Evolving focal cerebral ischemia in cats: spatial correlation of nuclear magnetic resonance imaging, cerebral blood flow, tetrazolium staining, and histopathology.

Abstract

The spatial correlation of nuclear magnetic resonance imaging (NMRI) and cerebral blood flow (CBF) may improve our ability to identify ischemic brain lesions and may provide further insight into the pathophysiology of early cerebral ischemia. Eleven pentobarbital-anesthetized adult cats underwent exposure of the common carotid arteries bilaterally and the right middle cerebral artery through a transorbital approach. Baseline NMRI images were obtained with a single spin-echo, multislice technique using a 0.6-T field, 0.4-cm slice thickness, and a surface coil. Focal ischemia was produced with right middle cerebral artery occlusion and potentiated with bilateral common carotid artery ligation. Sequential NMRI studies were then performed at 1, 2, 4, 6, and 12 hours or until CBF was determined in the same cats using [ l4 C]iodoantipyrine at either 2 (n = 2), 4 (n = 2), 6 (n = 2), or 12 (n = 1) hours after the time of occlusion. This protocol allowed temporal and spatial correlation of NMRI and CBF. Alternate 5-mm brain slices were incubated with 1 % 2,3,5-triphenyltetrazolium chloride (TTC) for 45 minutes at 37-41° C and frozen in liquid Freon for later autoradiographic CBF determination. Four cats were studied only with NMRI and TTC (not CBF). The correlation between areas of increased NMRI signal intensity observed in T2-weighted images (repetition time 2,000 msec, echo time 120 msec), vital staining with TTC, low CBF, and routine histology was evaluated. During the early phase (<6 hours), T2-weighted NMRI changes were localized to the central ischemic gray matter areas, as defined in the later CBF images, with no involvement of the white matter. By the twelfth hour the NMRI changes involved the entire ischemic area including gray and white matter. The initial visible changes seen on T2-weighted NMRI are suggestive of cellular edema, and the later changes are characteristic of vasogenic edema. The spread of NMRI changes compared with the ischemic area determined from autoradiographic CBF is consistent with the previously described biphasic evolution of ischemic injury. These data suggest that T2-weighted NMRI could be used clinically to delineate areas of acute ischemic stroke. (Stroke 1988; 19:28-37) T he sensitivity of nuclear magnetic resonance imaging (NMRI) to detect pathologic changes in a broad spectrum of neurologic diseases has been demonstrated. NMRI provides very accurate localization of cerebral lesions, with a sensitivity superior to that of conventional computed tomography (CT). 1 -6 Previous reports suggested the superiority of NMRI compared with CT in the early identification of ischemic injury 2 -3 -7 "" and indicated that ischemic changes were promptly and sharply demarcated from surrounding nonischemic parenchyma. T2-weighted images detect infarct and focal ischemia with high sensitivity but low specificity.12 Recent reports comparing CT and Received April 30, 1987; accepted August 11, 1987. NMRI in transient ischemic attacks 13 and cerebral infarction 14 propose that the sensitivity of ...

Nicardipine reduces ischemic brain injury. Magnetic resonance imaging/spectroscopy study in cats.

“…The changes were first seen in the dorsolateral frontal and parietal cortex and then progressed to involve the temporal cortex. A similar spatial evolution of brain edema following MCA occlusion in cats was recently reported by Bose et al 9 Five hours after MCA occlusion, the anatomic distribution of edema was considerably more widespread ( Figure 2). Signal enhancement was seen throughout most of the parietal and temporal lobes, the medial aspect of the head of the caudate, the lateral part of the globus pallidus, and most of the internal capsule.…”

“…We used proton magnetic resonance imaging (MRI) to detect alterations in brain tissue water content in nicardipine-treated and untreated (control) MCA-occluded cats. 9 Phosphorus-31 magnetic resonance spectroscopy (MRS) was performed concurrently to compare the extent of cerebral metabolic injury. Histochemical mapping of the viability of the electron transport chain enzymes was carried out with 2% 2,3,5-triphenyl tetrazolium chloride (TTC) to correlate spatially the evolution of ischemic tissue injury with the MRI/MRS results 5 hours after MCA occlusion.…”

Comparison between diffusion‐weighted imaging, ‐weighted, and postcontrast ‐weighted imaging after MR‐guided, high intensity, focused ultrasound treatment of uterine leiomyomata: Preliminary results

“…Vasogenic edema is defined as the "bulk flow of water" and is usually noted as increased signal intensity on a T 2 WI due to the increase in water in the tissue. 48,49 Thus, coupled with the signal intensity changes seen on DWI, which at acute times, reflect cytotoxic or cellular edema, may indicate that further tissue "destruction" may occur after treatment. In Fig.…”

Changes in Hippocampal Neuronal Activity During and After Unilateral Selective Hippocampal IschemiaIn Vivo

“…This fact necessitates showing the ischemic damage in early stage (ϳ4 h after ischemia induction). The 2,3,5-triphenyltetrazolium chloride method rests on the functioning of mitochondrial enzymes (Liszczak et al, 1984) and has been used by several groups to mark cerebral infarct area (Bose et al, 1988;Park et al, 1988;Hatfield et al, 1991;Goldlust et al, 1996;Kuroiwa et al, 2009;Popp et al, 2009). An obvious advantage of this method is its easy applicability, suitability for infarct volume evaluation and the immediate availability of results (Bederson et al, 1986;Mathews et al, 2000;Türeyen et al, 2004;Popp et al, 2009).…”