscopic study with nicardipine in cats with occluded middle cerebral arteries.

Hyperglycemia is often associated with an increased frequency of cerebrovascular disease and exacerbation of neuronal injury in focal ischemic cerebral infarction. We used a combination of high-field proton MR imaging and 1H and 31P MR spectroscopy to investigate whether hyperglycemia would adversely influence cerebral metabolism and eventual infarct size following unilateral occlusion of the middle cerebral artery (MCA) of cats pretreated with the calcium channel blocker nicardipine. Normoglycemic animals injected with 10 micrograms/kg of nicardipine (8 micrograms.kg-1.hr-1 maintenance dose) manifested only mild disturbances in phosphorus metabolism and cerebral pH regulation compared with untreated controls, and showed a significant reduction in infarct size 7 hr after MCA occlusion. By comparison, hyperglycemic cats (plasma glucose, 200-300 mg/dl) had significantly reduced cerebral high-energy phosphates, elevated lactic acid, and larger ischemic lesions in the occluded MCA territory, irrespective of whether they were treated with nicardipine. These results indicate that moderate hyperglycemia can exaggerate ischemic brain damage by enhancing formation of tissue lactic acid and impairing normal phosphorus metabolism. One implication of this study is that dextrose should not be provided to patients with acute ischemic stroke.

Animals↗