Effect of carotid artery ligation on regional cerebral blood flow in normotensive and spontaneously hypertensive rats.

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SUMMARY Cerebral vascular carbon dioxide (CO2) reactivities were compared in normotensive (NTR) and hypertensive (SHR) rats. Cerebral bloodflow (CBF) in cortex and thalamus were evaluated before and during one hour of hyperventilation. After one hour of hyperventilation brain lactate, pyruvate, and ATP concentrations were also determined. Significant and similar reductions of CBF due to hyperventilation induced hypocapnia were found in both NTR and SHR groups. In contrast the percent increase in cerebrovascular resistance (CVR) per unit decrease in paC0 2 was significant, indicating that hypocapnia induced vasoconstriction is greater in NTR than in SHR groups. During hyperventilation the average value for lactate in the NTR group was 3.98 mM/kg. In contrast it was 3.15 mM/kg in the SHR group, a significant difference (p < 0.05). When paCC>2 fell below 15 mm Hg the cerebral lactate increased strikingly in the NTR group and cortical CVR was reduced suggesting that an accumulation of the ischemic metabolites caused dilatation of the constricted cerebral vessels. In contrast the SHR group disclosed no such changes. The increase CVR characteristic of SHR appeared to diminish the cerebral vasoconstrictive response to hypo capnia. As a result ischemic metabolites in the brain do not increase in this group to the degree that they do in NTR.Stroke Vol 13, No 5, 1982 IT HAS BEEN KNOWN that hyperventilation leads to cally ventilated with a gas mixture of 70% N 2 0 and vasoconstriction of cerebral arteries with reduced cere 30% of 0 2 . One femoral artery was cannulated to bral blood flow (CBF) and cerebral oxygen tension, 1 ' 2 measure blood pressure and for anaerobic sampling of and consequently alters the brain metabolism. '• 3 4 The arterial blood for pC0 2 , p0 2 and pH determinations electroencephalographic changes during hyperventila with a Model 113 IL meter. The body temperature, tion are indistinguishable from those observed during measured in the rectum, was kept close to 37°C cerebral hypoxia. 5,6 throughout the experiment. Our previous studies 7-10 have demonstrated that The animals were divided into two experimental spontaneously hypertensive rats (SHR) are more sus groups: one for measurements of local CBF and the ceptible to cerebral ischemia than normotensive rats other for determinations of brain tissue metabolites. (NTR) following bilateral carotid occlusion, suggest ing that the cerebral vasoreactivities to changes of the Cerebral Blood Flowperfusion pressure might be different between SHR Twenty-two NTR and 22 SHR were used for this and NTR. In fact, the lower limit of cerebral autoregupurpose. The animal's head was fixed in a head holder, lation is significantly higher in SHR than NTR, and the and two small burr holes were made on the skull 2 mm increased cerebral vascular resistance due to the persis lateral to the bregma on each side for stereotaxic inser tent high blood pressure is responsible for such upward tion of teflon-coated platinum electrodes, one in the shift of the autoregulation in SHR...

Section: Cerebral Blood Flowmentioning

confidence: 99%

Effects of hyperventilation on cerebral blood flow and brain tissue metabolism in normotensive and spontaneously hypertensive rats.

Ishitsuka¹,

Fujishima²,

Nakatomi³

et al. 1982

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“…2 In an important contribution, Choki, et al have shown that 2 hours following bilateral carotid artery ligation, rCBF, measured autoradiographically with u C-antipyrine was significantly lower in SHR than in normotensive control rats (NTR). 3 Although this report has the important potential implication for the management of human patients that the severity of clinical outcome of a stroke will be influenced by the blood pressure prior to the stroke, this interpretation must be limited by some details of the experiment. Since more than 32 generations of selective inbreeding separate the SHR from the NTR parent Wistar stock which served as controls, there is the concern that some other genetic determinant of stroke outcome, unrelated to blood pressure, might be present in the SHR.…”

mentioning

confidence: 97%

Amelioration of cerebral ischemia by prior treatment of hypertension.

Halsey¹,

O'Brien²,

Strong³

1980

SUMMARY Bilateral carotid artery ligation was made in 14 SHR while rCBF was serially measured with hydrogen clearance. Blood pressure was controlled with an intra-arterial catheter connected to a reservoir. There was no significant correlation between blood pressure and rCBF prior to the carotid occlusion, but afterwards there was a progressirely increasingly negative correlation between mean arterial blood pressure and rCBF with time. These observations indicate that the severity of ischemia is greater in the presence of hypertension if the hypertension is present prior to the onset of ischemia and the blood pressure maintained constant thereafter. Stroke, Vol 11, No 3, 1980 EPIDEMIOLOGIC STUDIES over the past 2 decades have established a clear pathogenetic relationship between pre-existing hypertension and stroke morbidity and mortality, and even recurrence rate.

“…17 Therefore, bilateral carotid occlusion produces a decrease in cerebral blood flow amounting to only 50% of the normal value. 17 ' 18 Despite this degree of reduction in cerebral perfusion, the energy state of the tissue, as evaluated by biochemical analysis, remains unaltered provided the animal is normotensive. 1 …”

Section: Discussionmentioning

confidence: 99%

Incomplete transient ischemia: a non-destructive evaluation of in vivo cerebral metabolism and hemodynamics in rat brain.

Wiernsperger¹,

Sylvia²,

Jöbsis³

1981

SUMMARY Differential near infrared spectropbotometry was used to monitor sequential in vivo alterations in cerebral hemoglobin saturation, blood volume, and cytochrome c oxidase reduction/oxidation responses during and after a period of incomplete transient ischemia (acute, rerersible common carotid artery occlusion). In this study the rat brain was monitored non-lnvaslvely in the intact skull by trtnsiUumination. The data snow that an increase in cerebral deoxygenation of hemoglobin, which occurs simultaneously with a decrease in blood volume subsequent to carotid ligation, acts as a compensatory mechanism to assist in maintaining aerobic energy metabolism. The observations also demonstrate that in this spedes the effects of bilateral carotid occlusion on the cerebrorascular parameters are not necessarily irrevocable. The intramitochondrial metabolic alterations, as evaluated by cytochrome c oxidase redox transitions, are reversible as long as the systemic arterial blood pressure does not fall below a value of approximately 40 mm Hg. These data suggest the possibility of being able to use a critical reduction level of cytochrome c oxidase as an early indication of ischemia-induced cerebral metabolic dysfunction prior to major changes in high energy stores.Stroke, Vol 12, No 6, 1981THERE IS ample evidence to support a close coupling relationship of brain functional activity, oxidative energy metabolism, and cerebral blood flow. 1 " 4 Normally, cerebral blood flow, nutrient substrate delivery and oxygen sufficiency, are carefully regulated in direct proportion to regional tissue metabolic demands. However, in pathological states such as stroke-related oligemia, this regulatory capacity becomes impaired because the equilibrium between tissue metabolic supply and demand has been disturbed. Clinical assessment of progressive cerebral ischemic damage, therefore, demands a precise knowledge of sequential changes in the interrelationships between tissue energy metabolism and brain hemodynamics. The major route of cellular energy production, in the form of adenosine triphosphate (ATP), occurs via the process of oxidative phosphorylation. In terms of tissue oxygen consumption, O a utilization is directly proportional to the rate of electron transfer from cytochrome c oxidase (Cyt. a,a t ) to molecular oxygen. Since the Cyt. a,a» reduction/oxidation (redox) state is affected by variations in the level of tissue oxygenation within the physiological range in situ,' changes in the in vivo redox state of this enzyme may be used as an indicator of intracellular oxygen sufficiency and bioenergetics. 8 " 1 *In the present study, we have explored the consequences of incomplete transient ischemia (acute, reversible common carotid artery occlusion) on the tissue oxidative metabolic state and hemodynamic alterations in rat brain. A newly developed technique