Effects of Changes in Carbon Dioxide Pressure and Arterial Pressure on Blood Flow in Ischemic Regions of the Brain in Dogs

Abstract

The effect of locally induced cerebral ischemia on regional cerebral blood flow before and during elevation of Paco 2 was measured qualitatively in anesthetized dogs by a thermistor probe technique and a photographic method involving cerebral angiography. The flow response to changes in systemic arterial pressure was also noted in the ischemic zone. Increased Paco 2 resulted in increased flow to the ischemic zone and shrinkage of the area of ischemia, by virtue of collateral circulation from other arterial trunks. In no instance was "intracerebral steal," as previously reported, noted in response to increased Paco 2 , though there was no means of determining if the quantitative response in the ischemic area was similar to that in normal brain. Arteries and arterioles in the ischemic zone were seen to be constricted and irregular, rather than maximally dilated, as has been proposed. The percent decrease in pressure in the occluded arterial segment was much greater than in the patent cerebral arteries. Response to increased Paco 2 occurred even though intraarterial pressures were less than 40 mm Hg. There was preservation of the response to norepinephrine in the ischemic zone, despite reduction in flow; response to changes in Paco 2 persisted even after this had been lost. ADDITIONAL KEY WORDSintracerebral steal syndrome vasomotor paralysis collateral circulation tissue metabolites cerebral vasodilatation luxury perfusion syndrome heated thermistor transducer infrared absorption angiography• The variability and fluctuation of clinical symptoms in patients with occlusive cerebral vascular disease are thought to be related primarily to the extent of compensatory blood flow from the vascular beds surrounding the ischemic area, which eventually determines whether ischemia will be followed by infarction or recovery. It would, therefore, appear reasonable that cerebral vasodilating agents would diminish the area of ischemia by promoting collateral circulation, and this assumption has been the basis for a number of clinical therapeutic efforts (1-7). The lack of This study was supported by U. S. Public Health Service Grant NB 05820 03 and by funds from the Meyer Gold Grant.Received October 14, 1968. Accepted for publication February 6, 1969. conclusive results from these studies is partially due to lack of appropriate controls and to the intrinsic variability of the disease process. The physiologic events occurring in ischemic tissue have not been extensively measured, but occlusion of a major cortical artery has been shown to be followed by decreased flow in the ischemic area by several observers (8-10). showed that the decrease in tissue flow was associated with high Pco 2 , low pH, and low Po 2 in the brain parenchyma, factors which should promote more profound local vasodilatation than could be produced by systemic administration of vasodilating agents. Despite conditions presumed ideal for local vasodilatation, observation of ischemic brain tissue has revealed a great variability in the caliber of the ve...

Physostigmine induced reversal of ischemia following acute middle cerebral artery occlusion in the rat.

“…Whether this phenomenon exists or not is still a matter of debate as evidence has been provided for 23 " 27 and against it. 28 ' 22> M…”

Disordered Cholinergic Neurotransmission and Dysautoregulation After Acute Cerebral Infarction

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Effect of Pa CO CO2 on Blood Flow and Microvasculature of Ischemic and Nonischemic Cerebral Cortex

“…CBF response of nonischemic cortex was normal (mean ltLCBP(co ) = '•^•'A' ischemic cortex had no response (mean I ACBF(COt) = 0.10). cortex of animals of group 2, calculated from the fitted line, was 0.008 ml/g/min per 1-mm 32 Hg change of Paco 2 or approximately onethird that of nonischemic cortex. The mean IACBF(CO 2 ) f°r t^e ischemic hemispheres of the eight animals of group 2 was 0.67 ±0.…”