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.

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 α-adrenergic blockade on the cerebrovascular response to increased intracranial pressure after hemorrhage

1998 ◽  
Vol 89 (3) ◽  
pp. 454-459 ◽  
Author(s):  
Ingunn R. Rise ◽  
Ole J. Kirkeby
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Blood Loss ◽  
Treated Group ◽  
Control Group ◽  
Adrenergic Blockade ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Fine Print

Object. In this study the authors tested the hypothesis that hemorrhagic hypotension and high intracranial pressure induce an increase in cerebrovascular resistance that is caused by sympathetic compensatory mechanisms and can be modified by α-adrenergic blockade. Methods. Continuous measurements of cerebral blood flow were obtained using laser Doppler microprobes placed in the cerebral cortex in anesthetized pigs during induced hemorrhagic hypotension and high cerebrospinal fluid pressure. Eight pigs received 2 mg/kg phentolamine in 10 ml saline, and 13 pigs served as control animals. During high intracranial pressure occurring after blood loss, cerebral perfusion pressure (CPP) (p < 0.01) and cerebral blood flow (p < 0.01) decreased in both groups. Cerebrovascular resistance increased (p < 0.05) in the control group and decreased < 0.005) in the phentolamine-treated group. The cerebrovascular resistance was significantly lower in the phentolamine-treated group (p < 0.05) than in the control group. Cerebrovascular resistance increased at lower CPPs in the control group (linear correlation, r = 0.39, p < 0.01) and decreased with decreasing CPP in the phentolamine-treated group (linear correlation, r = 0.76, p < 0.001). Conclusions. This study shows that the deleterious effects on cerebral hemodynamics induced by blood loss in combination with high intracranial pressure are inhibited by α-adrenergic blockade. This suggests that these responses are caused by α-adrenergically mediated cerebral vasoconstriction.

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.

Cerebral blood flow regulation during experimental brain compression

1973 ◽  
Vol 39 (2) ◽  
pp. 186-196 ◽  
Author(s):  
J. Douglas Miller ◽  
Albert E. Stanek ◽  
Thomas W. Langfitt
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Raised Intracranial Pressure ◽  
Content Type ◽  
Brain Compression

✓ The effect of brain compression on cerebral blood flow was measured in 13 anesthetized, ventilated dogs by inflation of extradural balloons. The effects of the raised intracranial pressure, so produced, were correlated with the presence or absence of autoregulation of cerebral blood flow to induced changes of arterial pressure, which was tested immediately prior to each episode of inflation of the balloon. Cerebral blood flow was measured by a venous outflow method and monitored continuously, together with arterial and supratentorial intracranial pressure; arterial pCO2 and body temperature were held constant. Three stages were identified. When autoregulation to a change of arterial pressure was intact, initial inflation of the balloon did not reduce cerebral blood flow until the difference between arterial and intracranial pressure (which was taken to represent cerebral perfusion pressure) was less than 40 mm Hg. When autoregulation was impaired, which occurred after the first inflation of the balloon or was due to preceding arterial hypotension, raised intracranial pressure caused an immediate reduction of cerebral blood flow. At this stage of impaired autoregulation there was a tendency for hyperemia to develop on deflation of the balloon. Finally, after repeated inflation and deflation of the balloon, when brain swelling supervened, cerebral blood flow decreased steadily and failed to increase despite induced increases of arterial pressure and cerebral perfusion pressure.

scholarly journals Cerebral Blood Flow in Patients with Intracranial Pressure Elevation due to Traumatic Brain Edema

1976 ◽  
Vol 3 (1) ◽  
pp. 35-37 ◽  
Author(s):  
W. A. Tweed ◽  
Jørn Overgaard
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Brain Edema ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Monitoring And Control ◽  
Intracranial Pressure Elevation ◽  
Flow Through ◽  
And Control

SUMMARY:The object of this study was to determine if traumatic brain edema (BE) and increased intracranial pressure (ICP) reduce cerebral blood flow (CBF). Two groups of patients were studied, one with slight BE and ICP less than 20 mm Hg., the other with pronounced BE and ICP over 20 mm Hg. Although ICP was higher and cerebral perfusion pressure lower in pro-nounced edema there was only a small and non-significant reduction in CBF and no difference in cerebro-vascular resistance. Since traumatic BE does not increase resistance to blood flow through the brain, cerebral perfusion can be maintained if an adequate perfusion pressure is established. This in turn, demands the monitoring and control of ICP.

Hyperacute measurement of intracranial pressure, cerebral perfusion pressure, jugular venous oxygen saturation, and laser Doppler flowmetry, before and during removal of traumatic acute subdural hematoma

2001 ◽  
Vol 95 (4) ◽  
pp. 569-572 ◽  
Author(s):  
Bon H. Verweij ◽  
J. Paul Muizelaar ◽  
Federico C. Vinas
Keyword(s):  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Laser Doppler ◽  
Bone Flap ◽  
Acute Subdural Hematoma ◽  
Laser Doppler Flow ◽  
Content Type ◽  
Venous Oxygen Saturation ◽  
Fine Print

Object. The poor prognosis for traumatic acute subdural hematoma (ASDH) might be due to underlying primary brain damage, ischemia, or both. Ischemia in ASDH is likely caused by increased intracranial pressure (ICP) leading to decreased cerebral perfusion pressure (CPP), but the degree to which these phenomena occur is unknown. The authors report data obtained before and during removal of ASDH in five cases. Methods. Five patients who underwent emergency evacuation of ASDH were monitored. In all patients, without delaying treatment, a separate surgical team (including the senior author) placed an ICP monitor and a jugular bulb catheter, and in two patients a laser Doppler probe was placed. The ICP prior to removing the bone flap in the five patients was 85, 85, 50, 59, and greater than 40 mm Hg, resulting in CPPs of 25, 3, 25, 56, and less than 50 mm Hg, respectively. Removing the bone flap as well as opening the dura and removing the blood clot produced a significant decrease in ICP and an increase in CPP. Jugular venous oxygen saturation (SjvO2) increased in four patients and decreased in the other during removal of the hematoma. Laser Doppler flow also increased, to 217% and 211% compared with preevacuation flow. Conclusions. Intracranial pressure is higher than previously suspected and CPP is very low in patients with ASDH. Removal of the bone flap yielded a significant reduction in ICP, which was further decreased by opening the dura and evacuating the hematoma. The SjvO2 as well as laser Doppler flow increased in all patients but one immediately after removal of the hematoma.

Experimental cerebral oligemia and ischemia produced by intracranial hypertension

1975 ◽  
Vol 43 (3) ◽  
pp. 308-317 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Felix Durity ◽  
Robert Lounsbury ◽  
David I. Graham ◽  
Frank Welsh ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Neurological Function ◽  
Content Type ◽  
No Reflow ◽  
No Reflow Phenomenon ◽  
Complete Cerebral Ischemia ◽  
Fine Print

✓ Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 ± 4.2 ml/100 gm/min to 26.3 ± 4.4 (p < .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.

Regional cerebral blood flow, sensory evoked potentials, and intracranial pressure in dogs with MCA occlusion by embolization or trapping

1983 ◽  
Vol 58 (4) ◽  
pp. 500-507 ◽  
Author(s):  
Yoshikazu Okada ◽  
Takeshi Shima ◽  
Mitsuo Yamamoto ◽  
Tohru Uozumi
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Evoked Potentials ◽  
Regional Cerebral Blood Flow ◽  
Regional Cerebral Blood ◽  
Content Type ◽  
Sensory Evoked Potentials ◽  
Sensory Evoked ◽  
Fine Print

✓ Regional cerebral blood flow (rCBF), sensory evoked potentials (SEP), and intracranial pressure (ICP) were investigated in dogs with focal cerebral ischemia produced by a silicone cylinder embolus in the middle cerebral artery (MCA) trunk as compared to that produced by trapping the same vessel. These variables were measured at intervals of 1 hour for a period of 6 hours after MCA occlusion. In the embolized animals, rCBF decreased most extensively at the basal ganglia, from a control level of 53.9 ± 3.9 (mean ± SE) to 21.5 ± 2.7 ml/100 gm/min at the 6th hour. Sensory evoked potentials decreased progressively from the resting level of 100% to 53.0% ± 7.2% at the 3rd hour. Intracranial pressure, measured by epidural pressure on the occluded side, increased rapidly during the first 3 hours, from 10.6 ± 0.3 to about 30 cm H2O. In the animals with trapping, the decreases in rCBF and declines of SEP were significantly less than those in the embolized animals, and no evident brain swelling was observed. This study demonstrates that MCA trunk occlusion by silicone cylinder embolization produces a more marked decrease in deep CBF, with diminution of SEP and increase in ICP, than that produced by trapping.

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