Abstract
The circulatory effects of partial cerebral ischemia in dogs were studied by occluding the innominate and left subclavian arteries. Due to the collateral cerebral blood supply which was made more effective by an initial increase in arterial pressure, an effective cerebral ischemia did not occur unless the carotid back pressure was reduced to 30 mm. Hg or less. Reflex movements were not abolished in the cerebral is-chemic dogs if carotid back pressures were greater than 30 mm. Hg. Severe, sometimes fatal, vagal slowing of the heart occurred when carotid back pressures were below 30 mm. Hg. It was concluded that partial cerebral ischemia cannot be used as a substitute for anesthesia in studying the dynamics of hemorrhagic shock. Further investigation, using small doses of Na barbital to abolish movement and the vagal slowing of the heart, revealed that circulatory failure occurred in some dogs, but not in others, when the carotid back pressure was below 30 mm. Hg. By periodically occluding the aorta above the diaphragm for a few secs, and optically recording the pressure decline in the femoral artery, it was shown that the non-failure dogs maintained an increased peripheral runoff time, presumably due to increased peripheral resistance, during the ischemic period, but the failure dogs did not. However, circulatory failure did develop in the dogs which had maintained a normal blood pressure during the ischemic period, but only after the restoration of the cerebral circulation. The arterial pressures of both these dogs and those whose circulation failed during the ischemic period typically declined to a hypotensive level and remained there for several hrs. Pathologic signs resembling those found in hemorrhagic shock were found in all dogs regardless of whether circulatory failure occurred during or following a period of partial cerebral ischemia. There are indications that irreversible circulatory failure had started at the time the fall of blood pressure to shock levels began.

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