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.

The Cerebral Pharmacokinetics of Meperidine and Alfentanil in Conscious Sheep 

1997 ◽  
Vol 86 (6) ◽  
pp. 1317-1325 ◽  
Author(s):  
Richard N. Upton ◽  
Guy L. Ludbrook ◽  
Elke C. Gray ◽  
Clifford Grant
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Distribution Volume ◽  
Concentration Gradients ◽  
Variable Effect ◽  
Rate Of Penetration ◽  
Sagittal Sinus ◽  
Conscious Sheep ◽  
Kinetics Of ◽  
The Brain

Background Different opioids have different delays (hysteresis) between their concentrations in blood and their cerebral effects. Possible mechanisms include differences in their rate of penetration into the brain and differences in their distribution volume in the brain. There have been few in vivo studies of the cerebral kinetics of opioids to differentiate these mechanisms. Methods The cerebral kinetics of meperidine and alfentanil were examined using conscious sheep that were fitted with long-term monitoring equipment to measure relative changes in cerebral blood flow and opioid concentration gradients across the brain through frequent sampling of arterial and sagittal sinus blood. The data were compared using hybrid physiologic modeling with membrane-limited (consistent with mechanism 1) and flow-limited (consistent with mechanism 2) models of cerebral kinetics. Results Alfentanil had a variable effect on relative cerebral blood flow, whereas meperidine induced a transient increase. The arteriovenous concentration gradients were small after alfentanil but large after meperidine. The flow-limited model gave acceptable descriptions of observed sagittal sinus concentrations for alfentanil and meperidine, whereas the membrane-limited model collapsed to a flow-limited model. The half-lives of equilibrium between blood and brain were 6.3 and 0.8 min for meperidine and alfentanil, respectively: Conclusions The rate of penetration of both opioids into the brain was rapid and not rate-limiting. Large differences in the cerebral distribution volume of meperidine and alfentanil accounted for the respective delays in their peak brain concentration relative to blood.

Ex Vivo MuEtinuciear NMR Spectroscopy of Perfused, Respiring Rat Brain Slices: Model Studies of Hypoxia, Ischemia, and Excitotoxscit

1997 ◽  
Author(s):  
L. Litt ◽  
M.T. Espanol
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Nmr Spectroscopy ◽  
Clinical Care ◽  
Brain Slices ◽  
In Vivo Nmr ◽  
In Vivo Nmr Spectroscopy ◽  
Permanent Brain Damage ◽  
The Brain

We believe there are important roles for in vivo NMR spectroscopy techniques in studies of protection and treatment in stroke. Perhaps the primary utility of in vivo NMR spectroscopy is to establish the relevance of metabolic integrity, intracellular pH, and intracellular energy stores to concurrent changes occurring both at gross physiological levels (e.g., changes in cerebral blood flow, or blood oxygenation), and at microscopic or cellular levels. It has long been known that the brain is exquisitely sensitive to deprivations of oxygen, glucose, and cerebral blood flow. Routine human surgery on a limb takes place every day with tourniquets stopping all blood flow for up to two hours. In contrast, the deprivation of all blood flow to the brain (global ischemia) for approximately 5 minutes can result in severe, permanent brain damage. Research has gone on for more than 30 years to understand why the brain’s revival time is so much shorter, and to discover brain biochemical interventions that might dramatically extend the brain’s intolerance beyond 5 minutes, and therefore be relevant to protection and treatment of stroke. (Kogure and Hossmann, 1985; 1993) Stroke, defined as a permanent neurologic deficit arising from the death of brain cells, kills ∼ 150,000 people in the U.S.A. each year, and is the third leading cause of death (Feinleib et al., 1993). It is the next malady to escape, once one has dodged death from cardiovascular disease and cancer. Many, if not most, U.S.A. stroke victims will receive neurological clinical care not substantially different from what was provided 30 years ago. Most stroke patients will be put in intensive care units where blood pressure will be regulated and kept in a “safe” range, with the body given supportive care and the brain given an opportunity to heal itself. The problem of stroke is actually quite complex because there are several different kinds of stroke (ischemic, hemorrhagic, etc.), and because numerous systemic physiological factors are of relevance. Nevertheless, exciting advances in brain biochemistry suggest that stroke therapy and prophylaxis axe likely to improve dramatically in the near future (Zivin and Choi, 1991).

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%.

Blood-brain barrier permeability of 11C-labeled alcohols and 15O-labeled water

1976 ◽  
Vol 230 (2) ◽  
pp. 543-552 ◽  
Author(s):  
ME Raichle ◽  
JO Eichling ◽  
MG Straatmann ◽  
MJ Welch ◽  
KB Larson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Time Course ◽  
Brain Capillary ◽  
Permeability Characteristics ◽  
Permeability Surface ◽  
Brain Barrier Permeability ◽  
The Individual ◽  
The Brain

The extraction of 11C-labeled methanol, ethanol, and isopropanol, as well as 15O-labeled water by the brain during a single capillary transit, was studied in vivo in six adult rhesus monkeys by external detection of the time course of these tracers subsequent to their internal carotid artery injection. The data demonstrate the feasibility of accurately measuring brain permeability of highly diffusible substances by this technique and show that neither water nor the alcohols studied freely equilibrate with brain when the cerebral blood flow exceeds 30 ml/100 g min-1. At a cerebral blood flow of 50 ml/100 g min-1 only about 93% of an injected bolus of labeled water freely exchanges with brain, compared with methanol (93%), ethanol (97%), and isopropanol (99%). The brain capillary permeability-surface area (PS) products computed from these data were 0.023 cm3/s g-1 (water), 0.024 cm3/s g-1 (methanol), 0.030 cm3/s g-1 (ethanol), and 0.062 cm3/s g-1 (isopropanol). This sequence of PS products is consistent with the individual lipid solubilities of the alcohols studied and underscores the unique brain permeability characteristics of lipid-insoluble water.

scholarly journals Coupling between arterial and venous cerebral blood flow during postural change

2016 ◽  
Vol 311 (6) ◽  
pp. R1255-R1261 ◽  
Author(s):  
Shigehiko Ogoh ◽  
Takuro Washio ◽  
Hiroyuki Sasaki ◽  
Lonnie G. Petersen ◽  
Niels H. Secher ◽  
...  
Keyword(s):  
Blood Flow ◽  
Healthy Subjects ◽  
Internal Carotid ◽  
Jugular Vein ◽  
Venous Drainage ◽  
Postural Change ◽  
Venous Outflow ◽  
Venous Flow ◽  
End Tidal ◽  
The Brain

In supine humans the main drainage from the brain is through the internal jugular vein (IJV), but the vertebral veins (VV) become important during orthostatic stress because the IJV is partially collapsed. To identify the effect of this shift in venous drainage from the brain on the cerebral circulation, this study addressed both arterial and venous flow responses in the “anterior” and “posterior” parts of the brain when nine healthy subjects (5 men) were seated and flow was manipulated by hyperventilation and inhalation of 6% carbon dioxide (CO2). From a supine to a seated position, both internal carotid artery (ICA) and IJV blood flow decreased ( P = 0.004 and P = 0.002), while vertebral artery (VA) flow did not change ( P = 0.348) and VV flow increased ( P = 0.024). In both supine and seated positions the ICA response to manipulation of end-tidal CO2 tension was reflected in IJV ( r = 0.645 and r = 0.790, P < 0.001) and VV blood flow ( r = 0.771 and r = 0.828, P < 0.001). When seated, the decrease in ICA blood flow did not affect venous outflow, but the decrease in IJV blood flow was associated with the increase in VV blood flow ( r = 0.479, P = 0.044). In addition, the increase in VV blood flow when seated was reflected in VA blood flow ( r = 0.649, P = 0.004), and the two flows were coupled during manipulation of the end-tidal CO2 tension (supine, r = 0.551, P = 0.004; seated, r = 0.612, P < 0001). These results support that VV compensates for the reduction in IJV blood flow when seated and that VV may influence VA blood flow.

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.

scholarly journals Circulating tPA contributes to neurovascular coupling by a mechanism involving the endothelial NMDA receptors

2019 ◽  
Vol 40 (10) ◽  
pp. 2038-2054 ◽  
Author(s):  
Antoine Anfray ◽  
Antoine Drieu ◽  
Vincent Hingot ◽  
Yannick Hommet ◽  
Mervé Yetim ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Neurovascular Unit ◽  
Neurovascular Coupling ◽  
Laser Speckle ◽  
Tissue Type ◽  
Blood Flow Increase ◽  
The Brain

The increase of cerebral blood flow evoked by neuronal activity is essential to ensure enough energy supply to the brain. In the neurovascular unit, endothelial cells are ideally placed to regulate key neurovascular functions of the brain. Nevertheless, some outstanding questions remain about their exact role neurovascular coupling (NVC). Here, we postulated that the tissue-type plasminogen activator (tPA) present in the circulation might contribute to NVC by a mechanism dependent of its interaction with endothelial N-Methyl-D-Aspartate Receptor (NMDAR). To address this question, we used pharmacological and genetic approaches to interfere with vascular tPA-dependent NMDAR signaling, combined with laser speckle flowmetry, intravital microscopy and ultrafast functional ultrasound in vivo imaging. We found that the tPA present in the blood circulation is capable of potentiating the cerebral blood flow increase induced by the activation of the mouse somatosensorial cortex, and that this effect is mediated by a tPA-dependent activation of NMDAR expressed at the luminal part of endothelial cells of arteries. Although blood molecules, such as acetylcholine, bradykinin or ATP are known to regulate vascular tone and induce vessel dilation, our present data provide the first evidence that circulating tPA is capable of influencing neurovascular coupling (NVC).

scholarly journals In Vivo Measurements of Brain Glucose Transport Using the Reversible Michaelis–Menten Model and Simultaneous Measurements of Cerebral Blood Flow Changes during Hypoglycemia

2001 ◽  
Vol 21 (6) ◽  
pp. 653-663 ◽  
Author(s):  
In-Young Choi ◽  
Sang-Pil Lee ◽  
Seong-Gi Kim ◽  
Rolf Gruetter
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Transport ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Defense Mechanisms ◽  
Normal Brain ◽  
Brain Glucose ◽  
The Brain

Glucose is the major substrate that sustains normal brain function. When the brain glucose concentration approaches zero, glucose transport across the blood–brain barrier becomes rate limiting for metabolism during, for example, increased metabolic activity and hypoglycemia. Steady-state brain glucose concentrations in α-chloralose anesthetized rats were measured noninvasively as a function of plasma glucose. The relation between brain and plasma glucose was linear at 4.5 to 30 mmol/L plasma glucose, which is consistent with the reversible Michaelis–Menten model. When the model was fitted to the brain glucose measurements, the apparent Michaelis-Menten constant, Kt, was 3.3 ± 1.0 mmol/L, and the ratio of the maximal transport rate relative to CMRglc, Tmax/CMRglc, was 2.7 ± 0.1. This Kt is comparable to the authors' previous human data, suggesting that glucose transport kinetics in humans and rats are similar. Cerebral blood flow (CBF) was simultaneously assessed and constant above 2 mmol/L plasma glucose at 73 ± 6 mL 100 g−1 min−1. Extrapolation of the reversible Michaelis–Menten model to hypoglycemia correctly predicted the plasma glucose concentration (2.1 ± 0.6 mmol/L) at which brain glucose concentrations approached zero. At this point, CBF increased sharply by 57% ± 22%, suggesting that brain glucose concentration is the signal that triggers defense mechanisms aimed at improving glucose delivery to the brain during hypoglycemia.

scholarly journals Validation of Continuous Thermal Measurement of Cerebral Blood Flow by Arterial Pressure Change

1993 ◽  
Vol 13 (4) ◽  
pp. 693-701 ◽  
Author(s):  
Datong Wei ◽  
Mary Shea ◽  
Gerald M. Saidel ◽  
Stephen C. Jones
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Measurement System ◽  
Transient Flow ◽  
Thermal Fluctuations ◽  
Thermal Measurement ◽  
Flow Signal ◽  
Arterial Blood ◽  
The Brain

A thermal measurement system to monitor cerebral blood flow (CBF) continuously from the cortical surface is evaluated in vivo. It has a temperature resolution of better than 0.001°C (1 m°C) and can compensate for baseline temperature fluctuations in the brain tissue. A new approach has been developed to test the capability of monitoring dynamic CBF response. Transient CBF changes associated with changes in mean arterial blood pressure (MABP) caused by repeated bolus norepinephrine injections are used to examine the response of the measurement system in both the heated mode, sensitive to flow, and the unheated mode, sensitive only to temperature. Experiments on 13 rats demonstrate that changes in the MABP are closely correlated with those of temperature difference in the heated mode. Regression analysis shows a mean slope of 0.9 m°C/mm Hg in the heated mode, which is significantly different from zero (p < 0.002) and from the mean slope in the unheated mode (p < 0.002). This indicates that flow signal in the system output can be distinguished from the baseline thermal fluctuations. Thus, the system can be used to detect and study dynamic perfusion changes from the brain surface with minimal tissue damage. Furthermore, analysis of the data shows that the transient flow signal before autoregulation is linearly correlated with changes in MABP.

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.

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