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.

Effect of hypoxemia on the cardiovascular response to intracranial hypertension in postnatal lambs

1993 ◽  
Vol 265 (5) ◽  
pp. H1557-H1563 ◽  
Author(s):  
M. L. Kearney ◽  
J. E. Backofen ◽  
R. C. Koehler ◽  
M. D. Jones ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cardiovascular Response ◽  
Fetal Sheep ◽  
Peripheral Vasoconstriction ◽  
Significant Difference

Large increases in intracranial pressure in fetal sheep result in more potent peripheral vasoconstriction and better maintenance of cerebral O2 consumption (CMRO2) than in postnatal sheep. The fetus is exposed to a lower PO2. We tested the hypothesis that low PO2 in postnatal lambs potentiates peripheral vasoconstriction and better maintains cerebral perfusion pressure and CMRO2. Pentobarbital-anesthetized lambs, 2-7 days old, were ventilated with either room air (n = 7) or a low O2 mixture to reduce arterial O2 saturation to 50% (n = 7). Elevation of intracranial pressure to within 3-5 mmHg of baseline mean arterial pressure for 30 min by ventricular fluid infusion initially caused a similar increase in arterial pressure in the normoxic [11 +/- 3 (SE) mmHg] and hypoxic (14 +/- 2 mmHg) groups. Plasma catecholamines increased more rapidly in the hypoxic group. However, plasma vasopressin levels were substantially elevated by hypoxia alone and failed to increase further with elevated intracranial pressure. Moreover, there was no significant difference between groups in the steady-state increase in arterial pressure, and microsphere-determined blood flow to intestines, kidney, skin, and muscle did not decrease in either group. Consequently, cerebral perfusion pressure, regional cerebral blood flow, and CMRO2 were reduced similarly in both groups. Therefore, hypoxemia failed to potentiate the postnatal pressor response. Low PO2 is unlikely to be the major mechanism for the potent Cushing response in the fetus.

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.

scholarly journals The Effect of Indomethacin on Intracranial Pressure, Cerebral Perfusion and Extracellular Lactate and Glutamate Concentrations in Patients with Fulminant Hepatic Failure

2004 ◽  
Vol 24 (7) ◽  
pp. 798-804 ◽  
Author(s):  
Flemming Tofteng ◽  
Fin Stolze Larsen
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Early Death ◽  
Cerebral Blood Flow Autoregulation

Uncontrolled increase in intracranial pressure (ICP) continues to be one of the most significant causes of early death in patients with acute liver failure (ALF). In this study, we aimed to determine the effects of indomethacin on ICP and cerebral perfusion pressure in twelve patients with ALF and brain edema (9 females/3 males, median age 49,5 (range 21 to 64) yrs.). Also changes in cerebral perfusion determined by transcranial Doppler technique (Vmean) and jugular bulb oxygen saturation (SvjO2) were measured, as well as brain content of lactate and glutamate by microdialysis technique. Finally, we determined the cerebral blood flow autoregulation before and after indomethacin injection. We found that indomethacin reduced ICP from 30 (7 to 53) to 12 (4 to 33) mmHg ( P < 0.05). The cerebral perfusion pressure increased from 48 (0 to 119) to 65 (42 to 129) mmHg ( P < 0.05), while Vmean and SvjO2 on average remained unchanged at 68 (34 to 126) cm/s and 67 (28 to 82) %, respectively. The lactate and glutamate in the brain tissue were not altered (2.1 (1.8 to 7.8) mmol/l and 34 (2 to 268) μmol/l, respectively) after injection of indomethacin. Cerebral blood flow autoregulation was impaired in all patients before injection of indomethacin, but was not restored after administration of indomethacin. We conclude that a bolus injection of indomethacin reduces ICP and increases cerebral perfusion pressure without compromising cerebral perfusion or oxidative metabolism in patients with ALF. This finding indicates that indomethacin may be valuable as rescue treatment of uncontrolled intracranial hypertension in fulminant hepatic failure.

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.

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