Background and Purpose: Recent studies have suggested that cerebral in
farction influences autonomic activity and way contribute to sudden de
ath. The goal of this study was to examine effects of focal cerebral i
nfarction on mean arterial pressure and heart rate. Methods: Halothane
-anesthetized rats were assigned to two groups: stroke (n = 10), in wh
ich the middle cerebral artery or an adjacent vessel was embolized wit
h a silicone cylinder, and sham (n = 8), in which rats were sham embol
ized (saline). Arterial pressure and heart rate were measured for 90 m
inutes and again 24 hours after vascular occlusion. A change in electr
oencephalographic amplitude of -45% after embolization was used to det
ermine if a significant degree of infarction was present. Results: Vas
cular occlusion produced a significant increase in mean arterial press
ure at 10, 60, and 90 minutes (p<0.05). Changes in heart rate were sig
nificantly greater (p<0.05) than in sham-treated rats at 10 and 30 min
utes after embolization. In contrast, mean arterial pressure and heart
rate measured 24 hours after embolization were similar in both groups
. Anatomic analysis of the infarcted areas demonstrated that either in
sular cortex or amygdala was affected in all embolized rats. Conclusio
ns: This study indicates that cerebral infarction produces a transient
elevation of mean arterial pressure and heart rate. However, within 2
4 hours both parameters returned to preinfarcted levels. Our findings
are consistent with clinical reports that indicate that mean arterial
pressure and heart rate of stroke patients are similar to those of oth
er groups when they are admitted to the hospital, although other cardi
ovascular parameters are greatly altered.