Effect of intracisternal phentolamine on cerebral blood flow after subarachnoid injection of blood

1976 ◽  
Vol 44 (3) ◽  
pp. 353-358 ◽  
Author(s):  
Albert N. Martins ◽  
Norwyn Newby ◽  
Thomas F. Doyle ◽  
Arthur I. Kobrine ◽  
Archimedes Ramirez
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Subarachnoid Injection ◽  
Ischemic Encephalopathy ◽  
Hydrogen Clearance

✓ The hydrogen clearance method was used to measure total and focal cerebral blood flow (CBF) in the monkey before and for 5 hours after a simulated subarachnoid hemorrhage (SAH). Some monkeys also received 0.2 to 1.0 mg/kg phentolamine intracisternally 3 hours after SAH. Results show that SAH did not change cerebrovascular resistance, but as cerebral perfusion pressure decreased, CBF fell transiently. Phentolamine injected intracisternally 3 hours after SAH produced a significant fall in arterial blood pressure; cerebrovascular resistance did not change but CBF decreased significantly. These data indicate that intracisternal phentolamine cannot be considered potentially useful to treat ischemic encephalopathy after SAH.

Effect of reduced cerebral perfusion pressure on cerebral blood flow following inhibition of nitric oxide synthesis

1998 ◽  
Vol 89 (3) ◽  
pp. 448-453 ◽  
Author(s):  
Ingunn R. Rise ◽  
Ole J. Kirkeby
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Nitric Oxide Synthesis ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Fine Print

Object. The authors tested the hypothesis in a porcine model that inhibition of nitric oxide synthesis during reduced cerebral perfusion pressure (CPP) affected the relative cerebral blood flow (CBF) and the cerebrovascular resistance. Methods. The CPP was reduced by inducing high cerebrospinal fluid pressure and hemorrhagic hypotension. With continuous blood and intracranial pressure monitoring, relative CPP was estimated using the laser Doppler flowmetry technique in nine pigs that received 40 mg/kg nitro-l-arginine methyl ester (l-NAME) and in nine control animals. The l-NAME caused a decrease in relative CBF (p < 0.01) and increases in cerebrovascular resistance (p < 0.01), blood pressure (p < 0.05), and CPP (p < 0.001). During high intracranial pressure there were no significant differences between the treated animals and the controls. After hemorrhage, there was no significant difference between the groups initially, but 30 minutes later the cerebrovascular resistance was decreased in the control group and increased in the l-NAME group relative to baseline (p < 0.05). Combined hemorrhage and high intracranial pressure increased the difference between the two groups with regard to cerebrovascular resistance (p < 0.05). Conclusions. These results suggest that nitric oxide synthesis inhibition affects the autoregulatory response of the cerebral circulation after cardiovascular compensation has taken place. Nitric oxide synthesis inhibition enhanced the undesirable effects of high intracranial pressure during hypovolemia.

Effects of fluid-percussion brain injury on regional cerebral blood flow and pial arteriolar diameter

1986 ◽  
Vol 64 (5) ◽  
pp. 787-794 ◽  
Author(s):  
Douglas S. DeWitt ◽  
Larry W. Jenkins ◽  
Enoch P. Wei ◽  
Harry Lutz ◽  
Donald P. Becker ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Pial Arterioles ◽  
High Level ◽  
Arteriolar Diameter

✓ The effects of two levels of fluid-percussion brain injury on cerebral blood flow (CBF) and pial arteriolar diameter were investigated in cats. Regional CBF was measured using the radioactive microsphere technique. Experimental brain injury resulted in changes in arterial blood pressure, CBF, and pial arteriolar diameter that were related to the severity of the injury. Low-level injury (1.88 ± 0.11 atm, mean ± standard error of the mean) resulted in a slight transient increase in CBF which had returned to preinjury levels by 30 minutes. High-level injury (2.68 ± 0.19 atm) resulted in larger, statistically significant (p < 0.01) increases in whole-brain CBF, decreases in cerebrovascular resistance, and increases in pial arteriolar diameter 1 minute postinjury. One hour after injury, CBF had returned to preinjury levels while cerebral perfusion pressure was significantly (p < 0.01) reduced. There was no evidence of reduced CBF in any region studied. Pial arterioles dilated during the posttraumatic hypertensive period and then returned to control diameters within 1 hour after injury. Changes in the diameter of pial arterioles were significantly correlated with posttraumatic changes in CBF.

scholarly journals Carbon Dioxide Induced Changes in Cerebral Blood Flow and Flow Velocity: Role of Cerebrovascular Resistance and Effective Cerebral Perfusion Pressure

2015 ◽  
Vol 35 (9) ◽  
pp. 1470-1477 ◽  
Author(s):  
Frank Grüne ◽  
Stephan Kazmaier ◽  
Robert J Stolker ◽  
Gerhard H Visser ◽  
Andreas Weyland
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cerebrovascular Resistance ◽  
Flow Pressure ◽  
Induced Changes ◽  
Zero Flow

In addition to cerebrovascular resistance (CVR) zero flow pressure (ZFP), effective cerebral perfusion pressure (CPPe) and the resistance area product (RAP) are supplemental determinants of cerebral blood flow (CBF). Until now, the interrelationship of PaCO2 -induced changes in CBF, CVR, CPPe, ZFP, and RAP is not fully understood. In a controlled crossover trial, we investigated 10 anesthetized patients aiming at PaCO2 levels of 30, 37, 43, and 50 mm Hg. Cerebral blood flow was measured with a modified Kety-Schmidt-technique. Zero flow pressure and RAP was estimated by linear regression analysis of pressure–flow velocity relationships of the middle cerebral artery. Effective cerebral perfusion pressure was calculated as the difference between mean arterial pressure and ZFP, CVR as the ratio CPPe/CBF. Statistical analysis was performed by one-way RM-ANOVA. When comparing hypocapnia with hypercapnia, CBF showed a significant exponential reduction by 55% and mean VMCA by 41%. Effective cerebral perfusion pressure linearly decreased by 17% while ZFP increased from 14 to 29 mm Hg. Cerebrovascular resistance increased by 96% and RAP by 39%; despite these concordant changes in mean CVR and Doppler-derived RAP correlation between these variables was weak ( r = 0.43). In conclusion, under general anesthesia hypocapnia-induced reduction in CBF is caused by both an increase in CVR and a decrease in CPPe, as a consequence of an increase in ZFP.

Early hemodynamic changes in experimental intracerebral hemorrhage

1986 ◽  
Vol 65 (5) ◽  
pp. 697-703 ◽  
Author(s):  
Fredrik P. Nath ◽  
Alistair Jenkins ◽  
A. David Mendelow ◽  
David I. Graham ◽  
Graham M. Teasdale
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracerebral Hemorrhage ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Autologous Blood ◽  
Local Cerebral Blood Flow ◽  
Hemodynamic Changes ◽  
Content Type ◽  
Pressure Changes

✓ A model of experimental intracerebral hemorrhage is described in which carefully controlled volumes of autologous blood were injected at arterial pressure into the caudate nucleus of the rat. A comparison of intracranial pressure changes and local cerebral blood flow (CBF) was made between three groups of rats, each receiving different injection volumes, and sham-operated control rats by monitoring intraventricular pressure and by obtaining quantitative autoradiographic measurements of CBF within 1 minute of the experimental hemorrhage. Cerebral blood flow was reduced both around the hematoma and in the surrounding brain. This change was strongly volume-dependent and was not accompanied by significant alterations in cerebral perfusion pressure. This finding suggests that the degree of ischemia at the time of an intracerebral bleed depends on the size of the lesion, and implicates local squeezing of the microcirculation by the hematoma, rather than a generalized alteration in perfusion pressure, as the cause of ischemia.

Cerebral blood flow autoregulation in early experimental S. pneumoniae meningitis

2007 ◽  
Vol 102 (1) ◽  
pp. 72-78 ◽  
Author(s):  
Michael Pedersen ◽  
Christian T. Brandt ◽  
Gitte M. Knudsen ◽  
Christian Østergaard ◽  
Peter Skinhøj ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Arterial Blood ◽  
Norepinephrine Infusion ◽  
Intracisternal Injection ◽  
Cerebral Blood Flow Autoregulation

We studied cerebral blood flow (CBF) autoregulation and intracranial pressure (ICP) during normo- and hyperventilation in a rat model of Streptococcus pneumoniae meningitis. Meningitis was induced by intracisternal injection of S. pneumoniae. Mean arterial blood pressure (MAP), ICP, cerebral perfusion pressure (CPP, defined as MAP − ICP), and laser-Doppler CBF were measured in anesthetized infected rats ( n = 30) and saline-inoculated controls ( n = 30). CPP was either incrementally reduced by controlled hemorrhage or increased by intravenous norepinephrine infusion. Twelve hours postinoculation, rats were studied solely during normocapnia, whereas rats studied after 24 h were exposed to either normocapnia or to acute hypocapnia. In infected rats compared with control rats, ICP was unchanged at 12 h but increased at 24 h postinoculation (not significant and P < 0.01, respectively); hypocapnia did not lower ICP compared with normocapnia. Twelve hours postinoculation, CBF autoregulation was lost in all infected rats but preserved in all control rats ( P < 0.01). Twenty-four hours after inoculation, 10% of infected rats had preserved CBF autoregulation during normocapnia compared with 80% of control rats ( P < 0.01). In contrast, 60% of the infected rats and 100% of the control rats showed an intact CBF autoregulation during hypocapnia ( P < 0.05 for the comparison of infected rats at normocapnia vs. hypocapnia). In conclusion, CBF autoregulation is lost both at 12 and at 24 h after intracisternal inoculation of S. pneumoniae in rats. Impairment of CBF autoregulation precedes the increase in ICP, and acute hypocapnia may restore autoregulation without changing the ICP.

scholarly journals Model-derived assessment of cerebrovascular resistance and cerebral blood flow following traumatic brain injury

2010 ◽  
Vol 235 (4) ◽  
pp. 539-545 ◽  
Author(s):  
Michael L Daley ◽  
Nithya Narayanan ◽  
Charles W Leffler
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Cerebral Perfusion ◽  
The State ◽  
Cerebrovascular Resistance ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Cerebrovascular Regulation

The published guidelines point out the need for the development of methods that individualize patient cerebral perfusion management and minimize secondary ischemic complications associated with traumatic brain injury. A laboratory method has been developed to determine model-derived assessments of cerebrovascular resistance (mCVR) and cerebral blood flow (mCBF) from cerebrovascular pressure transmission, and the dynamic relationship between arterial blood pressure (ABP) and intracranial pressure (ICP). The aim of this two-fold study is to (1) evaluate relative changes in the model-derived parameters of mCVR and mCBF with the corresponding changes in the pial arteriolar vascular parameters of pial arteriolar resistance (PAR) and relative pial arteriolar blood flow (rPABF); and (2) examine the efficacy of the proposed modeling methodology for continuous assessment of the state of cerebrovascular regulation by evaluating relative changes in the model-derived parameters of CBF and cerebrovascular resistance in relation to changes of cerebral perfusion pressure prior to and following fluid percussion brain injury. Changes of ABP, ICP, PAR, relative arteriolar blood flow (rPABF) and the corresponding model-derived parameters of mCBF and mCVR induced by acute hypertensive challenge were evaluated before and following fluid percussion injury in piglets equipped with cranial windows. Before fluid percussion, hypertensive challenge resulted in a significant increase of PAR and mCVR, whereas both rPABF and mCBF remained constant. Following fluid percussion, hypertensive challenge resulted in a significant decrease of PAR and mCVR and consistent with impaired cerebrovascular regulation. Hypertensive challenge significantly increased both rPABF and mCBF, which approximately doubled with increased CPP with correlation values of r = 0.96 ( P < 0.01) and r = 0.97 ( P ≤ 0.01), respectively. The assessment of model-derived cerebrovascular resistance and CBF with changes of CPP provides a means to monitor continuously the state of cerebrovascular regulation.

Pressure-volume index as a function of cerebral perfusion pressure

1987 ◽  
Vol 67 (3) ◽  
pp. 377-380 ◽  
Author(s):  
W. John Gray ◽  
Michael J. Rosner
Keyword(s):  
Blood Flow ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Complex Function ◽  
Volume Index ◽  
Content Type ◽  
Adult Cats ◽  
Hydrogen Clearance ◽  
Fine Print

✓ The pressure-volume index (PVI) was measured in six adult cats while cerebral perfusion pressure (CPP) was reduced from normal levels to below the autoregulatory range by a continuous infusion of adenosine triphosphate. Anesthesia was induced with methohexital and maintained with an N2O:O2 (70%:30%) mixture. Body temperature, hematocrit, and PaCO2 were held constant throughout each experiment. Cerebral blood flow (CBF) was measured by the hydrogen clearance method. At CPP levels over 50 mm Hg, CBF remained relatively constant despite changes in CPP. Within this range, the PVI varied directly with CPP (PVI = 0.24 ml + 0.0013 mm Hg CPP). Below the autoregulatory range, CBF fell progressively with further decreases in CPP; in this range, PVI was found to increase as CPP fell (PVI = 0.84 ml − 0.0071 mm Hg CPP). These results indicate that the PVI is a complex function of CPP, varying directly with CPP within the autoregulatory range and indirectly with CPP below the autoregulatory range.

The effect of mannitol on cerebral blood flow

1973 ◽  
Vol 38 (4) ◽  
pp. 461-471 ◽  
Author(s):  
Ian H. Johnston ◽  
A. M. Harper
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Perfusion Pressure ◽  
Similar Response ◽  
Raised Intracranial Pressure ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Cerebral Metabolic Rate ◽  
Transient Rise

✓ The effect of mannitol on cerebral blood flow was studied in anesthetized baboons, both at normal and raised intracranial pressure. At normal intracranial pressure, rapid intravenous infusion of mannitol (1.5 gm/kg in 10 min) led to a sharp transient rise in cerebral blood flow during and immediately after the period of infusion. This was associated with a reduction in cerebrovascular resistance and a variable change in cerebral metabolic rate (CMRO2). Other parameters measured did not change significantly. A similar response was seen during hypercapnia. Under conditions of raised intracranial pressure (supratentorial subdural balloon) mannitol infusion did not alter cerebral blood flow in three of four animals. In the remaining animal, however, a marked increase in blood flow occurred without any concomitant change in cerebral perfusion pressure. When a further infusion of mannitol was subsequently given to these animals while the intracranial pressure was artificially maintained, there was very little change in cerebral blood flow. The possible causes of the increase in cerebral blood flow at normal intracranial pressure and the clinical implications of these findings are discussed.

Is cerebral perfusion pressure a major determinant of cerebral blood flow during head elevation in comatose patients with severe intracranial lesions?

2000 ◽  
Vol 92 (4) ◽  
pp. 606-614 ◽  
Author(s):  
Jean-Jacques Moraine ◽  
Jacques Berré ◽  
Christian Mélot
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Pressure Gradient ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Content Type ◽  
Head Elevation ◽  
Intracranial Lesions ◽  
Fine Print

Object. Head elevation as a treatment for lower intracranial pressure (ICP) in patients with intracranial hypertension has been challenged in recent years. Therefore, the authors studied the effect of head position on cerebral hemodynamics in patients with severe head injury.Methods. The effect of 0°, 15°, 30°, and 45° head elevation on ICP, cerebral blood flow (CBF), systemic arterial (PsaMonro) and jugular bulb (Pj) pressures calibrated to the level of the foramen of Monro, cerebral perfusion pressure (CPP), and the arteriovenous pressure gradient (PsaMonro − Pj) was studied in 37 patients who were comatose due to severe intracranial lesions. The CBF decreased gradually with head elevation from 0 to 45°, from 46.3 ± 4.8 to 28.7 ± 2.3 ml · min−1 · 100 g−1 (mean ± standard error, p < 0.01), and the PsaMonro − Pj from 80 ± 3 to 73 ± 3 mm Hg (p < 0.01). The CPP remained stable between 0° and 30° of head elevation, at 62 ± 3 mm Hg, and decreased from 62 ± 3 to 57 ± 4 mm Hg between 30° and 45° (p < 0.05). A simulation showed that the 38% decrease in CBF between 0° and 45° resulted from PsaMonro − Pj changes for 19% of the decrease, from a diversion of the venous drainage from the internal jugular veins to vertebral venous plexus for 15%, and from CPP changes for 4%.Conclusions. During head elevation the arteriovenous pressure gradient is the major determinant of CBF. The influence of CPP on CBF decreases from 0 to 45° of head elevation.

Effect of mannitol on cerebral blood flow and cerebral perfusion pressure in human head injury

1985 ◽  
Vol 63 (1) ◽  
pp. 43-48 ◽  
Author(s):  
A. David Mendelow ◽  
Graham M. Teasdale ◽  
Thomas Russell ◽  
John Flood ◽  
James Patterson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Severe Head Injury ◽  
Perfusion Pressure ◽  
Neuronal Damage ◽  
Content Type ◽  
Made In

✓ Patients with severe head injury frequently have evidence of elevated intracranial pressure (ICP) and ischemic neuronal damage at autopsy. Mannitol has been used clinically to reduce ICP with varying success, and it is possible that it is more effective in some types of head injury than in others. The aim of the present study was to determine the effect of mannitol on ICP, cerebral perfusion pressure (CPP), and cerebral blood flow (CBF) in patients with severe head injury, and to discover if these effects differed in different types of injury. Measurements of CPP, ICP, and CBF were made in 55 patients with severe head injury. In general, the resting level of CBF was higher in patients with diffuse injury (mean 50.2 ml/100 gm/min) than in those with focal injury (mean 39.8 ml/100 gm/min). Mannitol consistently reduced ICP and increased CPP and CBF by 10 to 20 minutes after infusion. The lowest flows (31.8 ml/100 gm/min) were recorded from the most damaged hemispheres of patients with focal injuries and elevated ICP. The baseline levels of flow did not correlate with ICP, CPP, Glasgow Coma Scale score, or outcome. Only four of the 55 patients had a CBF of less than 20 ml/100 gm/min in either or both hemispheres. The few low CBF's in this and other studies may reflect the steady-state conditions under which measurements are made in intensive care units, and that these patients have entered a phase of reperfusion.

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