Total Brain Blood Flow Research Articles

Regional blood flow in asphyxiated fetuses with seizures

OBJECTIVE: Our purpose was to determine ovine fetal regional blood flow changes during asphyxia of such severity that it results in seizures. STUDY DESIGN: Six ovine fetuses were exposed to severe asphyxia produced by maternal uterine artery occlusion for up to 90 minutes. Fetal blood pressure and heart rate, blood gases, acid base status, electrocorticogram, electromyogram and regional blood flow (radioactive microspheres) measurements were recorded. RESULTS: During the asphyxial insult pH fell from 7.39 ± 0.01 (mean ± SEM) to 6.99 ± 0.01 at 60 minutes, base excess from 4 ± 1 to –16 ± 1 mEq/L, and oxygen content from 3.5 ± 0.4 to 0.5 ± 0.1 mmol/L (p < 0.05). There was no significant change in fetal heart rate or blood pressure. The fetal electrocorticogram was profoundly suppressed during asphyxia, and seizure activity began 50 ± 19 minutes after the release of occlusion in all surviving animals. Blood flow increased to the heart and adrenals during asphyxia and decreased to spleen, gut, kidneys, and carcass (p < 0.05). There was no change in combined ventricular output and umbilical blood flow. There was no significant increase in total cerebral perfusion. CONCLUSION: When the ovine fetus is exposed to asphyxia of sufficient severity to produce neurologic damage (seizures), the pattern of redistribution of blood flow is comparable to the response to lesser asphyxia, except that a significant increase in total brain blood flow does not occur. This finding may have an important association with the development of long-term neurologic damage. (AM J OBSTET GYNECOL 1994;170:156-61.)

Regional cerebral blood flow in patients with internal carotid artery stenosis: Effects of nifedipine and nimodipine

Regional cerebral blood flow (rCBF) in 87 patients with CBF decreased due to unilateral stenosis of internal carotid artery was studied by using the133xenon infusion technique and a 30-detector setup. On the side of stenosis a decrease in the mean hemispheric blood flow (rCBFh) with an elevated deviation of rCBF from rCBFh was observed. Administration of a single oral dose of either nifedipine or nimodipine induced various changes in rCBF. A classification of their effects with due regard for changes in both the mean value of the hemispheric blood flow and the flow distribution is described. The decrease in both the interhemispheric difference of rCBFh and the deviation of rCBF from the hemispheric mean flow accompanying the increase of the total brain blood flow was considered as being the most beneficial drug effect. This positive reaction was found more frequently when nimodipine was used. In some patients nifedipine, and in fewer, nimodipine, induced nonbeneficial changes in rCBF with elevation of the interhemispheric difference and an increase in the number of ischemic and hyperemic regions on the side of stenosis. The types of drug effects after administration of a single dose were similar to those after two weeks of monotherapy. It is supported that this approach allows assessment of cerebral hemodynamics and drug effectiveness in cerebrovascular disorders.

Effects of indomethacin on brain blood flow and cerebral metabolism in hypoxic newborn piglets.

We tested the hypotheses that in newborn piglets indomethacin (Indo) pretreatment blunts the hyperemic brain blood flow (BF) and alters the cerebral metabolic responses to hypoxia and that these responses are dose dependent. We studied 23 chronically instrumented piglets exposed to graded hypoxia (O2 content: 7.1-0.4 microM O2/ml) after pretreatment with high (5 mg/kg, n = 8)-or low (0.3 mg/kg, n = 6)-dose Indo or placebo (diluent, n = 9). Total and regional brain BF increased significantly with decreasing O2 content values (P < 0.01) in all three groups. However, the rise in the brain BF curves with decreasing O2 content values was significantly (P < 0.05) lower in the high-compared with the low-dose group in all brain regions with the greatest effect in the caudal regions. Furthermore, the BF curves in the placebo-treated animals were similar to the low-dose group. The cerebral metabolic rate of O2 (CMR(O2)) and glucose metabolism were preserved in the three groups over all hypoxic ranges until severe hypoxia (O2 content < or = 1.1 microM O2/ml) was achieved in the high-dose group, when CMR(O2) decreased (P < 0.05), and glucose metabolism increased (P < 0.05). The mean arterial blood pressure in the high-dose group during severe hypoxia was 45 mmHg (P > 0.05). Although coupling of cerebral BF and CMR(O2) was preserved in the three groups, this association was significantly altered with high-dose pretreatment. We conclude that an attenuation in the hypoxia-induced brain perfusion by Indo is dose dependent. Alterations in CMR(O2) and glucose metabolism are observed with high-dose pretreatment during severe hypoxia, and the responses to hypoxia are similar with placebo and low-dose Indo pretreatment.

Effect of Sleep on Regional Blood Flow Distribution in Piglets

The regional distribution of blood flow to the brain and to other major organs was studied during wakefulness and sleep in growing piglets. A young group was studied at 6.8 +/- 1.3 d of age and an older group at 33.5 +/- 5.5 d. Two d before the experiments, we instrumented the animals for measurement of blood flow by the microsphere technique. We determined sleep state using EEG and behavioral criteria. Although we did not find significant differences in blood gas tensions and cardiac output with changes in behavioral states, we did note a number of important changes in brain and muscle blood flow with sleep. 1) Although total brain blood flow changed little between wakefulness and sleep at both ages, regional differences existed. Indeed, at both ages, during rapid eye movement sleep (active sleep), blood flow to the thalamus-hypothalamus and brainstem was significantly higher than during wakefulness (p less than 0.025); in older piglets, blood flow to these two regions was significantly lower in quiet sleep than in wakefulness (p less than 0.05). 2) Blood flow to most skeletal muscle groups, and particularly to the diaphragm, was lower during sleep than during wakefulness. 3) Age did not have a significant effect on the regional distribution of blood flow during sleep. We conclude that behavioral states influence the regional distribution of blood flow in early life, but not in an age-dependent fashion. We speculate that, because no difference was observed in other hemodynamic variables, the regional changes in organ blood flow with sleep most probably reflect the differences in local metabolic needs.

Nimodipine has no effect on the cerebral circulation in conscious pigs, despite an increase in cardiac output

1. We studied the effects of four doses of nimodipine (0.5, 1, 2 and 4 micrograms kg-1 min-1) on systemic haemodynamics and on regional vascular beds, in particular the cerebral circulation, in conscious pigs. 2. Nimodipine caused dose-dependent, probably reflex-mediated, increases in heart rate (42% with the highest dose) and cardiac output (54%), while arterial blood pressure was only minimally affected. Left ventricular end-diastolic pressure and systemic vascular resistance decreased dose-dependently (35-40% at the highest dose) while stroke volume remained unchanged. 3. Total brain blood flow was not affected by the drug. Furthermore, we could not demonstrate any regional cerebral differences, as blood flows to both cerebral hemispheres as well as the diencephalon, cerebellum and brain stem remained unchanged. 4. Blood flow to the kidneys, liver, small intestine and skin also did not change. Nimodipine caused dose-dependent increases in blood flow to the stomach (95%), myocardium (97%) and adrenal glands (102%), while blood flow to skeletal muscles (267%) increased most. 5. It is concluded that in the conscious pig, nimodipine is an arterial vasodilator which shows some selectivity for the skeletal muscle vasculature but does not increase total or regional cerebral blood flow.

Regional cerebral blood flow response during and after acute asphyxia in newborn piglets.

The hemodynamic response during and after acute asphyxia was studied in 14 newborn piglets. An apnea-like asphyxial insult was produced in paralyzed mechanically ventilated piglets by discontinuing ventilation until the piglets became bradycardic (heart rate less than 80 beats/min). Seven piglets had organ blood flow measured by microspheres at control, during asphyxia (PO2 = 16 +/- 11 Torr, pH = 7.31 +/- 0.07, PCO2 = 47 +/- 9 Torr), and during recovery from asphyxia. During acute asphyxia, rapid organ blood flow redistribution occurred, producing decreased renal and skeletal muscle blood flow, while coronary blood flow increased. Although total brain blood flow changed little during asphyxia, regional cerebral blood flow (rCBF) analysis revealed significant nonhomogeneous blood flow distribution within the brain during asphyxia, with decreases to the cerebral gray and white matter and the choroid plexus, whereas brain stem structures had increased flow. During recovery with reventilation, total brain blood flow increased 24% above control, with a more uniform distribution and increased flow to all brain regions. The time course of rCBF changes during acute asphyxia was then determined in seven additional piglets with CBF measurements made sequentially at 30-60 s, 60-120 s, and 120-180 s of asphyxia. The vasoconstriction seen in cortical structures, concurrent with the reduction in skeletal and kidney blood flow, known to be sympathetically mediated, suggest a selective reflex effect in this brain region. The more gradual and progressive vasodilation in brain stem regions during asphyxia is consistent with chemical control. These findings demonstrate significant regional heterogeneity in CBF regulation in newborn piglets.

Con: The EEG should not be monitored during cardiopulmonary bypass

N EUROPSYCHIATRIC complications continue to be one of the major problems following open heart surgery, despite great improvements in operative and extracorporeal perfusion techniques.‘T2 There are wide variations in the reported incidence of cerebral dysfunction, ranging from 1% to 53%~.~-~ This variation may be related to the criteria selected and indicates that there is room for improvement in the monitoring methods used. Various types of EEG monitoring have been advocated and applied to monitor brain function in the operating room (OR), and particularly to assess the adequacy of cerebral function during clinical cardiopulmonary bypass (CPB) procedures. ‘-lo There is no available means of noninvasive monitoring other than the EEG for detection of cerebral dysfunction during general anesthesia and CPB. Therefore, instead of debating whether we should use EEG monitoring during open heart surgery, we should ask, “Does this type of monitoring provide sufficient warning of inadequate cerebral circulation or of focal embolic phenomena to allow corrective measures that can result in prevention of postoperative cerebral dysfunction ?” Following careful review of published data and of our experience with the EEG, I am forced to conclude that the answer is “no.” Recent literature supporting the usefulness of intraoperative monitoring of the EEG during CPB has usually been anecdotal. In accordance with their observations and bias, the authors generally express a degree of enthusiasm, and there are only occasional notes of caution. If intraoperative monitoring of the EEG is to be of value in the OR for detection of cerebral dysfunction during CPB, however, several criteria must be satisfied. First, the entire brain is at risk and must be amenable to monitoring. Second, personnel and equipment must be available for correct recording and interpretation of the EEGs. Third, it is necessary to monitor brain dysfunction under hypothermia, anesthesia, and various forms of pharmacologic intervention. Fourth, corrective measures must be possible if and when changes in the EEG are found; and when corrective steps are taken, the benefit should outweigh the risk to patients whose EEGs indicate (correctly or falsely) that they will suffer deficits. Let us examine the first criterion, which concerns the relationship between electroencephalography and regional brain function. The EEG can record only the electrical activity arising from the cerebral cortex, thus limiting anatomic resolution of the EEG to the superficial brain structures. Deeper brain structures, including the brain stem, have little effect on the recorded EEG. Still, some authors go so far as to state that EEG activity correlates well with cerebral metabolism and regional cerebral blood flow (CBF), even when CBF and cerebral metabolic rate for oxygen (CMROJ measurements reflect total brain blood flow and oxygen consumption of the entire brain.” However, these relationships are not valid when the patient is experiencing hypoxic brain injury, has a tumor, is receiving certain anesthetics, or is asleep.12*i3 This clearly casts doubt on the value of intraoperative EEG monitoring. Most authorities would agree that the principal causes of diffuse cerebral damage are altered characteristics of CPB perfusion or the occurrence of a microembolism. However, there is no evidence that EEG monitoring is capable of differentiating between these problems. If a patient has a microembolism in some part of the brain, can the simplified EEG detect this problem, or is a more sophisticated EEG program required? How many leads are needed to pick up the microembolism? These questions are still unanswered. The second criterion concerns the availability of qualified personnel and equipment for

Intracranial Arteriovenous Malformation: Relationships between Clinical and Radiographic Factors and Cerebral Blood Flow

Arteriovenous malformations (AVMs) dramatically alter normal cerebral circulatory dynamics. Clinical and radiographic data from 62 patients were analyzed to determine their impact on total brain blood flow (TBF) measured by single-photon emission computed tomography. 48% of patients presented with hemorrhage and 34% with progressive deficits. 37% had angiographic steal and 21% developed postoperative hyperemic complications. 40% were under 30 years old, 45% were between 30 and 50 years of age, and 15% were over 50. TBF was less than 70 ml/100 gm/min in 32% of patients, between 70 and 84 ml/100 gm/min in 40%, and greater than 84 ml/100 gm/min in 27%. Female patients had higher TBF than males; 42% of females but only 17% of males had values greater than 84 ml/100 gm/min (p less than 0.05). A trend toward decreased TBF with advancing age was noted. Intracranial hemorrhage was associated with lower TBF; 47% of patients with hemorrhage and 19% of those without had TBF of less than 70 ml/100 gm/min (p less than 0.05). 89% of patients with AVMs less than 5 cm in diameter had TBF of less than or equal to 84 ml/100 gm/min, and 65% of those with larger AVMs had similarly low flows (p less than 0.05). A trend toward lower TBF was observed in patients with unfavorable outcomes.

Prolonged hypercarbia in the awake newborn piglet: effect on brain blood flow and cardiac output.

In adults, exposure to prolonged hypercarbia results in a normalization of the extravascular brain pH associated with a reduction in brain blood flow (BBF). Following prolonged hypercarbia, sudden normalization of the arterial PCO2 also produces a change in the extravascular brain pH to an alkaline state, resulting in a marked decrease in BBF. We examined these physiologic phenomena in newborn subjects by exposing seven awake, spontaneously breathing newborn piglets to 4 h of sustained hypercarbia (PaCO2: 60-70 mm Hg) followed by a 45-min normocarbic period. Total and regional BBF, cardiac output (radionuclide-labeled microsphere method), arterial blood pressure, plasma catecholamine and lactate concentrations, blood gases, oxygen contents, and hematocrits were measured during a baseline period, at 1/2, 2, and 4 h of sustained hypercarbia and 1/4 and 3/4 h following an abrupt onset of normocarbia. The initial 2.5-fold increase in total BBF during hypercarbia persisted for 2 h and at 4 h decreased significantly below the level of the 30-min hypercarbic measurement, although the values still remained 2-fold above the baseline values. Brain tissue pH was reduced at the onset of hypercarbia, remaining unchanged throughout the hypercarbic period. Both total BBF and brain tissue pH returned to baseline values following the return to normocarbia. Changes in regional BBF were similar to that of total BBF with the exception of the boundary zone (periventricular area in the frontoparietal region of the cerebrum, adjacent to the caudate nucleus) and the parietal area (site of the brain tissue pH electrode), where a significant decrease from the peak hyperemia was not observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension.

Profound arterial hypotension is a commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

Porcine Brain and Myocardial Perfusion During Enflurane Anesthesia Without and With Nitrous Oxide

Summary: Brain and myocardial blood flow (MBF) were examined in 10 previously instrumented swine during isocapnic conditions using 15 μm in diameter radionuclide-labeled microspheres that were injected into the left atrium. Minimum alveolar concentration (MAC) of enflurane required to prevent 50% of the pigs from responding by gross purposeful movement to a noxious stimulus was 1.66%. In pigs, 50% nitrous oxide decreased enflurane requirement for 1.0 MAC anesthesia by 0.82%. Each animal was studied during the following conditions: (a) unanesthetized (control); (b) 1.0 MAC enflurane anesthesia (1.66% end-tidal concentration); (c) 1.5 MAC (2.49%) enflurane anesthesia; (d) the equivalent of 1.0 and 1.5 MAC anesthesia produced by enflurane (0.84 and 1.67%) plus 50% nitrous oxide. Cerebral and total brain blood flow values were the same as control values during both levels of enflurane anesthesia. However, blood flow in the brainstem and cerebellum exhibited a dose-related increase; the increment of 28% for each of these regions at 1.5 MAC achieved statistical significance. Vascular resistance in all regions of the brain decreased with enflurane anesthesia. Substitution of 50% nitrous oxide for enflurane to maintain the same level of anesthesia markedly increased cerebral blood flow. At 1.0 and 1.5 MAC anesthesia produced using enflurane plus 50% nitrous oxide, cerebral blood flow was 151 and 183% of the control value, respectively. During enflurane plus nitrous oxide anesthesia equivalent to 1.5 MAC, cerebellar and brain stem blood flow were 135 and 180% of respective control values. MBF in all regions decreased in a doserelated manner with enflurane anesthesia. At 1.5 MAC enflurane, perfusion values in the walls of the left and the right ventricles were 52 and 59% of respective control values. During both levels of enflurane plus 50% nitrous oxide anesthesia, transmural MBF in all regions remained close to awake values. Subendocardial/subepicardial perfusion ratio in both ventricles exceeded 1.00 during all steps of the protocol, thereby suggesting that subendocardial O2 delivery kept pace with O2 demand. These experiments have demonstrated that usage of 50% N2O with enflurane to produce equipotent anesthesia resulted in a dramatic increase in cerebral blood flow while MBF remained near awake value.

Porcine Brain and Myocardial Perfusion During Enflurane Anesthesia Without and With Nitrous Oxide

Brain and myocardial blood flow (MBF) were examined in 10 previously instrumented swine during isocapnic conditions using 15 micron in diameter radionuclide-labeled microspheres that were injected into the left atrium. Minimum alveolar concentration (MAC) of enflurane required to prevent 50% of the pigs from responding by gross purposeful movement to a noxious stimulus was 1.66%. In pigs, 50% nitrous oxide decreased enflurane requirement for 1.0 MAC anesthesia by 0.82%. Each animal was studied during the following conditions: (a) unanesthetized (control); (b) 1.0 MAC enflurane anesthesia (1.66% end-tidal concentration); (c) 1.5 MAC (2.49%) enflurane anesthesia; (d) the equivalent of 1.0 and 1.5 MAC anesthesia produced by enflurane (0.84 and 1.67%) plus 50% nitrous oxide. Cerebral and total brain blood flow values were the same as control values during both levels of enflurane anesthesia. However, blood flow in the brainstem and cerebellum exhibited a dose-related increase; the increment of 28% for each of these regions at 1.5 MAC achieved statistical significance. Vascular resistance in all regions of the brain decreased with enflurane anesthesia. Substitution of 50% nitrous oxide for enflurane to maintain the same level of anesthesia markedly increased cerebral blood flow. At 1.0 and 1.5 MAC anesthesia produced using enflurane plus 50% nitrous oxide, cerebral blood flow was 151 and 183% of the control value, respectively. During enflurane plus nitrous oxide anesthesia equivalent to 1.5 MAC, cerebellar and brain stem blood flow were 135 and 180% of respective control values. MBF in all regions decreased in a dose-related manner with enflurane anesthesia. At 1.5 MAC enflurane, perfusion values in the walls of the left and the right ventricles were 52 and 59% of respective control values. During both levels of enflurane plus 50% nitrous oxide anesthesia, transmural MBF in all regions remained close to awake values. Subendocardial/subepicardial perfusion ration in both ventricles exceeded 1.00 during all steps of the protocol, thereby suggesting that subendocardial O2 delivery kept pace with O2 demand. These experiments have demonstrated that usage of 50% N2O with enflurane to produce equipotent anesthesia resulted in a dramatic increase in cerebral blood flow while MBF remained near awake value.

CHANGES IN EPINEPHRINE (E) AND MEAN ARTERIAL BLOOD PRESSURE (MABP) DURING HYPERCARBIA (HC): EFFECTS ON BRAIN BLOOD FLOW (BBF) IN THE NEWBORN PIGLET

We have previously shown that HC results in spontaneous elevations of MABP and pressure passive increases in brain blood flow (BBF) in the newborn piglet. We further analyzed the mechanism of this phenomena by correlating these changes with acid base and plasma E data in 20 awake newborn piglets where HC (PaCO2:50-60 mmHg) was induced by breathing 15% CO2. During HC, E, MABP, and BBF increased significantly (p<0.05). The increase in MABP was directly related to E (r=.71 p<0.001). However, both E and MABP also demonstrated a significant correlation with the decrease in arterial blood pH (pH vs E:r=-.91, p<0.001; pH vs MABP:r=-.84 p<0.001) and the increase in base deficit (BD) (BD vs E:r=0.83, p<0.001), BD vs MABP:r=0.84 p<0.001). PaCO2 was not related to the E or MABP increase. The increase in total BBF (TBBF) and regional BBF were directly related to the elevations of MABP (TBBF:r=0.58 p<0.01 cerebrum r=0.57 p<0.01, cerebellum:r=0.67 p<0.01, boundary zone r=0.62 p<0.01 and periventricular area r=.76 p<0.001). We conclude that HC induced hypertension and brain hyperperfusion is partly due to catecholamine (epineprine) release which in turn is mediated through concurrent metabolic acidosis.

False positive digoxin results in infant sera with some commercial RIA methodologies

The normal aging human brain experiences global decreases in metabolism, but whether this affects the topography of brain metabolism is unknown. Here we describe PET-based measurements of brain glucose uptake, oxygen utilization, and blood flow in cognitively normal adults from 20 to 82 years of age. Age-related decreases in brain glucose uptake exceed that of oxygen use, resulting in loss of brain aerobic glycolysis (AG). Whereas the topographies of total brain glucose uptake, oxygen utilization, and blood flow remain largely stable with age, brain AG topography changes significantly. Brain regions with high AG in young adults show the greatest change, as do regions with prolonged developmental transcriptional features (i.e., neoteny). The normal aging human brain thus undergoes characteristic metabolic changes, largely driven by global loss and topographic changes in brain AG.

Effect of aminophylline on brain blood flow in the newborn piglet.

The effect of 6 mg/kg of aminophylline on brain blood flow was examined in newborn piglets. Arterial plasma aminophylline concentration averaged 7 mg/l. Total brain, regional brain (cerebrum, cerebellum and stem) and eye blood flow as well as the total brain oxygen consumption were not altered by aminophylline treatment. Choroid plexus blood flow was five times higher than the total brain blood flow in these newborn piglets. In contrast to brain blood flow, choroid plexus blood flow decreased significantly following aminophylline administration.

Ventral medullary extracellular fluid pH and blood flow during hypoxia.

Vascular responses of the ventral medulla and total brain to 30-60 min of isocapnic hypoxia (PaO2 = 32 +/- 2 Torr) were examined using radioactive microspheres in anesthetized, paralyzed, and artificially ventilated cats. Ventral medullary extracellular fluid (ECF) pH was measured using pH microelectrodes with tip diameters of 1-2 micrometers. Total brain blood flow (Q) increased significantly from a control value of 53 +/- 8 (mean +/- SE) to 160 +/- 42 ml.100 g-1.min-1 following 30-60 min of hypoxia. Ventral medullary Q increased from 28 +/- 5 to 97 +/- 20 ml.100 g-1.min-1 and ECF pH decreased by 0.15 +/- 0.06 pH U. Q responses are attributable to decreased vascular resistance as arterial pressure remained constant. The sensitivity of the ventral medullary vasculature to isocapnic hypoxia did not differ from that of the brain as a whole. The results show that under the conditions of our experiment, the ventral medullary vascular response to hypoxia is not sufficient to stabilize local ECF pH. The observation of simultaneously reduced pH and increased Q is consistent with a role for ECF H+ in mediating the cerebrovascular response to hypoxia.

Sympathetic regulation of cephalic blood flow.

Blood flow to bilateral tissues (cranial and extracranial) was studied by means of the particle distribution method in two groups of anesthetized dogs (five using 25-mu radioactive microspheres, six using 15-mu microspheres) and five anesthetized stumptail Macaques monkeys (8-mj spheres) during unilateral sympathetic stimulation. The stimulatory parameters were adjusted to produce maximum pupillary dilatation. In the five dogs hemispheric and regional cerebral blood flow decreased but not significantly. Flow to the extracranial tissues decreased 82%. Hemispheric brain blood flow averaged 0.70 ml/min/gm for Paco2 of 40 mm Hg. In the six dogs sympathetic stimulation did not significantly decrease cerebral blood flow but decreased flow to extracranial tissues (72.3%). At an average Paco2 of 33.2 mm Hg, hemispheric blood flow to the unstimulated side averaged 0.51 ml/min/gm. In the five monkeys findings were essentially the same as those observed in the dogs. The hemispheric blood flow averaged 0.36 ml/min/gm on the nonstimulated side for an average Paco2 of 36.6 mm Hg. Under the conditions studied, electrical stimulation of the cervical sympathetic nerves does not appear to modify regional or total brain blood flow in dogs and Macaques monkeys. The vascular response in oral and other extracranial tissues is very dramatic, however.

Cerebral fluid dynamics and brain regional blood flow in experimental hydrocephalus.

Cerebral blood flow was measured by the indicator fractionation technique in normal, acute hydrocephalic, chronic compensated hydrocephalic and craniectomized hydrocephalic cats. In the five normal cats the mean total brain blood flow was 136.1 ml/min/100 g dry weight. The six acute hydrocephalic animals demonstrated a relatively uniform 22% reduction in total blood flow. In eight chronic hydrocephalic cats CBF increased to the point where there was only an overall 7% decrease. In three hydrocephalic and craniectomized cats the CBF was reduced by 30.6%. In the acute phases there was a decrease in the number of blood vessels. Chronic compensated hydrocephalic brains had somewhat more vessels than the normal, whereas the craniectomized, massively hydrocephalic brain had a dramatic increase in both the number and caliber of blood vessels. These results clearly demonstrate that in acute obstructive hydrocephalus in cats, there is a significant decrease in CBF. The blood vessels revert to normal in shunted cats.

Total cerebral blood flow in the monkey measured by hydrogen clearance.

Simple hydrogen-sensitive polarographical electrodes of thin platinum wire were inserted into the torcular Herophili of Rhesus monkeys. Hydrogen was administered by inhalation for ten minutes, after which the hydrogen clearance was recorded from torcular blood. At a Paco 2 of 32 mm Hg (SD ± 2.3), flow in the fast flow compartment was 102 ml/100 gm per minute (SD ± 19.1), and flow in the slow flow compartment was 28 ml/100 gm per minute (SD ± 5.8). Mean total cerebral blood flow was 52 ml/100 gm per minute (SD ± 10.5). Coefficient of variation was less than 10%. Our experience suggests that one may reliably measure average total cerebral blood flow in the experimental setting by following the clearance of hydrogen from torcular blood. The method is relatively simple, inexpensive and radiation-free. It can be easily combined with the standard hydrogen clearance technique for measuring local tissue blood flow, thereby permitting the simultaneous recording of both local and total brain blood flow.

Regional cerebral blood flow in dogs using a particle-distribution method.

SummaryIn this study a known activity of microspheres labeled with 169Yb was injected into the left heart of lightly anesthetized dogs. Prior to injection of microspheres, cardiac output was determined by the isotope dilution technique using 42K or 86Rb. Blood flow to the cerebral cortex, white matter, thalamus, cerebellum, and caudate nucleus was determined in ml/min·g from fractional distribution of particles in tissue samples. Total brain blood flow in ml/min·g was estimated from the radioactivity observed in the remaining brain tissue. Comparison of dogs breathing air with dogs breathing 5% CO2 showed that flow values were significantly increased (p<.05) with 5% CO2 for all areas except white matter. Old dogs tended to show higher flow values than young dogs. Flow values obtained in this study were compared with values reported by others using different methods. The distribution of the particles in the brain was checked by autoradiography.