Cerebral Oxygen Uptake Research Articles

Hypertension with hemodilution prevents multifocal cerebral hypoperfusion after cardiac arrest in dogs.

Improved neurological outcome with postarrest hypertensive hemodilution in an earlier study could be the result of more homogeneous cerebral perfusion and improved O2 delivery. We explored global, regional, and local cerebral blood flow by stable xenon-enhanced computed tomography and global cerebral metabolism in our dog cardiac arrest model. Ventricular fibrillation cardiac arrest of 12.5 minutes was reversed by brief cardiopulmonary bypass, followed by life support to 4 hours postarrest. We compared control group I (n = 5; mean arterial blood pressure, 100 mm Hg; hematocrit, greater than or equal to 35%) with immediately postarrest reflow-promoted group II (n = 5; mean arterial blood pressure, 140-110 mm Hg; hypervolemic hemodilution with plasma substitute to hematocrit, 20-25%). After initial hyperemia in both groups, during the "delayed hypoperfusion phase" at 1-4 hours postarrest, global cerebral blood flow was 51-60% of baseline in group I versus 85-100% of baseline in group II (p less than 0.01). Percentages of brain tissue voxels with no flow, trickle flow, or low flow were lower (p less than 0.01) and mean regional cerebral blood flow values were higher in group II (p less than 0.01). Global cerebral oxygen uptake recovered to near baseline values at 3-4 hours postarrest in both groups. Postarrest arterial O2 content, however, in hemodiluted group II was 40-50% of that in group I. Thus, the O2 uptake/delivery ratio was increased (worsened) in both groups at 2-4 hours postarrest. After prolonged cardiac arrest, immediately induced moderate hypertensive hemodilution to hematocrit 20-25% can normalize cerebral blood flow patterns (improve homogeneity of cerebral perfusion), but does not improve cerebral O2 delivery, since the flow benefit is offset by decreased arterial O2 content. Individualized titration of hematocrit or hemodilution with acellular O2 carrying blood substitute (stroma-free hemoglobin or fluorocarbon solution) would be required to improve O2 uptake/delivery ratio.

Fetal heart rate variability and cerebral oxygen consumption in fetal sheep during asphyxia

This study was designed to examine the relationship between fetal heart rate variability and fetal cerebral oxygen uptake. Fetal sheep were chronically prepared with catheters and electrodes to determine cerebral blood flow (microsphere method), cerebral arteriovenous oxygen difference, and the electrocardiogram. An adjustable occluder was placed on the maternal common internal iliac artery to induce fetal asphyxia by reducing uterine blood flow. Fetal heart rate variability tended to decrease in the first 11 min of asphyxia, when cerebral oxygen consumption was approximately 53% of control. Despite stable cerebral oxygen consumption and worsening metabolic acidosis, however, fetal heart rate variability progressively returned towards normal by 36 min. There was no relationship between the depression of FHR variability and the degree of reduction of cerebral oxygen consumption. Nor was there any relationship between an alteration in regional cerebral blood flow or myocardial blood flow and the return of FHR variability with increasing duration of asphyxia. We conclude that there is an association between loss of fetal heart rate variability and reduced cerebral oxygen consumption, but the reduced variability does not persist with time at this degree of reduced cerebral metabolism in fetal sheep. This appears to be at variance with human clinical experience. Among the explanations for this may be insufficiently severe asphyxia, a species difference, removal of an inhibitor to FHR variability, or progressive use of other substrates for metabolism.

Improved blood flow during prolonged cardiopulmonary resuscitation with 30% duty cycle in infant pigs.

Sustained compression is recommended to maximize myocardial and cerebral blood flow during cardiopulmonary resuscitation (CPR) in adults and children. We compared myocardial and cerebral perfusion during CPR in three groups of 2-week-old anesthetized swine using compression rates and duty cycles (duration of compression/total cycle time) of 100 per minute, 60%; 100 per minute, 30%; and 150 per minute, 30%. Ventricular fibrillation was induced and CPR was begun immediately with a sternal pneumatic compressor. Epinephrine was continuously infused during CPR. Microsphere-determined blood flow and arterial and sagittal sinus blood gas measurements were made before cardiac arrest was induced and after 5, 10, 20, 35, and 50 minutes of CPR. At 5 minutes of CPR, ventricular and cerebral blood flows were greater than 25 ml.min-1 x 100 g-1 and were not significantly different between groups. When CPR was prolonged, however, myocardial and cerebral blood flows were significantly higher with the 30% duty cycle than with the 60% duty cycle. By 35 minutes, all myocardial regions had less than 5 ml.min-1 x 100 g-1 flow with the 60% duty cycle. In contrast, CPR with the 30% duty cycle at either compression rate provided more than 25 ml.min-1 x 100 g-1 to all ventricular regions for 50 minutes. By 20 minutes, most brain regions received 50% less flow with the 60% duty cycle compared with animals undergoing CPR with the 30% duty cycle (p less than 0.05). Cerebral oxygen uptake was better preserved with the 30% duty cycle. Chest deformation from loss of recoil was greater with the 60% duty cycle compared with the 30% duty cycle. We conclude that the shorter duty cycle provides markedly superior myocardial and cerebral perfusion during 50 minutes of CPR in this infant swine model. These data do not support recommendations for prolonged compression at rates of 100 per minute during CPR in infants and children.

Cerebral blood flow and metabolism in affective disorders

International Journal of Geriatric PsychiatryVolume 6, Issue 6 p. 423-430 Article Cerebral blood flow and metabolism in affective disorders Eileen M. Joyce, Eileen M. Joyce Laboratory of Clinical Studies, National Instiute on Alcohol Abuse and Alcoholism, NIH Building 10, Bethesda, MD 20892, USASearch for more papers by this author Eileen M. Joyce, Eileen M. Joyce Laboratory of Clinical Studies, National Instiute on Alcohol Abuse and Alcoholism, NIH Building 10, Bethesda, MD 20892, USASearch for more papers by this author First published: June 1991 https://doi.org/10.1002/gps.930060615Citations: 4AboutRelatedInformationPDFPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessClose modalShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume6, Issue6June 1991Pages 423-430 RelatedInformation RecommendedEffects of morphine and naloxone on cerebral blood flow and metabolism in experimental subarachnoid hemorrhageJ. Hauerberg, M. Juhler, Acta Neurologica ScandinavicaCerebral blood flow and metabolism following subarachnoid haemorrhage: cerebral oxygen uptake and global blood flow during the acute period in patients with SAHM. Jakobsen, E. Enevoldsen, P. Bjerre, Acta Neurologica ScandinavicaCerebral blood flow and metabolism following subarachnoid haemorrhage: effect of subarachnoid bloodM. Jakobsen, T. Skjødt, E. Enevoldsen, Acta Neurologica ScandinavicaEffects of sevoflurane on intracranial pressure, cerebral blood flow and cerebral metabolism: A dose‐response study in patients subjected to craniotomy for cerebral tumoursH. Bundgaard, G. VON Oettingen, K. M. Larsen, U. Landsfeldt, K. A. Jensen, E. Nielsen, G. E. Cold, Acta Anaesthesiologica ScandinavicaCerebral blood flow findings in moyamoya disease in adultsE. Dietrichs, A. Dahl, R. Nyberg-Hansen, D. Russell, K. Rootwelt, T. Veger, Acta Neurologica Scandinavica

Cerebral blood flow and metabolism following subarachnoid haemorrhage: cerebral oxygen uptake and global blood flow during the acute period in patients with SAH

Forty-eight patients with subarachnoid haemorrhage were studied with repeated rCBF and CMRO2 measurements. Cortical rCBF was measured using xenon-inhalation technique. CMRO2 was calculated as AVDO2 x CBF. When first studied the 29 conscious patients showed relative hyperaemia with CBF at 50 ml and reduced CMRO2 at 2.17 ml. In the following week CBF decreased to 41. CMRO2 remained reduced and constant. The 19 unconscious patients showed initially pronounced reduction in CMRO2 to 1.26, followed by gradual increase to 1.73 in 4-5 days. Simultaneously CBF increased from 18 ml to slightly above 30 ml. In the conscious patients the early reduction in CMRO2 and the concomitant luxury perfusion may be explained by global ischaemia because of very high ICP at the time of the haemorrhage. The reduced CBF in the unconscious group could be due to increased ICP, as ventricular drainage increased CBF to levels of relative hyperaemia as demonstrated in one case. As no decrease in CMRO2 was seen during the first 2 weeks, it is suggested that ischaemia at the time of aneurysm rupture is the most important single factor in reduction of global CMRO2.

Cerebral perfusion and oxygen uptake studies in patients with intracranial tumors.

Cerebral perfusion and oxygen uptake studies in patients with intracranial tumors.

Partitioning and Extraction of Glucose Regulates Cerebral Glucose Utilization in Newborn Dogs

We investigated the amount of fasting steady-state systemic glucose production utilized by the neonatal canine cerebral cortex. The relationship of systemic glucose production and cerebral glucose utilization were analyzed as functions of cerebral blood flow, cerebral oxygen uptake, and indirect measures of alternate fuel utilization. Fasting arterial blood glucose was 3.36 mM and glucose production was 49.6 mumol/kg/min. Average cerebral blood flow was 0.83 ml/g/min, and cerebral glucose uptake was 0.60 +/- 0.15 mumol/g/min. 36.6% of systemic glucose production was utilized by the cerebral cortex. There were no correlations between systemic glucose production, cerebral blood flow, or cerebral glucose uptake with blood glucose concentration. Furthermore, total cerebral glucose uptake was static across a wide range of glucose levels. Nonetheless, the percent of glucose production used by the brain was an inverse function of systemic glucose production (r = -0.71, p less than 0.001). The cerebral extraction of glucose (27.6 +/- 4.1%) decreased as a function of increasing blood glucose levels (r = -0.51, p less than 0.05), while brain uptake index correlated with increasing systemic glucose production (r = 0.61, p less than 0.02). We can conclude that the canine neonatal cerebral cortex may utilize only 37% of systemic glucose production. At low rates of glucose turnover, a larger proportion of systemic glucose production is allotted to the brain. Mechanisms that may regulate total cerebral glucose influx may be glucose permeability, or the increased extraction of glucose at lower blood glucose levels.

Cerebral blood flow and metabolism in fasting neonatal piglets.

Cerebral blood flow and cerebral metabolism were studied in 8 fasting neonatal piglets. Cerebral blood flow was not significantly different (p greater than 0.1) at 24 h (75.0 +/- 30.7 ml/min/100 g) and 48 h (74.2 +/- 32.3 ml/min/100 g) of age. Blood glucose concentration was lower in 48-hour-old fasted piglets (1.27 +/- 0.60 mmol/l) in comparison with 24-hour-old fasted animals (2.90 +/- 0.52 mmol/l), and cerebral glucose utilisation rate was also reduced in the 48-hour-old piglets (17.6 +/- 6.0 mumol/min/100 g at 48 h, 34.2 +/- 12.2 mumol/min/100 g at 24 h). Blood lactate concentration and cerebral lactate utilisation rate were not significantly different at 24 and 48 h of age. Brain lactate utilisation accounted for approximately 10% of cerebral oxygen utilisation at 48 h in fasted piglets. Cerebral glucose and lactate utilisation at 48 h accounted for approximately 66% of cerebral oxygen uptake, indicating that other substrates make a major contribution to cerebral metabolic requirements in fasting neonatal piglets.

Cerebral Metabolic Response to Neonatal Hypoglycemia in Growth-Retarded Dogs

The cerebral metabolic effects of hypoglycemia due to intrauterine growth retardation were studied in newborn dogs. Intrauterine growth retardation was induced in newborn dogs after 3 days of maternal nutritional deprivation (birth weight 251 +/- 7 versus 227 +/- 7 g, p less than 0.01). After birth, growth retarded pups developed fasting neonatal hypoglycemia which lasted from 3 to 9 h of life. The cerebral arteriovenous differences for glucose, oxygen, and ketone bodies were not different between growth-retarded pups or those from age-matched controls. The cerebral venous efflux of lactate was reduced, whereas the extraction of glucose (relative to blood glucose) was enhanced among growth-retarded pups. Cerebral glycogen content was lower in pups with growth retardation whereas phosphoenolpyruvate and pyruvate concentrations were augmented among growth-retarded pups. The latter may reflect a more oxidized cytoplasmic redox state but may also be due to diminished lactate efflux from the brain. Cerebral ATP content was not affected during periods of reduced blood glucose levels. These results suggest that in newborn dogs hypoglycemia associated with intrauterine growth retardation alters cerebral metabolism by increasing cerebral extraction of glucose and decreasing CNS efflux of lactate. We speculate that the net effect is increased lactate utilization within oxidative pathways and preservation of cerebral oxygen uptake. Cerebral glucose utilization is directed away from glycogen synthesis and toward glycolysis. Lactate oxidation rather than release to the systemic circulation may maintain cerebral ATP production in growth-retarded hypoglycemic newborn dogs.

Allocation of systemic glucose output to cerebral utilization as a function of fetal canine growth.

To determine whether the neonatal canine brain consumes a major proportion of the systemic glucose production, we investigated the cerebral glucose requirement and hepatic glucose production in beagle pups. Sixteen pups received D-[6-3H]-glucose to determine systemic glucose production. Cerebral blood flow was measured by [N-methyl-14C]antipyrine, and the brain uptake index (BUI) of glucose was determined using 2-[14C]deoxy-D-glucose. Glucose production was 49.6 +/- 11.0 mumol.kg-1.min-1. Cerebral blood flow was 0.83 ml.g-1.min-1; cerebral uptake of glucose was 0.60 +/- 0.15 mumol.g-1.min-1. Of the total glucose production 36.6 +/- 7.9% was accounted for by the cerebral uptake of glucose. Brain-to-body weight and brain-to-liver weight ratios were the greatest in the smallest pups, suggesting brain sparing. The effect of growth status on cerebral substrate availability could not be correlated with cerebral uptake of glucose or oxygen or with systemic glucose production. However, the percentage of systemic glucose production allotted to the cerebral cortex increased with increasing body weight (r = 0.50, P less than 0.05). Cerebral glucose entry measured by BUI was demonstrated to be 0.108 +/- 0.014; BUI inversely correlated with canine birth weight (r = -0.832, P less than 0.001). We conclude that the percentage of glucose production utilized by the neonatal canine brain is not proportionately larger in the smaller pups despite a proportionately larger brain. Because the absolute cerebral glucose utilization may be static, we speculate that BUI (glucose entry) may be less of a rate-limiting factor for cerebral glucose entry in the smallest pups.

Cerebral metabolism in the newborn lamb with polycythemia.

Infants with polycythemia and hyperviscosity are known to have a reduced cerebral blood flow. Eight newborn lambs were studied to determine what effect the reduction in cerebral blood flow might have on the cerebral delivery and uptake of oxygen, glucose, lactate, pyruvate, beta-hydroxybutyrate, and acetoacetate. Measurements of cerebral blood flow, hematocrit, blood viscosity as well as delivery and uptake of the forementioned substrates were made during a control period and at 60, 180, and 300 min after an exchange transfusion with packed newborn red blood cells was performed to increase the hematocrit. Sixty min after the exchange transfusion, cerebral blood flow fell while cerebral oxygen delivery and uptake were stable. Although arterial glucose concentration remained unchanged, there was a significant fall in cerebral glucose delivery. At 180 min after the exchange transfusion, the arterial glucose concentration fell from 90 to 70 mg/100 ml causing the cerebral glucose delivery to further decrease. This resulted in a significant fall in the cerebral glucose uptake and glucose:oxygen quotient. At 300 min arterial glucose concentration remained low but a rise in cerebral blood flow resulted in a small increase in the cerebral glucose delivery and consequently the cerebral glucose uptake and glucose:oxygen quotient returned to normal. We conclude that polycythemia results in a decrease in cerebral glucose delivery and uptake during normoglycemia.

The in vivo effect of bilirubin and sulfisoxazole on cerebral oxygen, glucose, and lactate metabolism in newborn piglets.

Bilirubin inhibits in vitro oxidative phosphorylation and glycolysis. This study investigated the in vivo effect of bilirubin on cerebral oxygen, glucose, and lactate uptake in newborn piglets. Seventeen 2- to 4-day-old piglets were divided into three groups and examined as follows: group 1 = control (C); group 2 = control with sulfisoxazole; and group 3 = experimental, given bilirubin with sulfisoxazole. In the experimental group, bilirubin was infused for 4 h. The cerebral bilirubin content in the bilirubin-infused group was 11.0 +/- 1.4 nmol/g of cerebral cortex (mean +/- SEM), consistent with levels found in infants with kernicterus. However, this level of brain bilirubin had no major, acute effects on cerebral uptake of oxygen, glucose, or lactate despite producing lethargy and ataxia which were consistent with bilirubin intoxication. This suggests that mitochondrial changes may not be involved in vivo in acute bilirubin encephalopathy.

Cerebral metabolism during cross-circulation in experimental hepatic failure in the pig.

The effect of hepatic assistance on cerebral metabolism was evaluated in a series using cross-circulation, anticipating increased efficiency of hepatic support. The experimental model for liver failure was pigs with totally devascularized liver. Cross-circulation with a normal sibling pig, cross-circulation with inflow in the donor directly into the portal vein and cross-perfusion with isolated perfused liver starting 20 h after elimination of liver function in the recipient and lasting for 3 h did not increase survival. Before cross-circulation in these three groups, the cerebral flow and oxygen uptake were decreased; during the cross-circulation a significant but temporary increase was found. In experiments with early and prolonged perfusion with isolated perfused liver no changes in cerebral flow, oxygen or glucose uptake were found, and these variables were still normal 6 h after termination of the perfusion. The survival time was significantly increased. In the control group a significant rise in blood and CSF ammonia was found with a mean CSF/blood ratio of 0.92. After cross-circulation, the CSF/blood ratio was 0.52 and 0.62, respectively, indicating a proportionally greater elimination of ammonia from the cerebrospinal fluid than from the blood. Cross-circulation did not significantly change the alpha-ketoglutarate, glutamate or glutamine CSF concentrations. After prolonged cross-perfusion, the ammonia blood/CSF ratio was 0.24. It is concluded that by extended extracorporeal hepatic assistance it is possible to increase survival and to prevent changes in cerebral metabolism and ammonia accumulating in the cerebrospinal fluid.

Effect of epinephrine on cerebral and myocardial perfusion in an infant animal preparation of cardiopulmonary resuscitation.

We assessed the efficacy of conventional cardiopulmonary resuscitation (CPR) in 2-week-old piglets. We determined intrathoracic vascular pressures, cerebral (CBF) and myocardial blood flows (MBF), and cerebral oxygen uptake during conventional CPR in this infant animal preparation and contrasted these results with those of previous work on adult animals. We further examined the effects of the infusion of epinephrine on these pressures and flows and on cerebral oxygen uptake, which has not been previously evaluated in adult preparations. Conventional CPR was performed on pentobarbital-anesthetized piglets with a 20% sternal displacement with the use of a pneumatic piston compressor. Chest recoil was incomplete, leading to an 18% to 27% reduction in anteroposterior diameter during the relaxation phase. Aortic and right atrial pressures in excess of 80 mm Hg were generated. These pressures are greater than those generally obtained in adult animals with similar percent pulsatile displacements. CBF and MBF were also initially greater than those reported in adult animals undergoing conventional CPR. However, when CPR was prolonged beyond 20 min, aortic pressure fell and CBF and MBF declined to the near-zero levels seen in adult preparations. At 5 min of CPR, CBF and MBF were 24 +/- 7 and 27 +/- 7 ml . min-1 x 100 g-1 (50% and 17% of the values during cardiac arrest), respectively. With the continuous infusion of epinephrine (4 micrograms/kg/min) in another group of animals, MBF was significantly greater at 20 min of CPR and CBF and cerebral O2 uptake were greater at 35 min of CPR as a result of higher perfusion pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Does glucose administration affect the cerebral response to fetal asphyxia?

This study was designed to test whether the fetal brain has an increased resistance towards asphyxia at high levels of blood-glucose, compared with low levels. 35 fetal sheep were exteriorized and investigated under general anesthesia. Cerebral blood flow (CBF) was estimated with the 133Xenon-washout method. Cerebral uptake of oxygen, glucose, and lactate was measured. Somatosensory evoked potentials (SEP) were recorded. The fetuses were subjected to controlled asphyxia by ventilating the ewes with gas mixtures low in oxygen. The blood sugar levels of the fetuses were varied over a four-fold range. During normal oxygenation of the fetus variations in the blood glucose concentration induced considerable changes in the cerebral glucose uptake, whereas CBF and oxygen uptake were unaffected. During asphyxia, hyperglycemia was associated with rapid development of acidosis and reduction in cerebral oxygen consumption together with deterioration of the neurophysiological characteristics of the brain. Far from being beneficial during asphyxia, fetal hyperglycemia appeared to reduce the tolerance of the fetal brain towards asphyxia. This report together with other evidence provides support for the view that extra glucose might be disadvantageous for the asphyxiated fetus.

The effect of dihydroergotoxine on lipid peroxidation in vitro.

Dihydroergotoxine mesylate (DHET), an ergot alkaloid derivative, is widely used to treat senile cerebral vascular insufficiency. Aspects of this age-related phenomenon may be due to deterioration by lipid oxidation of cellular membranes. DHET stabilizes EEG alpha frequencies, increases cerebral blood flow and oxygen uptake and accumulates in lipid-rich structures of the brain. The effect of DHET was studied on iron-catalyzed peroxidation of liposomes as measured by the thiobarbituric acid assay. It was found that DHET inhibits peroxidation in vitro in a dose-dependent manner. These results suggest that DHET acts in part as a lipid antioxidant when used to treat senile cerebral vascular insufficiency.

Nitroprusside-hypotension: cerebral blood flow and cerebral oxygen consumption in neurosurgical patients.

The effects of nitroprusside-induced hypotension on cerebral blood flow and cerebral oxygen consumption were investigated in nine patients scheduled for cerebral arterial aneurysm surgery. Anesthesia was maintained with nitrous oxide/oxygen and fentanyl; muscle relaxation was achieved with pancuronium; PaCO2 was maintained at 4.79-5.32 kPa. Mean arterial pressure was reduced to 50 mmHg by nitroprusside infusion after opening of the dura. Measurements were recorded and blood samples were taken 15 min before induction of hypotension, during stable hypotension and 15 min after termination of nitroprusside infusion. Measurements included: cerebral blood flow, using the argon-washin technique, cardiac output (thermodilution), mean arterial pressure and heart rate. Cerebral blood flow averaged 56 +/- 6 min . 100 g before hypotension. Nitroprusside produced hypotension but did not significantly alter cerebral blood flow (61 +/- 7 ml/min . 100 g). Cerebral blood flow remained virtually at preinfusion values upon cessation of infusion (53 +/- 6 ml/min . 100 g). Cerebral oxygen uptake averaged 3 +/- 0.2 ml/min . 100 g before hypotension and did not change significantly during hypotension (3.3 +/- 0.3 ml/min . 100 g) and after termination of hypotension (2.7 +/- -0.3 ml/min . 100 g). In two patients nitroprusside produced a 17 and 20% increase, respectively, in cerebral blood flow with no change in cerebral oxygen consumption, together with a marked increase in cardiac output and heart rate.

Cerebral blood flow and oxygen uptake in endotoxic shock. An experimental study in dogs.

Cerebral blood flow (CBF), cerebral oxygen uptake (CMRO2) and central haemodynamics in anaesthetized dogs with controlled ventilation were studied at intervals for 2 h following an intravenous injection of E. coli endotoxin, 1.0-1.5 mg/kg. CBF showed a 30% decrease within 15 min after the endotoxin administration, while the arterial blood pressure was still not markedly depressed. Autoregulation to arterial blood pressure changes was maintained during endotoxinaemia and the cerebrovascular reaction to changes in arterial carbon dioxide tension (PaCO2) depressed. Normocapnic animals (PaCO2) greater than or equal to 4.0 kPa) showed an increase in CMRO2 of over 40%, that was obvious 1 h after the administration of endotoxin. The intracranial pressure was decreased with 5 min of the administration of endotoxin irrespective of the prevailing arterial blood pressure. Thereafter, it was raised above the control level. Two hours after endotoxin increased protein concentrations in cerebrospinal fluid were seen, results compatible with blood-brain barrier damage and penetration of other substances; e.g. monoamines released during endotoxinaemia could thus be expected to have a direct influence on both cerebral blood flow and metabolism.

Cerebral Blood Flow and Cerebral Metabolism in Children Following Cardiac Surgery with Deep Hypothermia and Circulatory Arrest. Clinical Course and Follow-Up of Psychomotor Development

Between November 1975 and June 1977, 49 children underwent repair of complicated cardiac defects with the aid of deep hypothermia. Circulatory arrest was used in 28 cases. Nine children died (18%) due to early postoperative heart failure. A decisive cause of death in terms of important cardiovascular defects, which were either unknown or not correctable at the time of repair, was found in 6 patients. Children with complicated forms of congenital heart disease requiring an extensive repair were overrepresented among those who died. Hence, there was an excess in the duration of bypass among nonsurvivors (p less than 0.01) whereas the patient's age at operation, the use of circulatory arrest and the duration of aortic occlusion had no bearing on operative mortality. Cerebral blood flow (CBF) and cerebral metabolism were studied in 9 survivors. A negative correlation (r = -0.67) was found between the duration of circulatory arrest and CBF measured directly after surgery. CBF was reduced to values below 0.2 ml . g-1 . min-1 in 3 children with long periods of circulatory arrest. The cerebral uptake of oxygen and glucose was normal both before and after surgery. Two separate interviews with the parents were performed, the first one 3-22 months and the second one about 3 years after surgery. No serious neurological symptoms or psychomotor disturbances were reported. However, in 3 children operated with circulatory arrest, difficulties in performing more delicate motor activities were noted by the parents. The findings indicate that circulatory arrest should be used with caution and total arrest periods exceeding 60 min avoided.

The electroencephalogram, blood flow, and oxygen uptake in rabbit cerebrum.

In the present study, the relationships among electroencephalographic (EEG) amplitude shifts, cerebral blood flow (CBF), and cerebral oxygen uptake (CMRO2) have been characterized in halothane-anesthetized rabbits. CBF was measured by timed collection of venous effluent from the superior sagittal sinus. CMRO2 was calculated as the product of CBF and the arteriovenous difference in oxygen content. The depth of anesthesia in the first series of experiments was maintained at a constant level that was characterized by spontaneous EEG shifts from high- to low-voltage states (HV-LV shifts). These shifts were associated with transient decreases in mean arterial pressure (MAP), which averaged 23 +/- 2 mm Hg (n = 17). Ninety seconds after spontaneous HV-LV shifts, MAP had returned to its original value, CBF had increased by 26 +/- 7% (n = 8), and CMRO2 had increased 22 +/- 4% (n = 7). In a second series of experiments, HV-LV shifts were induced by a 90-s application of a standardized nociceptive stimulus (n = 13). Following these stimulation-induced HV-LV shifts, CBF increased 28 +/- 5% and CMRO2 increased 27 +/- 4%. Under scopolamine (0.35 mg/kg, i.v., n = 8), no change in CBF was observed following HV-LV shifts induced by 90-s of stimulation, although CMRO2 increased significantly by 14 +/- 3%. After 300 s of post-scopolamine stimulation, however, both CBF and CMRO2 had significantly increased by 12 +/- 3 and 15 +/- 3% (n = 8) of control, respectively. These results demonstrate that HV-LV shifts, whether spontaneous or stimulation-induced, are associated with significant increases in both CBF and CMRO2. Because the early (90-s) increases in CBF but not those in CMRO2 could be blocked by scopolamine, we suggest that the cerebral vasodilatation that occurs during the early phase of HV-LV shifts involves cholinergic mechanisms. Because scopolamine could not block the increase in CBF observed after 300 s of stimulation, we suggest that the final value of CBF obtained after an HV-LV shift is determined by a combination of both cholinergic and noncholinergic factors.