Risk area and infarct area relations in the hypertensive stroke-prone rat.

Abstract

Our purpose was to characterize the surface area of the infarct and the surface area at risk of infarction as defined spatially by arterial anastomoses to determine whether position, size, or shape of the infarct and the area at risk were related in stroke-prone rats or hybrid rats. Stroke-prone rats (n = 18; mean +/- SEM blood pressure, 182 +/- 8 mm Hg) and hybrid rats (n = 18; mean +/- SEM blood pressure, 147 +/- 6 mm Hg; p < 0.05) were anesthetized and the left middle cerebral artery was occluded with a ligature. The rats were killed 7 days later, arterial anastomoses were made visible with latex, the brains were fixed in formalin, and film recorded the infarct and anastomoses. Anastomoses and infarcts were digitized for measurements of risk area, luminal width, and infarct area. Mean risk area was similar in size, length, width, and variability in stroke-prone rats (area, 85 +/- 5 mm2) and hybrid rats (area, 84 +/- 7 mm2; p > 0.05), whereas mean infarct area was larger, longer, wider, and less variable in stroke-prone rats (area, 53 +/- 6 mm2) than in hybrid rats (area, 15 +/- 11 mm2; p < 0.05). Infarct length was appreciably greater than infarct width in both groups, indicating that infarct shape was not amorphous. Spatial overlap maps indicated that the infarct area common to all stroke-prone rats was positioned centrally in the risk area and was surrounded by a variable infarct area, which indicated that the likelihood of infarction increased with distance from the anastomoses. Shape factors for both risk area and infarct area were significantly different within each rat group, which indicated that infarct shape did not uniformly parallel the anastomotic sites that determined risk area shape (p < 0.05). Risk area anastomoses and border zone width were linearly correlated in size and both were significantly wider in hybrid rats than in stroke-prone rats (p < 0.05), which suggests that the narrower border zone tissue was perfused by narrower anastomoses. We conclude that the position of the infarct within the risk area relates to luminal widths of conterminous anastomoses that define the risk area, but not to the size or shape of the area at risk of infarction defined spatially by the anastomoses.