A venous outflow method for continuously monitoring cerebral blood flow in the rat

1986 ◽  
Vol 250 (2) ◽  
pp. H304-H312
Author(s):  
S. Morii ◽  
A. C. Ngai ◽  
K. R. Ko ◽  
H. R. Winn
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Venous Blood ◽  
Tracer Technique ◽  
Excellent Correlation ◽  
Venous Outflow ◽  
Sagittal Sinus ◽  
Wide Range ◽  
Microsphere Method

We analyzed the retroglenoid venous outflow (VOF) technique in the rat to document the validity of this method of measuring cerebral blood flow (CBF). Stereotypic changes in CBF were obtained with VOF during hypercarbia and hypotension. O2 content of retroglenoid venous blood did not differ significantly from O2 content of blood obtained from the sagittal sinus, suggesting minimal extracerebral contamination of the retroglenoid venous blood. This lack of extracerebral contamination was further analyzed using a double tracer technique (125I-labeled serum albumin, 22Na) that quantitated minimal extracerebral contamination in the retroglenoid vein. CBF measurements were made simultaneously using microsphere and VOF methods, and excellent correlation was found between the two techniques over a wide range of CBF during normoxia, hypoxia, and normoxic hypocarbia and hypercarbia. However, a decrease in the ratio of VOF to microsphere CBF was observed during severe normoxic hypotension (mean arterial pressure = 41 +/- 4 mmHg). VOF represented 18% of total CBF as measured by microsphere method. This study indicates that the retroglenoid outflow technique in rats is a valid method of measuring CBF.

Cerebral sodium extraction in the dog: a test for extracerebral contamination

1980 ◽  
Vol 238 (6) ◽  
pp. H868-H875
Author(s):  
L. G. D'Alecy ◽  
C. J. Rose ◽  
S. A. Sellers ◽  
J. P. Manfredi
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Sympathetic Stimulation ◽  
Single Drop ◽  
Venous Outflow ◽  
Sagittal Sinus ◽  
The Common ◽  
The Mean ◽  
Alpha Chloralose

The single-pass extraction of sodium was measured with and without sympathetic stimulation in dogs anesthetized with alpha-chloralose. A mixture of the test (24Na) and reference ([125I]RISA) substances was injected as a bolus into the common carotid artery. Single-drop samples were taken at approximately 1-s intervals from the sagittal sinus and the temporal sinus while cerebral blood flow was continuously measured at the temporal sinus by the venous outflow technique. The extraction measurements were used to test for extracerebral contamination of venous outflow. The mean integral extraction determined from sagittal sinus samples was 2.2% during control conditions and 3.0% during sympathetic stimulation. The mean temporal sinus extraction of sodium was 6.9% during control and 2.7% during sympathetic stimulation. If true cerebral sodium extraction is assumed to be 1.4% and extracerebral sodium extraction is 60%, then these data indicate that extracerebral contamination is less than 10%.

Cerebral venous outflow and arterial microsphere flow with elevated venous pressure

1983 ◽  
Vol 244 (4) ◽  
pp. H505-H512
Author(s):  
E. M. Wagner ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Cerebral Autoregulation ◽  
Regional Cerebral Blood Flow ◽  
Venous Pressure ◽  
Regional Cerebral Blood ◽  
Venous Outflow ◽  
Pressure Elevation ◽  
Cerebral Venous Pressure

The cerebral blood flow response to cerebral venous pressure elevation was studied in pentobarbital-anesthetized dogs using the cerebral venous outflow and radiolabeled microsphere techniques. Cerebral venous pressure elevation resulted in a significant reduction in cerebral venous outflow at a pressure of approximately 2.0 mmHg (referenced at the level of the external auditory meatus). At higher pressures, cerebral venous outflow decreased at a rate of 0.5 ml x min-1 x mmHg-1. Mean arterial pressure was 102.0 mmHg, and thus cerebral perfusion pressure (mean arterial pressure minus cerebral venous pressure) was well within the range for cerebral autoregulation. These results were obtained regardless of whether cerebrospinal fluid pressure was allowed to rise concomitantly with cerebral venous pressure (11 dogs) or was maintained at atmospheric pressure (7 dogs). However, simultaneous measurement of cerebral venous outflow and total and regional cerebral blood flow with the radiolabeled microsphere technique with venous pressure elevation (6 dogs) produced discrepant results. As cerebral venous pressure was elevated to approximately 16.0 mmHg, cerebral venous outflow decreased to 40% of control while total and regional cerebral blood flow values remained unchanged, so that regional and cerebral vascular resistances decreased. These results suggest that cerebral venous pressure elevation opens intracranial venous anastomotic channels and diverts blood flow from the measured venous drainage through other drainage sites. In addition, our results suggest that the dominant mechanism of cerebral autoregulation is metabolic, not myogenic.

scholarly journals An Ultrasonic Doppler Venous Outflow Method for the Continuous Measurement of Cerebral Blood Flow in Conscious Sheep

1994 ◽  
Vol 14 (4) ◽  
pp. 680-688 ◽  
Author(s):  
Richard Upton ◽  
Cliff Grant ◽  
Guy Ludbrook
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Continuous Measurement ◽  
Venous Outflow ◽  
Sagittal Sinus ◽  
Global Cerebral Blood Flow ◽  
Conscious Sheep ◽  
End Tidal ◽  
The Brain

A pulsed ultrasonic Doppler venous outflow method was developed for the continuous measurement of global cerebral blood flow (CBF) in conscious sheep. The sheep were prepared under anesthesia with a “suture down”-style ultrasonic flow probe on the dorsal sagittal sinus placed via a trephine hole. Angiographic and dye studies showed that the dorsal sagittal sinus at the point of placement of the probe collected the majority of the blood from the cerebral hemispheres. Studies of the blood velocity profile across the sinus showed that the dimensions of the dorsal sagittal sinus changed minimally with changes in CBF in vivo. The velocity measurements were calibrated under anesthesia against an in vivo direct venous outflow method. Control CBF values for six sheep ranged from 31 to 53 ml/min for the area of brain described above; for two sheep in which the weight of the brain was determined, this gave total CBF values of approximately 34 and 30 ml min−1 100 g−1. The CBF measured varied in the expected manner with changes in the end-tidal CO2 concentration in expired breath and showed transient reductions with the barbiturate thiopentone and transient increases with the opiate alfentanil. It is concluded that the method is simple and accurate.

scholarly journals Cerebral blood flow during hypoxic hypoxia with plasma-based hemoglobin at reduced hematocrit

1998 ◽  
Vol 274 (6) ◽  
pp. H1933-H1942 ◽  
Author(s):  
John A. Ulatowski ◽  
Enrico Bucci ◽  
Anna Razynska ◽  
Richard J. Traystman ◽  
Raymond C. Koehler
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Hemoglobin Concentration ◽  
Hypoxic Hypoxia ◽  
Control Group ◽  
Hemoglobin Solution ◽  
Sagittal Sinus ◽  
Wide Range ◽  
Anemia Group ◽  
The Brain

We determined whether cerebral blood flow (CBF) remained related to arterial O2 content ([Formula: see text]) during hypoxic hypoxia when hematocrit and hemoglobin concentration were independently varied with cell-free, tetramerically stabilized hemoglobin transfusion. Three groups of pentobarbital sodium-anesthetized cats were studied with graded reductions in arterial O2saturation to 50%: 1) a control group with a hematocrit of 31 ± 1% (mean ± SE; n = 7); 2) an anemia group with a hematocrit of 21 ± 1% that underwent an isovolumic exchange transfusion with an albumin solution ( n = 8); and 3) a group transfused with an intramolecularly cross-linked hemoglobin solution to decrease hematocrit to 21 ± 1% ( n = 10). Total arterial hemoglobin concentration (g/dl) after hemoglobin transfusion (8.8 ± 0.2) was intermediate between that of the control (10.3 ± 0.3) and albumin (7.2 ± 0.4) groups. Forebrain CBF increased after albumin and hemoglobin transfusion at normoxic O2 tensions to levels attained at equivalent reductions in [Formula: see text] in the control group during graded hypoxia. Over a wide range of arterial O2 saturation and sagittal sinus[Formula: see text], CBF remained greater in the albumin group. When CBF was plotted against[Formula: see text] for all three groups, a single relationship was formed. Cerebral O2 transport, O2 consumption, and fractional O2 extraction were constant during hypoxia and equivalent among groups. We conclude that CBF remains related to [Formula: see text] during hypoxemia when hematocrit is reduced with and without proportional reductions in O2-carrying capacity. Thus O2 transport to the brain is well regulated at a constant level independently of alterations in hematocrit, hemoglobin concentration, and O2 saturation.

Progressive hypoxia until brain electrical silence: a useful model for studying protective interventions

1988 ◽  
Vol 66 (11) ◽  
pp. 1398-1406 ◽  
Author(s):  
Carl F. Cartheuser
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Time Course ◽  
Venous Blood ◽  
Hypoxia Tolerance ◽  
Sagittal Sinus ◽  
Progressive Hypoxia ◽  
Time Courses ◽  
Blood Data

Anesthetized spontaneously breathing rats, fitted with epicortical electrodes and catheters for sampling arterial, venous, and cerebral venous blood, were exposed to standardized progressive hypoxia. Three minutes of hypoxia sequentially caused hyperpnea, hypopnea, apnea, and cessation of electrocorticogram "spiking," of synchronization, and of background in electroencephalogram (EEG). Blood data and cerebral blood flow and metabolism were measured throughout and at "insults," i.e., at apnea and cessation events, to clarify their interdependence. Arterial and brain venous Po2 fell linearly with inspired oxygen (final value of 2% at 280 s). Hyperpnea induced arterial alkalosis; subsequent hypopnea led to near-normal Pco2 and pH when EEG ceased. Hypercapnia was more pronounced in cerebral than in systemic venous blood; time courses of pH changes were similar. Sagittal sinus blood pressure and outflow were linearly related and resembled the time course of local cerebral blood flow. Blood flow increased by 25% at apnea and only 60% at EEG silence. Cerebral metabolic rate of O2 rose during the hyperpnea phase and fell exponentially thereafter. Cerebral glucose uptake and lactate release increased within the first 3 min but fell abruptly when cortico-electric spiking ceased. Time courses of cerebral O2 consumption and spike rate were linearly related; both showed inverse linear relations to cerebral perfusion. The hypoxic insults were well defined by blood data; critical Po2 values were lower than previously assumed. This model is proving to be a useful, controlled method by which mechanisms of cerebral hypoxia tolerance may be studied in vivo.

Cerebral blood flow and oxygen consumption in the newborn dog

1978 ◽  
Vol 234 (5) ◽  
pp. R209-R215
Author(s):  
M. J. Hernandez ◽  
R. W. Brennan ◽  
R. C. Vannucci ◽  
G. S. Bowman
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Superior Sagittal Sinus ◽  
Venous Blood ◽  
Arterial Pco2 ◽  
Content Difference ◽  
Cerebral Metabolic Rate ◽  
Sagittal Sinus ◽  
Newborn Brain ◽  
Arterial Blood

Cerebral blood flow (CBF), CBF responses to changes in arterial CO2 tension, and cerebral metabolic rate for oxygen (CMRO2) were measured in newborn dogs, by means of a modification of the Kety and Schmidt technique employing 133Xe. Mongrel dogs of 1-7 days of age were paralyzed and passively ventilated with 70% N2O and 30% O2. CBF was derived by analysis of paired serial 20-microliter samples of arterial and of cerebral venous blood from the superior sagittal sinus. At an arterial PCO2 of 36.9 +/- 3.7 Torr and a mean arterial blood pressure of 62 +/- 10 Torr, CBF was 23 +/- 8 ml/min per 100 g. The arteriovenous oxygen content difference averaged 5.6 vol%, and CMRO2 was 1.13 +/- 0.30 ml O2/min per 100 g. CBF increased or decreased by 0.58 ml/min/100 g per Torr change in PCO2. Our results suggest that in the newborn, basal CBF and CBF responses to CO2 are considerably lower than in the adult and parallel the lower metabolic needs of the newborn brain.

The assessment of pathological changes in cerebral blood flow in hypertensive rats with stress-induced intracranial hemorrhage using Doppler OCT: Particularities of arterial and venous alterations/Die Beurteilung von pathologischen Veränderungen der Hirndurchblutung bei hypertensiven Ratten mit Stress-induzierten intrakraniellen Blutungen mittels Doppler-OCT: Besonderheiten von arteriellen und venösen Veränderungen

2013 ◽  
Vol 2 (2) ◽  
Author(s):  
Oxana V. Semyachkina-Glushkovskaya ◽  
Vladislav V. Lychagov ◽  
Olga A. Bibikova ◽  
Igor A. Semyachkin-Glushkovskiy ◽  
Sergey S. Sindeev ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Hemorrhage ◽  
Venous Insufficiency ◽  
Hypertensive Rats ◽  
Arterial Tree ◽  
Venous Outflow ◽  
Venous Circulation ◽  
Latent Stage ◽  
Doppler Oct

AbstractHemorrhagic insult is a major source of morbidity and mortality in both adults and newborn babies in the developed countries. The mechanisms underlying the non-traumatic rupture of cerebral vessels are not fully clear, but there is strong evidence that stress, which is associated with an increase in arterial blood pressure, plays a crucial role in the development of acute intracranial hemorrhage (ICH), and alterations in cerebral blood flow (CBF) may contribute to the pathogenesis of ICH. The problem is that there are no effective diagnostic methods that allow for a prognosis of risk to be made for the development of ICH. Therefore, quantitative assessment of CBF may significantly advance the understanding of the nature of ICH. The aim of this study was to determine the particularities of alterations in arterial and venous cerebral circulation in hypertensive rats at different stages of stress-related development of ICH using three-dimensional Doppler optical coherence tomography (DOCT).Experiments were performed in mongrel adult rats. To induce ICH, hypertensive rats underwent stress (effect of severe sound, 120 dB during 2 h). To induce the renal hypertension (two kidneys, one clip) the rats were clipped at the left renal artery with a silver clip. Seven weeks after clipping, the hypertensive rats were used in the experiment. The monitoring of CBF was performed in anesthetized rats with fixed heads using a commercially available swept source OCT system (OCS1300SS; Thorlabs) in the masked period of ICH (4 h after stress) and during ICH (24 h after stress).It could be shown that in stressed rats, compared with non-stressed animals, the latent stage of stress-induced ICH (4 h after stress-off) is characterized by an increase in diameter of the superior sagittal vein with decrease in speed of the blood flow in the venous network, whereas no changes in the CBF in the arterial tree were found in this period. These facts suggest that the masked period of ICH is accompanied by decreasing venous outflow and the development of venous insufficiency. The incidence of ICH, 24 h after stress, is associated with progression of pathological alterations in cerebral venous circulation. All hypertensive rats with ICH demonstrated a greater increase in the diameter of the superior sagittal vein than stressed rats at the latent stage of ICH (in 2.5-fold,In summary, using DOCT we have shown that the latent stage of stress-induced ICH is characterized by a decrease in venous outflow. The incidence of ICH is associated with the progression of pathological alterations in cerebral venous circulation that is accompanied by a decrease in blood flow in the arterial tree. The evaluation of cerebral venous insufficiency is an important diagnostic approach for the prognosis of the risk of developing cerebral hypotension and ICH.

Direct Cerebral Vasodilatory Effects of Sevoflurane and Isoflurane 

1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
End Tidal

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P<0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.

scholarly journals Venous blood ammonia can be associated with cerebral blood flow in hepatic encephalopathy

Hepatology ◽  
2013 ◽  
Vol 58 (2) ◽  
pp. 832-833 ◽  
Author(s):  
Gang Zheng ◽  
Long Jiang Zhang ◽  
Yue Cao ◽  
Guang Ming Lu
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Hepatic Encephalopathy ◽  
Venous Blood ◽  
Blood Ammonia

scholarly journals Type A botulinum toxin (disport) in treatment of chronic forms of primary headache

2008 ◽  
Vol 7 (5-1) ◽  
pp. 270-275
Author(s):  
M. V. Napriyenko ◽  
V. Yu. Oknin ◽  
A. G. Sazonova ◽  
L. M. Kudayeva
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Botulinum Toxin ◽  
Pilot Study ◽  
Doppler Ultrasonography ◽  
Primary Headache ◽  
Arterial Blood Flow ◽  
Venous Outflow ◽  
Arterial Blood ◽  
Daily Headache

The aim of this investigation is to study the effect of BTA on the cerebral blood flow in patients with chronic daily headache. The analysis of Doppler ultrasonography and transcranial Dopplergraphy findings has shown the following: after the treatment 34% of the patients had no extravasal effect and in 66% of the patients it became moderate and after the treatment normal venous outflow was found in 58% of the patients . The results of the pilot study demonstrate the effect of BT-A injection on the cerebral blood flow by means of optimizing both the arterial blood flow and the venous outflow from the cavity of the skull.

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