Regulation of cerebral blood flow after asphyxia in neonatal lambs

In a postasphyxia neonatal lamb model, the responses of the cerebral circulation to hypoxic hypoxia and changes in systemic arterial blood pressure were examined. Ventilated newborn lambs (n = 14) were subjected to a gradual asphyxial insult, resuscitated, and returned to control ventilator settings. During the time 2-5 hours after asphyxia, the responses of cerebral blood flow (CBF), cerebral oxygen delivery (OD), cerebral oxygen consumption (CMRO2), and cerebral fractional oxygen extraction (E) to changes in either arterial oxygen content (CaO2) or mean arterial blood pressure (MAP) were assessed. These data were compared with measurements from nonasphyxiated lambs (n = 7). With hypoxia (n = 7), cerebral blood flow increased (CBF = 646/CaO2 + 44) compared with nonasphyxiated lambs (CBF = 1121/CaO2 + 11). In asphyxiated lambs, cerebral oxygen delivery decreased (OD = 0.41 CaO2 + 6.87), but cerebral oxygen consumption remained stable due to a proportional increase in cerebral fractional oxygen extraction (E = -0.014 CaO2 + 0.65). In nonasphyxiated lambs, cerebral oxygen delivery, consumption, and fractional extraction were unchanged with hypoxia. In response to alterations in blood pressure, both cerebral blood flow (CBF = 0.84 MAP + 6.62) and oxygen delivery (OD = 0.13 MAP + 0.77) were pressure-passive. With hypotension, cerebral fractional oxygen extraction increased (E = -0.003 MAP + 0.69) but not enough to prevent a decrease in cerebral oxygen consumption (CMRO2 = 0.042 MAP + 1.79). In nonasphyxiated lambs, cerebral blood flow, oxygen delivery, consumption, and fractional extraction did not vary with blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Studies on cerebral blood flow and oxygen metabolism in patients with established cerebral infarcts undergoing omental transposition

Regional cerebral blood flow, blood volume, fractional oxygen extraction, and oxygen consumption were measured by positron emission tomography in 4 stroke patients prior to and 6 months following omental transposition surgery. Preoperatively, 3 patients showed the typical picture of established infarction with a matched reduction in flow and oxygen metabolism and a normal oxygen extraction fraction in the symptomatic hemisphere. One patient showed a chronically impaired perfusion reserve with a proportionally greater reduction in flow than oxygen metabolism and a compensatory rise in oxygen extraction ratio. No change in the physiological parameters was demonstrated in the postoperative studies.     

Borderzone ischemia

Positron emission tomography was used to measure cerebral perfusion and metabolism in 7 patients with severe carotid stenosis. None of the patients had sustained a major stroke, and all had a normal neurological examination except 1 patient with a mild neurological deficit from a capsular lacuna. Cerebral blood flow (CBF), cerebral blood volume, the cerebral blood flow/cerebral blood volume ratio, oxygen metabolism, and the fractional extraction of oxygen by the brain were measured in the cerebral cortex of both hemispheres in the anterior and middle cerebral artery distributions, in the borderzone regions between the anterior and middle cerebral arteries (anterior borderzone), and between the middle cerebral and posterior cerebral arteries (posterior borderzone). Results obtained in patients were compared, using Student's t test, to those obtained in 6 neurologically normal, elderly volunteers. Cerebral blood flow and the cerebral blood flow/cerebral blood volume ratio were both significantly decreased (p less than 0.025 and p less than 0.05, respectively) in the anterior borderzone ipsilateral to the carotid stenosis. In the same region there was a tendency toward a rising fractional extraction of oxygen with the oxygen metabolism maintained in the low-normal range. Cerebral blood flow was also significantly decreased (p less than 0.05) in the contralateral anterior borderzone. Hemodynamic and metabolic variables in other vascular territories were not significantly different from values obtained in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)     

In vivo disturbance of the oxidative metabolism of glucose in human cerebral gliomas

Abnormalities in the oxidative metabolism of glucose in human cerebral gliomas have been studied in seven patients using positron emission tomography. Measurements of regional cerebral blood flow and oxygen consumption were obtained using the oxygen-15 steady-state inhalation technique. Values of regional cerebral glucose consumption were obtained using fluorine 18-labeled 2-fluoro-2-deoxy-D-glucose and a simplification of the method of Sokoloff. Functional values were obtained for regions of tumor and brain tissue in the middle cerebral artery territory of the contralateral cortex. Values of regional glucose consumption were calculated for both regions using a value of the lumped constant quoted for normal brain tissue (0.42). Tumor regional cerebral blood flow was comparable to that in the contralateral cortex, whereas regional cerebral oxygen consumption was depressed. This depression resulted in low tumor values of the fractional oxygen extraction ratio (0.21 +/- 0.07), indicating that oxygen supply exceeded the metabolic demand. In contrast, tumor regional cerebral glucose consumption was not depressed and regional glucose extraction ratios were similar for tumor and brain tissue. The metabolic uncoupling between regional oxygen consumption and regional glucose consumption (CMRO2/CMRGlu = 0.24 +/- 0.07 ml of oxygen per milligram of glucose) is indicative of increased aerobic glycolysis.     

Cerebral haemodynamic changes after extracranial-intracranial bypass surgery.

Regional cerebral blood flow, oxygen utilisation, fractional oxygen extraction, and cerebral blood volume were measured by positron emission tomography in twelve patients with carotid artery occlusion. Follow-up studies were carried out at a mean interval of eleven weeks after extracranial-intracranial bypass surgery. Clinical improvement was observed in three patients who had presented with frequent transient ischaemic attacks. One patient with multiple vascular occlusions suffered a stroke at the time of surgery. Follow-up studies showed an increase of regional cerebral blood flow in only two of the twelve patients. In the group as a whole, there was no significant change of cerebral blood flow, oxygen consumption or fractional oxygen extraction after bypass surgery. The most consistent post-operative change, observed in eleven of the twelve patients, was a fall of cerebral blood volume in the cortical territory of the bypassed carotid artery (p less than 0.01). This effect was most marked in patients with bilateral carotid occlusion, in whom there was often an accompanying fall of blood volume in the contralateral hemisphere. The post-operative findings were consistent with an increase of regional cerebral perfusion pressure as a result of the bypass procedure. Although this effect is potentially of value, those patients with most to gain from bypass surgery may also run the highest risk of peri-operative cerebral ischaemia.     

Disturbance of oxidative metabolism of glucose in recent human cerebral infarcts

Eight patients with recent cerebral hemispheric infarction were studied with positron emission tomography and the oxygen-15 steady-state inhalation and [¹⁸F]deoxyglucose techniques to obtain values of regional cerebral blood flow, oxygen consumption, and glucose metabolism. The Sokoloff equation, used to calculate glucose metabolism, was simplified to exclude the exponential terms containing the rate constants. A value of the lumped constant quoted for normal brain (0.42) was used for infarcted regions and contralateral hemisphere. Mean regional cerebral blood flow, oxygen consumption, and glucose metabolism were all significantly depressed within the infarcts compared with the mirror regions in the contralateral cerebral hemisphere. The mean fractional extraction of oxygen was low, indicating an adequate supply of oxygen for residual oxidative metabolism. Regional oxygen consumption and glucose metabolism were significantly correlated within the infarcts, but with a relationship of 2 moles of oxygen per mole of glucose—one-third that in the contralateral hemisphere and in normal brain. Although these results suggest that the metabolizing tissue of a recent cerebral infarct utilizes aerobic glycolysis, caution about the validity of this pathophysiological observation is dictated by limitations in current positron emission tomographic tracer methodology.     

Hypertension induced changes in cerebral capillary permeability to water are mediated by afferent neuronal connections from the carotid sinus to the brain

The effects of acute opiate receptor stimulation on regional cerebral oxygen consumption and blood flow were examined in 9 regions of the artificially respired, alpha-chloralose-anesthetized cat. Regional cerebral arterial and venous oxygen saturation were examined microspectrophotometrically and regional cerebral blood flow was monitored using radioactively tagged microspheres (15 +/- 3 micron in diameter). Oxygen consumption was calculated as the product of flow and oxygen extraction. In 8 cats, after control cerebral blood flow was obtained, and in 8 experimental cats after this same measurement was obtained before and 40 min after the administration of 1.5 mg/kg morphine sulfate; the cats' heads were simultaneously sawed in 3 places and quickly frozen in liquid nitrogen-cooled propane. Systolic and diastolic blood pressure were significantly decreased by treatment. The heterogeneity of venous oxygen saturation was significantly reduced by morphine. Average cerebral blood flow, oxygen extraction and consumption were not altered significantly by morphine. Regional cerebral blood flow in the hypothalamus, thalamic oxygen extraction, and hypothalamic and thalamic oxygen consumption were significantly decreased by treatment. This low dose of morphine may produce changes in cerebral neuronal and/or synthetic activity which lowers oxygen consumption in some regions rich in opiate receptors, while not affecting overall brain oxygen supply or consumption.     

Hemodynamic and metabolic effects of cerebral arteriovenous malformations studied by positron emission tomography

Seventeen patients with an intracranial arteriovenous malformation were studied with positron emission tomography. Cerebral blood flow, cerebral blood volume, oxygen extraction fraction, and glucose and oxygen metabolism were evaluated in both hemispheres, excluding the area of the malformation itself. Patients were divided into three groups according to the size of their malformation, and results obtained were compared with studies in healthy volunteers. The glucose metabolism was significantly (p less than 0.01) decreased in the ipsilateral hemisphere in all patients. The cerebral blood volume was significantly increased (p less than 0.001) ipsilaterally in the three groups, and contralaterally in patients with medium- and large-sized arteriovenous malformations. The cerebral blood volume to cerebral blood flow ration, an index of vascular mean transit time, was significantly increased (p less than 0.005) ipsilaterally in patients with medium- and large-sized malformations and contralaterally in patients with large ones. Cerebral blood flow, oxygen extraction fraction, and oxygen metabolism were within the normal range bilaterally in all three groups, but oxygen extraction fraction tended to be higher in patients with larger lesions. The lack of significant change in oxygen metabolism suggests that oxygen metabolism in cortical areas remote from the arteriovenous malformation has been maintained by compensatory hemodynamic mechanisms. These data reveal widespread metabolic and hemodynamic consequences of arteriovenous malformations and suggest that they are associated with impairment of glucose metabolism, both in ipsilateral regions remote from the lesion and in the contralateral hemisphere in patients with large lesions.     

Studies on regional cerebral oxygen utilisation and cognitive function in multiple sclerosis.

Regional cerebral oxygen utilisation (rCMRO2), oxygen extraction (rOER), blood flow (rCBF), and blood volume (rCBV) have been determined for fifteen patients with multiple sclerosis in remission using positron emission tomography (PET). Cerebral oxygen utilisation and blood flow were significantly reduced in both white matter and peripheral cortical grey matter in the multiple sclerosis patients compared to a group of normal controls. No evidence of regional cerebral ischaemia in the multiple sclerosis group was found. Lowest levels of cerebral oxygen utilisation were found in patients with cerebral atrophy, and in patients in whom a significant fall in present full-scale IQ from estimated pre-morbid levels had occurred. No correlation was found between rCMRO2 values and severity of locomotor dysfunction or clinical disease duration.     

Effect of morphine on regional cerebral oxygen consumption and supply

The effects of acute opiate receptor stimulation on regional cerebral oxygen consumptilon and blood flow were examined in 9 regions of the artificially respired, α-chloralose-anesthetized cat. Regional cerebral arterial and venous oxygen saturation were examined microspectrophotometrically and regional cerebral blood flow was monitored using radioactively tagged microspheres (15 ± 3 μm in diameter). Oxygen consumption was calculated as the product of flow and oxygen extraction. In 8 cats, after control cerebral blood flow was obtained, and in 8 experimental cats after this same measurement was obtained before and 40 min after the administration of 1.5 mg/kg morphine sulfate; the cats' heads were simultaneously sawed in 3 places and quickly frozen in liquid nitrogen-cooled propane. Systolic and diastolic blood pressure were significantly decreased by treatment. The heterogeneity of venous oxygen saturation was significantly reduced by morphine. Average cerebral blood flow, oxygen extraction and consumption were not altered significantly by morphine. Regional cerebral blood flow in the hypothalamus, thalamic oxygen extraction, and hypothalamic and thalamic oxygen consumption were significantly decreased by treatment. This low dose of morphine may produce changes in cerebral neuronal and/or synthetic activity which lowers oxygen consumption in some regions rich in opiate receptors, while not affecting overall brain oxygen supply or consumption.     

Effects of acetazolamide on cerebral blood flow, blood volume, and oxygen metabolism: a positron emission tomography study with healthy volunteers.

To evaluate changes in cerebral hemodynamics and metabolism induced by acetazolamide in healthy subjects, positron emission tomography studies for measurement of cerebral perfusion and oxygen consumption were performed. Sixteen healthy volunteers underwent positron emission tomography studies with 15O-gas and water before and after intravenous administration of acetazolamide. Dynamic positron emission tomography data were acquired after bolus injection of H2[15O] and bolus inhalation of 15O2. Cerebral blood flow, metabolic rate of oxygen, and arterial-to-capillary blood volume images were calculated using the three-weighted integral method. The images of cerebral blood volume were calculated using the bolus inhalation technique of C[15O]. The scans for cerebral blood flow and volume and metabolic rate of oxygen after acetazolamide challenge were performed at 10, 20, and 30 minutes after drug injection. The parametric images obtained under the two conditions at baseline and after acetazolamide administration were compared. The global and regional values for cerebral blood flow and volume and arterial-to-capillary blood volume increased significantly after acetazolamide administration compared with the baseline condition, whereas no difference in metabolic rate of oxygen was observed. Acetazolamide-induced increases in both blood flow and volume in the normal brain occurred as a vasodilatory reaction of functioning vessels. The increase in arterial-to-capillary blood volume made the major contribution to the cerebral blood volume increase, indicating that the raise in cerebral blood flow during the acetazolamide challenge is closely related to arterial-to-capillary vasomotor responsiveness.     

High-intensity area in the deep white matter indicating hemodynamic compromise in internal carotid artery occlusive disorders

We used positron emission tomography and magnetic resonance imaging to evaluate 16 patients with transient ischemic attacks or minor strokes and unilateral internal carotid occlusive disease, five with stenosis, and 11 with occlusion. Cerebral blood flow, cerebral metabolic rate of oxygen, oxygen extraction fraction, cerebral blood volume, and T2-weighted magnetic resonance images obtained at 1.5-T were analyzed. Irrespective of vascular disease, patients with a confluent high-intensity area in the middle centrum semiovale had substantially decreased cerebral blood flow and ratio of cerebral blood flow to blood volume in the middle cerebral artery distribution of the cortex, with a substantially increased oxygen extraction fraction. We concluded that the confluent high-intensity area in the deep white matter region indicates hemodynamic compromise in the affected hemisphere in internal carotid artery occlusive disease.     

Cerebral blood flow and oxygen metabolism in rett syndrome

Positron emission tomography was performed on six patients with Rett syndrome to investigate cerebral blood flow and oxygen metabolism, and the results were compared with the concurrent clinical status of the patients. The cerebral metabolic rate of oxygen (CMRO2) was low in five patients, and oxygen extraction fraction was low in four patients; both had a tendency to decline with advancing age. Although the cause is unknown, it is suggested that impaired oxidative metabolism exists in Rett syndrome. An analysis of the distribution among brain regions showed that the ratios of values for the frontal cortex to those for the temporal cortex for both cerebral blood flow and CMRO2 were lower than those for the controls, which may indicate the loss of hyperfrontality in Rett syndrome.     

Response of the cerebral circulation to profound hypocarbia in neonatal lambs

Hyperventilation to extremely low arterial carbon dioxide tension (PaCO2) has been used in the management of persistent pulmonary hypertension in newborn infants. With progressive hypocarbia, cerebral vasoconstriction occurs, raising the concern that extreme hypocarbia may result in cerebral oxygen deprivation. Therefore, I evaluated regulation of the cerebral circulation during acute hypocarbia in 10 newborn lambs. Whole-brain and regional blood flows measured using radioactive microspheres, arterial and venous (sagittal sinus) blood gases, and oxygen contents were measured in each lamb at four arterial carbon dioxide tensions. Whole-brain oxygen delivery, oxygen consumption, and fractional oxygen extraction were calculated. Finally, arterial and venous lactate concentrations were measured to assess cerebral lactate production. Whole-brain blood flow (CBF) decreased in a nonlinear fashion as PaCO2 ranged from 46 to 12 mm Hg [In(CBF) = 0.025(PaCO2) + 3.38; r = 0.70, p less than 0.001]. Similar responses were demonstrated for all regional blood flows examined. Cerebral fractional oxygen extraction (E) increased in a nonlinear fashion [In(1-E) = 0.023(PaCO2)-1.37; r = 0.80, p less than 0.001], and cerebral metabolic rate for oxygen was unchanged with hypocarbia. Cerebral venous lactate concentration increased significantly (3.49 +/- 0.23 vs. 2.01 +/- 0.22 mM, p less than 0.001) during severe hypocarbia (PaCO2 of less than 22 mm Hg), and the arterial-venous lactate concentration difference became negative. These results demonstrate uniform responses of whole-brain and regional blood flows and stable cerebral oxygen consumption during moderate and severe hypocarbia. Although there is evidence for cerebral lactate production during severe hypocarbia, this is not likely to indicate cerebral hypoxia as oxygen consumption does not change.     

大骨瓣减压对不同年龄重型颅脑创伤患者脑血流量及脑代谢的影响

目的 探讨大骨瓣减压对不同年龄重型颅脑创伤患者脑血流量及脑代谢的影响.方法 将71例重型颅脑创伤患者分为＜30岁组、30～50岁组和＞50岁组.每组又分为治疗组和对照组,大骨瓣减压手术前后行桡动脉和颈内静脉血气分析及血糖、血乳酸、血红蛋白监测,计算动脉-颈内静脉血糖差、颈内静脉-动脉乳酸差以及脑氧摄取率,TCD测定脑血流量.结果 术后第1天开始,≤50岁治疗组患者的脑血流量和脑氧摄取率均明显大于对照组;＞50岁治疗组患者的脑血流量明显高于对照组,脑氧摄取率明显低于对照组(P＜0.05).术后第3天开始,≤50岁治疗组患者的动脉-颈内静脉血糖差明显高于对照组,颈内静脉-动脉乳酸差明显低于对照组;＞50岁治疗组患者的动脉-颈内静脉血糖差明显低于对照组(P＜0.05),颈内静脉-动脉乳酸差明显高于对照组(P＜0.05).结论 大骨瓣减压能增加50岁以下重型颅脑创伤患者的脑血流量和脑氧代谢,能增加50岁以上患者的脑血流量并降低脑氧代谢.

Abstract：

Objective To explore the effects of decompressive craniectomy on cerebral blood flow volume and brain metabolism in different aged patients with severe traumatic brain injury.Method 71 cases were divided into three groups according age:group A( ＜30 years) ,group B(30 ～50 years) ,group C ( ＞ 50 years).Each group was divided into decompressive craniectomy ( DC ) treatment group and control group.Monitor dynamically blood gas analysis, glucose, lactic acid, hemoglobin in radial artery and internal jugular venous bulb, accounting the cerebral oxygen extraction ( CEO2 ) and the D - values of glucose and lactic acid respectively between radial artery and internal jugular venous bulb.Color doppler ultrasonography was used to determine the cerebral blood flow volume(CBFV).Results From the 1 st to 7th day, the CBFV and CEO2 of DC group were significantly greater than control group in group A and group B.The CBFV was significantly greater than control group while the CEO2 was lower than control group in group C ( P ＜ 0.05 ).From third day, the D - values of glucose of DC group was significantly higher than control group while the D - values of lactic acid was lower than control group in group A and group B, the D - values of glucose of DC group was significantly lower than control group while the D - values of lactic acid was higher than control group in group C( P ＜ 0.05 ).Conclusions Decompression craniectomy can increase the CBFV and brain oxygen metabolism in STBI patients before age 50 and increase the CBFV in patients after age 50 whereas decrease the brain oxygeon metabolism.     

Cerebral blood flow and metabolism in normotensive and hypertensive patients with transient neurologic deficits

We used positron emission tomography to examine retrospectively the effects of blood pressure on regional cerebral blood flow and oxygen metabolism in seven normotensive and eight hypertensive patients with a history of transient neurologic deficits. In the hypertensive patients, a decrease in regional cerebral blood flow was closely related to blood pressure; these changes were most pronounced in the supratentorial structures, especially the striatum and thalamus. In contrast, the regional cerebral metabolic rate for oxygen was less related to blood pressure. Consequently, the regional oxygen extraction fraction was increased in the hypertensive patients, while regional cerebral blood volume and the regional cerebral blood flow volume ratio were unchanged. Multivariate regression analysis confirmed that hypertension was an independent factor affecting regional cerebral blood flow. The analysis also disclosed that age, sex, hematocrit, smoking, and PaCO2 affected regional cerebral blood flow. These findings suggest that the hemodynamic reserve in hypertensive individuals is reduced, which may predispose them to cerebral ischemia and perhaps stroke, even during small decreases in cerebral perfusion pressure.     

Fetal cerebral blood flow and metabolism during oligemia and early postoligemic reperfusion

The early time period following ischemia may be of pathogenetic importance in hypoxic-ischemic brain injury. Global cerebral oligemia was induced in ten late gestation fetal sheep by inflation of a balloon occluder around the brachiocephalic artery. Cerebral blood flow, oxygen, glucose, and lactate net flux, and oxygen delivery were measured by the Fick principle following 1 h of oligemia and at 5, 30, and 60 min of postoligemic reperfusion. During oligemia, cerebral blood flow decreased by 74 +/- 10% (mean +/- SD) and oxygen consumption decreased by 34 +/- 24%. The glucose:oxygen quotient was elevated throughout the oligemic period. In the early (5 min) reperfusion period, blood flow and oxygen delivery were not different from control but oxygen consumption was persistently depressed by 27 +/- 32%; fractional extraction of oxygen was 0.38 +/- 0.10 during control and 0.24 +/- 0.09 during early reperfusion. The venous oxygen tension increased modestly from 15.2 +/- 2.4 to 18.0 +/- 1.7 mm Hg; the postoligemic venous pO2 was limited by the lack of reactive hyperemia combined with the low arterial pO2 of the intrauterine environment. Postoligemic carbohydrate fluxes could not be differentiated from control possibly due to blood-brain barrier limitations. These factors may be related to the relative resistance of the fetal brain to hypoxic-ischemic injury.     

Regional cerebral oxygen consumption, blood flow, and blood volume in healthy human aging.

Using high-resolution positron emission tomography and the oxygen 15 continuous inhalation method, we examined the changes in cerebral metabolic rate of oxygen, blood flow, blood volume, and oxygen extraction fraction as a function of age in 25 optimally healthy, unmedicated volunteers who ranged in age from 20 to 68 years. Subjects were strictly selected for absence of cerebrovascular risk factors, dementia, or mental disorders; they had neither biological nor clinical abnormalities, and no focal anomaly on computed tomographic scan. Regions of interest were determined according to the anatomical structures defined on corresponding computed tomographic scan cuts obtained using a stereotaxic head-positioning method. This same method was also used for positron emission tomographic imaging. There was no significant effect of aging on PaCO2 values, hematocrit, arterial blood pressure, cholesterol and triglyceride levels, and blood glucose levels. In most cerebral cortex gyri, the cerebral metabolic rate of oxygen significantly decreased with age according to a linear pattern, with the same magnitude (about -6% per decade) in all four lobes and on both sides. This effect of age on cortical cerebral metabolic rate of oxygen persisted when the possible influence of cortical atrophy, gender, and head size were partialled out. In contrast, the white matter, deep gray nuclei, thalamus, and cerebellum were not significantly affected. The cerebral blood volume declined with a similar pattern to cerebral metabolic rate of oxygen, while changes in cerebral blood flow were less significant, presumably because of larger variance of data across subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of adrenergic drugs on cerebral blood flow, metabolism, and evoked potentials after delayed cardiopulmonary resuscitation in dogs

BACKGROUND AND PURPOSE: Epinephrine administration during cardiopulmonary resuscitation increases cerebral blood flow by increasing arterial pressure. We tested whether potential beta-adrenergic effects of epinephrine directly influence cerebral blood flow and oxygen consumption independently of raising perfusion pressure. METHODS: Four groups of seven anesthetized dogs were subjected to 8 minutes of fibrillatory arrest followed by 6 minutes of chest compression, ventricular defibrillation, and 4 hours of spontaneous circulation. Cerebral perfusion pressure was increased to approximately equivalent ranges during resuscitation by either 1) epinephrine infusion, 2) epinephrine infusion after pretreatment with the lipophilic beta-adrenergic antagonist pindolol, 3) infusion of the alpha-adrenergic agonist phenylephrine, or 4) descending aortic balloon inflation without pressor agents. RESULTS: We found no difference in cerebral blood flow, oxygen extraction, or oxygen consumption during chest compression among groups. After ventricular defibrillation, depressed levels of cerebral blood flow, cerebral oxygen consumption, and somatosensory evoked potential amplitude were not different among groups. CONCLUSIONS: We detected no evidence that after 8 minutes of complete ischemia, epinephrine administration during resuscitation substantially influences cerebral blood flow or cerebral oxygen consumption independent of its action of raising arterial pressure or or that epinephrine has a negative impact on immediate metabolic or electrophysiological recovery attributable to its beta-adrenergic activity.     

Acute poisoning with triethyltin in the rat. Changes in cerebral blood flow, cerebral oxygen consumption, arterial and cerebral venous blood gases

Experiments were conducted with rats in two groups. In group 1 (survival group) triethyltin was administered i.p. once in a dose of 2.5 mg/kg body weight and in group 2 (terminal group) the animals received triethyltin in a dose of 9 mg/kg of body weight. Twelve and twenty-four hours after triethyltin injection a decrease of 30 to 40% in cerebral blood flow was observed in both groups. A decrease of systemic arterial blood pressure and changes in hematocrit value were found at that time. Progressive bradycardia was noted in all animals at all times of observation. Additionally, 48 h after intoxication, cerebral blood flow was increased in both groups by 13 to 24% above control values. The described changes were accompanied by macroscopic features of brain edema and changes in the cerebral vascular network. Cerebral oxygen consumption was augmented by about 18% 12 h after triethyltin injection in group 1. After 24 h it decreased by about 60% compared with control values, and after 48 h it returned to normal. In group 2 cerebral oxygen consumption was decreased significantly throughout the observation period. This reflects the state of cerebral metabolism at these stages of cerebral edema. The results underscore the necessity of simultaneous monitoring of cerebral blood flow and blood gases in order to distinguish between the particular stages of brain edema revealed by biochemical tests.