Cerebral Venous Oxygen Research Articles

Effectiveness of the Cobra aortic catheter for dual-temperature management during adult cardiac surgery

Objectives: In animals the Cardeon Cobra catheter (Cardeon Corp, Cupertino, Calif) allows independent control of aortic arch and descending aortic temperatures and profoundly reduces cerebral embolization during bypass. This investigation describes the first clinical use of the device during adult cardiac surgery. The purpose of the study was to confirm that the Cobra catheter delivers adequate cerebral and systemic perfusion while providing simultaneous cerebral hypothermia and systemic normothermia during cardiopulmonary bypass. Methods: In a prospective multicenter study the Cobra aortic catheter was placed in 20 adults undergoing cardiopulmonary bypass. Arch and corporeal temperatures, bypass flows, and arterial blood pressures were recorded intraoperatively. Jugular bulb and mixed venous oxygen saturation was used to assess the adequacy of cerebral and systemic perfusion. Results: Surgeons at 3 institutions placed the Cobra catheter in patients undergoing coronary artery bypass grafting (n = 13), valve (n = 3), and combined valve-bypass (n = 4) operations. Mean total bypass flows of 2.1 ± 0.2 L · min−1 · −2 maintained mean arterial pressures in arch and descending aortic circulations of greater than 55 mm Hg. A mean differential of 4.3°C between arch and descending aortic temperatures was established before crossclamp application, and a mean maximum temperature differential of 7°C was established during bypass. A 2.4°C temperature differential was maintained at crossclamp removal. Cerebral and systemic venous oxygen saturation remained greater than 65% during bypass. Conclusions: The Cobra device met all expectations for an arterial cannula with adequate perfusion to the arch and corporeal circulations. Dual perfusion with the Cobra catheter allows for independent temperature control during cardiopulmonary bypass with simultaneous cerebral hypothermia and systemic normothermia.J Thorac Cardiovasc Surg 2003;125:378-84

Developmental and neurologic outcomes late after neonatal corrective surgery

J Thorac Cardiovasc Surg 2002;124:425-7

Optoacoustic technique for noninvasive monitoring of blood oxygenation: a feasibility study.

Replacement of invasive monitoring of cerebral venous oxygenation with noninvasive techniques offers great promise in the management of life-threatening neurologic illnesses including traumatic brain injury. We developed and built an optoacoustic system to noninvasively monitor cerebral venous oxygenation; the system includes a nanosecond Nd:YAG laser and a specially designed optoacoustic probe. We tested the system in vitro in sheep blood with experimentally varied oxygenation. Our results demonstrated that (1) the amplitude and temporal profile of the optoacoustic waves increase with blood oxygenation in the range from 24% to 92%, (2) optoacoustic signals can be detected despite optical and acoustic attenuation by thick bone, and (3) the system is capable of real-time and continuous measurements. These results suggest that the optoacoustic technique is technically feasible for continuous, noninvasive monitoring of cerebral venous oxygenation.

Continuous jugular venous oximetry in the neurointensive care unit--a brief review.

To describe the technique of continuous jugular venous oxygen saturation (SjVO(2)) monitoring and review its applications in the neurointensive care unit (NICU), with special reference to the management of raised intracranial pressure (ICP) following severe acute brain injury. This narrative review is based on a selection of current literature on SjVO(2) monitoring in conjunction with local experience using this technique. Despite limitations, the use of SjVO(2) monitoring has the potential to impact on patient care in the NICU. The placement of the catheter is relatively simple. Studies have confirmed that abnormalities in cerebral venous oxygen saturation are associated with adverse outcome following traumatic brain injury. There is evidence that SjVO(2) may be a useful adjunct to ICP monitoring of patients with intracranial hypertension. Furthermore, managing cerebral extraction of oxygen in conjunction with cerebral perfusion pressure may result in an improved outcome. Further research in this area is needed. Other indications for SjVO(2) monitoring include subarachnoid hemorrhage, cardiopulmonary bypass and following ischemic stroke. In the past, the management of severe acute brain injury was targeted at ICP and perfusion pressure with little consideration for the metabolic requirements of the injured brain. SjVO(2) monitoring is another tool the intensivist can use to obtain information about the global oxygen requirements of the injured brain on a continuous basis. Whether this will impact on care in the long term remains to be seen.

Adequate cerebral perfusion pressure during rewarming to prevent ischemic deterioration after therapeutic hypothermia

Ischemic deterioration during rewarming is one of the most notable clinical complications after successful therapeutic cerebral hypothermia, but the mechanism is not completely understood. Hypothermia may cause vasoconstriction and relative ischemia, especially with insufficient cerebral perfusion pressure (CPP). Various parameters were evaluated to determine the critical CPP threshold to avoid ischemia during rewarming. Cat experimental head injury was induced by inflating an epidural rubber balloon, and intracranial pressure was maintained at 30 mmHg. During rewarming after cerebral hypothermia, CPP was maintained at ≥ 120 mmHg (n = 16), 90 mmHg (n = 11), 60 mmHg (n = 11), and 40 mmHg (n = 4) by controlling the blood pressure. Cerebral blood flow, cerebral metabolic rate for oxygen, arteriovenous difference of oxygen (AVDO2), cerebral venous oxygen saturation (ScvO2), and extracellular glutamate concentrations were monitored by glutamate oxidase electrode. After rewarming, the cerebral metabolic parameters were almost restored to the pre-injury level in animals with CPP of more than 90 mmHg. However, in the animals with CPP = 60 mmHg, all parameters significantly deteriorated and indicated misery perfusion; ScvO2 was low (29.5 ± 1.1%), AVDO2 was significantly high (9.9 ± 0.8 ml 100 g-1 min-1) (one-way analysis of variance, p < 0.05), and electron microscopic features showed subcellular ischemic change. Extracellular glutamate significantly increased during the rewarming period only in the CPP = 40 mmHg group. CPP less than 60 mmHg during rewarming causes secondary ischemic insult, which might indicate continuation of cerebral vasoconstriction in hypothermia. CPP higher than 90 mmHg is required to avoid the potential risk of relative ischemia after hypothermia. [Neurol Res 2002; 24: 271-280]

Effect of Combined Hyperventilation and Mannitol on Cerebral Blood Flow and Cerebral O2 Metabolism during a Craniectomy

Background: There are therapies to lower intracranial pressure (ICP) including head elevation, hyperventilation, diuretics injection, intravenous mannitol, hypothermia, cerebrospinal fluid drainage, and cerebral resection in neurosurgical patients. However in recent reports, hyperventilation followed by mannitol administration may lead to cerebral ischemia. Therefore, we investigated the effect of 0.5 -1.0 g/kg mannitol administration on jugular venous oxygen saturation () and cerebral arterialjugular venous oxygen content difference () at 25-30 mmHg and 35-40 mmHg in patients undergoing neurosurgery. Methods: We studied 17 patients undergoing neurosurgery in the Ajou University Hospital. Anesthesia was induced with fentanyl, midazolam, thiopental, and vecuronium, and maintained with -Air-Isoflorane, a continuous infusion of fentanyl, and vecuronium. Patients were divided into two groups. Group 1 (n = 10) which is 25-30 mmHg and Group 2 (n = 7) which is 35-40 mmHg by controlling ventilator. Measurements of and in following time intervals: I = preinjection of mannitol, II = postinjection 20 minutes of mannitol, III = postinjection 40 minutes of mannitol were obtained for each group. 0.5-1.0 g/kg mannitol was administered intravenously just at duramater opening. Results: Hemodynamics and hematologics were not significantly different among the two groups. of each group are as follows; Group 1; I (70.3 8.1%), II (66.3 6.9%), III (69.1 7.9%) and Group 2; I (78.6 7.4%), II (75.1 8.1%), III (76.0 11.2%). Hyperventilation significantly decreased . was not significantly different but in II was significantly decreased compared with I and III in Group 1 (20% patients). Conclusions: Mannitol produced a change of and during hyperventilation. Therefore, intravenous mannitol during hyperventilation should be given cautiously according to the patients status because it may cause cerebral ischemia in critical patients.

Simultaneous measurement of local cortical blood flow and tissue oxygen saturation by Near infra-red Laser Doppler flowmetry and remission spectroscopy in the pig brain.

In the current study we evaluated the combined use of Near-infrared Laser-Doppler flowmetry (NiLDF) and Remission Spectroscopy (RS) for measurement of regional perfusion and oxygen saturation of the cerebral cortex. An epidural probe for combined measurements of NiLDF and RS was placed above the parietal or frontal cortex of nine anesthetized juvenile pigs. Cerebral perfusion pressure (CPP) was stepwise decreased by intracisternal infusion of artificial CSF at clamped arterial blood pressure (baseline, CPP50, CPP40, CPP30 mmHg, ischemia). Subsequent reperfusion was followed for 3 h. Regional cerebral blood flow (rCBF) was measured with colored microspheres (CMS) and compared with corresponding NiLDF values during CMS injection. Cerebral venous oxygen saturation was measured in blood samples withdrawn from the sagittal sinus and compared with simultaneous recordings of tissue oxygenation during blood withdrawal. Linear regression analysis resulted in a significant correlation (p < 0.001) for changes in regional perfusion during CPP decrease and reperfusion, as measured with CMS and NiLDF (r = 0.92, n = 39). A significant correlation was also found for tissue oxygen saturation--as measured with RS--and cerebral venous oxygen saturation (r = 0.85, n = 67). Although the problem of spatial variability remains to be solved, the combined use of NiLDF and RS allows continuous and non-invasive monitoring of changes of key parameters of oxygen metabolism within the cerebral cortex.

Appropriate cerebral perfusion pressure during rewarming after therapeutic hypothermia.

This study evaluated the cerebral ischemic parameters during the rewarming period after therapeutic hypothermia to determine the critical cerebral perfusion pressure (CPP) threshold to avoid ischemic deterioration. Cat experimental head injury was induced by inflation of an epidural rubber balloon to maintain intracranial pressure at 30 mmHg under hypothermia. During the rewarming period, CPP was maintained at > or = 120 mmHg, 90 mmHg, and 60 mmHg by controlling the blood pressure. CBF, CMRO2, AVDO2, and cerebral venous oxygen saturation (ScvO2) were measured. Brain extracellular glutamate concentrations were also measured by a dialysis electrode. Histological preparations of all brains were examined under an electron microscope. The cerebral metabolic parameters in animals with CPP of more than 90 mmHg returned to the base values after rewarming. However, ScvO2 was significantly lower (27 +/- 6%) and AVDO2 was significantly higher (9.4 +/- 1.8 ml/100 g/min) after rewarming in the animals with CPP = 60 mmHg, which indicated misery perfusion. Animals with CPP = 60 mmHg also showed increased extracellular glutamate concentration and histological ischemic damage (mitochondrial swelling). CPP of 60 mmHg during the rewarming period is associated with irreversible ischemia, which indicates continuation of cerebral vasoconstriction. Therefore, a CPP of greater than 90 mmHg is required to avoid cerebral ischemia.

Systems analysis of functional magnetic resonance imaging data using a physiologic model of venous oxygenation.

The authors revisit a simple mathematical model, presented in previous work, that characterizes the response of cerebral venous oxygenation to changes in blood flow and oxygen consumption. This physiologically based model can qualitatively duplicate the results of several recent empirical studies in which other authors have tested the hypothesis of linearity in the functional magnetic resonance imaging (fMRI) response to task activation, in that the experimentally found nearly linear behavior of the system and also its subtle departures from linearity are both predicted by simulations of the model. The model is simple enough that its equations can be explicitly solved. Moreover, an amended model that incorporates a varying cerebral blood volume parameter is found to have similar if not better consistency with the empirical data; indeed, this "extended" model is shown to be solvable by the same differential equation as the authors' simple one, wherein the volume is fixed as a constant. These investigations lend further indirect support to the blood oxygen level-dependent hypothesis of venous deoxyhemoglobin as the primary mechanism for fMRI signal changes during task activation, as well as for the authors' simple system as a useful physiologic model thereof. Although the authors' mathematical model does not formally represent a linear system with respect to the flow input, its underlying linear character may help partially explain the "nearly" linear behavior of the fMRI response.

Effect of hyperventilation on brain tissue oxygenation and cerebrovenous PO 2 in rats

Previous studies have shown that cortical tissue oxygenation is impaired during hyperventilation. However, it is important to quantify the effect of hyperventilation on brain tissue PO 2 and cerebrovenous PO 2 simultaneously especially since cerebral venous oxygenation is often used to assess brain tissue oxygenation. The present study was designed to measure the sagittal sinus PO 2 (PvO 2), brain tissue PO 2 in the thalamus (PtO 2), and brain temperature (Bt) simultaneously during acute hyperventilation. Isoflurane-anesthetized rats were hyperventilated for 10 min during which time the arterial carbon dioxide tension (PaCO 2) dropped from 40.3+4.9 mmHg to 23.5+2.8 mmHg. PtO 2 declined from 26.0±4.2 mmHg to 14.8±5.2 mmHg ( P=0.004) while brain temperature decreased from 36.5+0.3°C to 36.2+0.3°C ( P=0.02). However, PvO 2 and arterial blood pressure (BP) did not change during hyperventilation. The maintenance of PvO 2 when perfusion is thought to decline and PtO 2 decreases suggests that there may be a diffusion limitation, possibly due to selective perfusion. Therefore, cerebrovenous PO 2 may not give a good assessment of brain tissue oxygenation especially in conditions of acute hyperventilation, and deeper brain regions other than the cortex also show impaired tissue oxygenation following hyperventilation.

Effect of AMPA on cerebral cortical oxygen balance of ischemic rat brain.

We tested the hypothesis that the excitatory neurotransmitter receptor agonist, alpha amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), would worsen cerebral cortical oxygen supply/consumption balance during focal ischemia. In this study, we compared regional cerebral blood flow, arterial and venous O2 saturation, O2 extraction and oxygen consumption of ischemic and AMPA treated ischemic and control regions of rat brain. Ischemia was induced by middle cerebral artery (MCA) occlusion in isoflurane (1.4%) anesthetized Wistar rats. Twenty minutes after MCA occlusion, 10(-5) M AMPA was applied to the ischemic cortex (IC) for a period of 40 min; the fluid was changed every 10 min. After 1 hr of ischemia, animals were sacrificed and regional cerebral blood flow (rCBF) was determined using the C14-iodoantipyrine autoradiographic technique. Regional arterial and venous oxygen saturation were determined microspectrophotometrically. In control, the cerebral blood flow and oxygen consumption of the IC were significantly lower than the contralateral cortex (rCBF: 46 +/- 20 vs. 81 +/- 39 ml/min/100g, O2 consumption: 2.8 +/- 1.4 vs. 3.6 +/- 1.4 ml O2/min/100g). 10(-5) M AMPA did not significantly alter regional cerebral blood flow and oxygen consumption of the IC, but did decrease the average venous O2 saturation of the IC from 50.2 +/- 3.9% to 46.7 +/- 1.6%. AMPA also significantly increased the frequency of small veins with less than 45% O2 saturation in the IC (8 out of 56 veins in IC vs. 18 out of 56 veins in AMPA treated IC). Thus, topical application of 10(-5) M AMPA to the ischemic area worsens cerebral O2 balance and suggests that excitatory amino acids contribute to the degree of cerebral ischemia.

No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury.

Hyperventilation has been used for many years in the management of patients with traumatic brain injury (TBI). Concern has been raised that hyperventilation could lead to cerebral ischemia; these concerns have been magnified by reports of reduced cerebral blood flow (CBF) early after severe TBI. The authors tested the hypothesis that moderate hyperventilation induced early after TBI would not produce a reduction in CBF severe enough to cause cerebral energy failure (CBF that is insufficient to meet metabolic needs). Nine patients were studied a mean of 11.2+/-1.6 hours (range 8-14 hours) after TBI occurred. The patients' mean Glasgow Coma Scale score was 5.6+/-1.8 and their mean age 27+/-9 years; eight of the patients were male. Intracranial pressure (ICP), mean arterial blood pressure, and jugular venous oxygen content were monitored and cerebral perfusion pressure was maintained at a level higher than 70 mm Hg by using vasopressors when needed. Measurements of CBF, cerebral blood volume (CBV), cerebral metabolic rate for oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral venous oxygen content (CvO2) were made before and after 30 minutes of hyperventilation to a PaCO2 of 30+/-2 mm Hg. Ten age-matched healthy volunteers were used as normocapnic controls. Global CBF, CBV, and CvO2 did not differ between the two groups, but in the TBI patients CMRO2 and OEF were reduced (1.59+/-0.44 ml/100 g/minute [p < 0.01] and 0.31+/-0.06 [p < 0.0001], respectively). During hyperventilation, global CBF decreased to 25.5+/-8.7 ml/100 g/minute (p < 0.0009), CBV fell to 2.8+/-0.56 ml/100 g (p < 0.001), OEF rose to 0.45+/-0.13 (p < 0.02), and CvO2 fell to 8.3+/-3 vol% (p < 0.02); CMRO2 remained unchanged. The authors conclude that early, brief, moderate hyperventilation does not impair global cerebral metabolism in patients with severe TBI and, thus, is unlikely to cause further neurological injury. Additional studies are needed to assess focal changes, the effects of more severe hyperventilation, and the effects of hyperventilation in the setting of increased ICP.

The Effect of Hyperventilation and Hyperoxia on Cerebral Venous Oxygen Saturation in Patients with Traumatic Brain Injury

The Effect of Hyperventilation and Hyperoxia on Cerebral Venous Oxygen Saturation in Patients with Traumatic Brain Injury

Cerebral venous and tissue gases and arteriovenous shunting in the dog.

Cerebral venous blood gas values have been used to indicate brain tissue oxygenation. However, it is not clear how cerebral tissue and venous measures may vary under physiologic conditions caused by arteriovenous shunt. The purpose of this study was to measure brain tissue and local cerebral venous oxygen (PO2) and carbon dioxide (P(CO2)) partial pressure during changes in ventilation and to calculate shunt fraction. Eight dogs were anesthetized with isoflurane. After a craniotomy, a Neurotrend probe (Diametrics Inc., St. Paul, MN) that measures P(O2), P(CO2), pH, and temperature was inserted into brain tissue, and a small vein that drained the same tissue was catheterized. Arterial, cerebral venous, and brain tissue P(O2) and Pco2 were measured during random changes in ventilation to produce five different levels of inspired oxygen (room air, 40%, 60%, 80%, 95%) at each of three different end-tidal Pco2 (20 mm Hg, 40 mm Hg, 60 mm Hg). Arteriovenous shunt was calculated from oxygen and C(O2) content in artery, vein, and tissue, representing capillary. Tissue P(CO2) was 8 mm Hg greater than vein Pco2 during hypocapnia and this difference increased to 20 mm Hg during hypercapnia. Vein P(O2) was 8 mm Hg higher than tissue P(O2) during hypocapnia, and this difference increased to 40 mm Hg during hypercapnia. Shunt fraction increased from 10%-20% during hypocapnia to 50%-60% during hypercapnia. These results show that brain vein and tissue P(O2) and P(CO2) differ because of arteriovenous shunting and this difference is increased as end-tidal P(CO2) increases. We found, in dogs, that the gradient between brain venous and tissue P(O2) and PCO2 is increased with increased arterial P(CO2). The divergence between tissue and venous gases can be described by arterial to venous shunting.

Misery perfusion caused by cerebral hypothermia improved by vasopressor administration

Therapeutic cerebral hypothermia is widely used for the treatment of severe head injury and cerebral ischemia. The effects of cerebral hypothermia on the cerebral blood flow (CBF) and metabolism, and cerebral vasculature in the normal brain were investigated. Thirty-four adult cats were divided into four groups. CBF was monitored by hydrogen clearance. Arteriovenous oxygen difference (AVD02) and cerebral venous oxygen saturation (ScvO2) were measured in blood samples from the superior sagittal sinus. The cerebral metabolic rate of oxygen (CMRO2) and cerebral vascular resistance (CVR) were calculated. The cerebral blood volume (CBV) was measured using technetium-99m-labeled human serum albumin in 12 cats. Deep cerebral temperature was cooled from 37° C to 25° C using a water-circulating blanket. In the hypothermia group (Croup A: n = 10), CBF (51.2 ± 8.3 ml 100 g–1 min–1 at 37° C) decreased with lower brain temperature (6.1 ±2.7 at 25°C). CMRO2 (2.24 ± 0.75ml 100g–1 min–1 at 37° C) was also decreased (0.52 ±0.20 at25°C). AVDO2 (4.3 ± 1.0 ml 100 g–1 min–1 at 37° C) increased significantly at 31°C (6.6 ± 1.8; p < 0.05) and ScvO2 (67.8 ± 7.9% at 37°C) decreased significantly at 29° C (53.7± 9.7; p < 0.05). CBV (5.3 ± 1.2% at 37°C) decreased significantly at 29°C (3.7± 1.0;p < 0.05) and CVR (3.2 ±0.7 mmHg ml–1 100g–1 min–1 at 37° C) increased significantly at 29° C (13.8 ±5.2; p < 0.01). The combined effect of hypothermia with vasopressor (noradrenalin) (Croup B: n = 6) or barbiturate (thiopental) administration (Croup C: n = 6) on the cerebral metabolic parameters were also examined. Hypothermia with noradrenalin administration significantly improved the ischemic parameters (AVDO2 was 4.7± 1.4ml 100g min–1 at 31°C and ScvO2 was 72.2±6.4% at 29°C). However, hypothermia with barbiturate administration did not improve these metabolic parameters. These results suggest that hypothermia may cause vasoconstriction and misery perfusion in the brain. This potential risk of relative ischemia can be avoided by combination with vasopressor administration. [Neurol Res 1999; 21: 585–592]

Cerebral Venous and Tissue Gases and Arteriovenous Shunting in the Dog

Cerebral venous blood gas values have been used to indicate brain tissue oxygenation. However, it is not clear how cerebral tissue and venous measures may vary under physiologic conditions caused by arteriovenous shunt. The purpose of this study was to measure brain tissue and local cerebral venous oxygen (PO2) and carbon dioxide (PCO2) partial pressure during changes in ventilation and to calculate shunt fraction. Eight dogs were anesthetized with isoflurane. After a craniotomy, a Neurotrend probe (Diametrics Inc., St. Paul, MN) that measures PO2, PCO2, pH, and temperature was inserted into brain tissue, and a small vein that drained the same tissue was catheterized. Arterial, cerebral venous, and brain tissue PO2 and PCO2 were measured during random changes in ventilation to produce five different levels of inspired oxygen (room air, 40%, 60%, 80%, 95%) at each of three different end-tidal PCO2 (20 mm Hg, 40 mm Hg, 60 mm Hg). Arteriovenous shunt was calculated from oxygen and CO2 content in artery, vein, and tissue, representing capillary. Tissue PCO2 was 8 mm Hg greater than vein PCO2 during hypocapnia and this difference increased to 20 mm Hg during hypercapnia. Vein PO2 was 8 mm Hg higher than tissue PO2 during hypocapnia, and this difference increased to 40 mm Hg during hypercapnia. Shunt fraction increased from 10%–20% during hypocapnia to 50%–60% during hypercapnia. These results show that brain vein and tissue PO2 and PCO2 differ because of arteriovenous shunting and this difference is increased as end-tidal PCO2 increases. Implications We found, in dogs, that the gradient between brain venous and tissue PO2 and PCO2 is increased with increased arterial PCO2. The divergence between tissue and venous gases can be described by arterial to venous shunting.

Delayed impairment of cerebral oxygenation after deep hypothermic circulatory arrest in children

Background. Clinical studies of deep hypothermic circulatory arrest (DHCA) have focused only on the immediate postoperative period. However, experimental findings suggest impairment of cerebral oxygenation at 2 to 8 hours after reperfusion. Methods. In 10 children who had DHCA for heart operations, transcerebral differences of hemoglobin oxygen saturation and plasma hypoxanthine, xanthine, and lactoferrin concentrations were measured in concurrently obtained cerebral venous, arterial, and mixed venous samples up to 10 hours postoperatively. Results. Compared with preoperative levels (57% ± 7%), cerebral venous oxygen saturation was not significantly reduced until 2 hours (44% ± 6%) and 6 hours (42% ± 5%) after DHCA ( p < 0.05). A statistically significant transcerebral (ie, cerebral vein versus artery) concentration difference of hypoxanthine was observed at 30 minutes (3.6 ± 0.9 μmol/L), 1 hour (3.4 ± 1.1 μmol/L), and 2 hours (3.1 ± 0.8 μmol/L) after DHCA but not preoperatively (0.4 ± 0.2 μmol/L). A transcerebral concentration difference of lactoferrin occurred 30 minutes after DHCA (196 ± 70 μg/mL) but not preoperatively (16 ± 20 μg/mL). Conclusions. Cerebral venous oxygen saturation of hemoglobin decreased as late as 2 to 6 hours after DHCA, in association with impaired cerebral energy status. Neutrophil activation in the cerebral circulation occurred 30 minutes after reperfusion.

Propranolol blocks cocaine-induced cerebral vasodilation in newborn sheep.

The objective of this study was to test the hypothesis that cocaine-induced cerebral vasodilation in newborn sheep is mediated via beta-adrenergic receptor activation. The cerebral effects of a single intravenous injection of cocaine (4 mg/kg) given 30 mins after pretreatment with propranolol (1 mg/kg) were studied and compared with the results from a previous study using an identical cocaine protocol without propranolol pretreatment. Seven chronically catheterized, unanesthetized newborn sheep (6 +/- 1 days old). Cerebral blood flow using radiolabeled microspheres, mean arterial blood pressure (MAP), heart rate, and cerebral arterial and venous oxygen content were measured at baseline, after administration of propranolol, and 0.5, 5, 15, and 60 mins after cocaine injection. Cerebrovascular resistance was calculated as the MAP divided by the cerebral blood flow. Propranolol injection alone caused no systemic or cerebral physiologic changes other than an 11 +/- 2% (mean +/- SEM) decrease in heart rate, which was sustained after cocaine injection. In contrast to previous studies showing cerebral vasodilation (25% decrease in cerebrovascular resistance) and acute hypertension (57% increase in MAP) 30 secs after cocaine injection, there were no changes in cerebrovascular resistance after cocaine injection and after propranolol pretreatment and there was only a 23 +/- 7% increase in MAP 30 secs after injection, with a return to baseline by 15 mins. Cocaine and norepinephrine levels were similar to those previously reported in the newborn sheep after an injection of 4 mg/kg cocaine. Propranolol blocks cocaine-induced cerebral vasodilation and blunts the acute hypertension in newborn sheep, suggesting that cocaine's cerebrovascular effects in the developing brain are mediated, at least in part, by beta-adrenergic receptor activation.

Quantification of dynamic changes in cerebral venous oxygenation with MR phase imaging at 1.9 T

A double-echo magnetic resonance (MR) phase imaging method was used to measure the time-dependent changes in regional cerebral venous blood oxygenation during neural stimulation. Our results showed that a finger opposition task induced an absolute increase of blood oxygenation level of deltaY = 0.16+/-0.05 (n = 6), which was measured in the small veins located in the left central sulcus. It was observed that there is a long temporal delay of approximately 27 sec after the onset of the task to reach the steady-state venous oxygenation. This work demonstrated that MRI is a powerful clinical tool for in vivo monitoring of the dynamic nature of organ-specific venous blood oxygenation.

Quantification of dynamic changes in cerebral venous oxygenation with MR phase imaging at 1.9 T

Quantification of dynamic changes in cerebral venous oxygenation with MR phase imaging at 1.9 T