Cerebral blood flow and evoked potentials during Cushing response in sheep

1989 ◽  
Vol 256 (3) ◽  
pp. H779-H788
Author(s):  
R. C. Koehler ◽  
J. E. Backofen ◽  
R. W. McPherson ◽  
M. D. Jones ◽  
M. C. Rogers ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Evoked Potentials ◽  
Aortic Pressure ◽  
Base Line ◽  
Auditory Evoked Responses ◽  
Cushing Response

We determined how alterations in systemic hemodynamics, characteristic of the Cushing response, are related to changes in cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), and brain electrical conductive function, as assessed by somatosensory-evoked potentials (SEP) and brain stem auditory-evoked responses (BAER). In three groups of eight pentobarbital-anesthetized sheep, intracranial pressure was gradually elevated to within 50, 25, or 0 mmHg of base-line mean arterial pressure and then held constant for 40 min by intraventricular infusion of mock cerebrospinal fluid. Microsphere-determined CBF fell when cerebral perfusion pressure was less than 50 mmHg. CMRO2 fell when CBF fell greater than 30-40%. Mean aortic pressure and cardiac output increased when CBF fell greater than 40%, i.e., at approximately the level at which CMRO2 fell. Furthermore, the magnitude of the increase in arterial pressure and cardiac output correlated with the reduction of CMRO2. SEP latency did not increase unless CBF fell greater than 55-65%, corresponding to a 20-30% reduction of CMRO2. Increased latency of BAER wave V was associated with a fall in midbrain blood flow of greater than 65-70%. Thus increase in SEP and BAER latencies required reductions of flow greater than those required to elicit a systemic response. This demonstrates that there is a range of intracranial pressure over which the increase in arterial pressure preserves sufficient CBF to sustain minimal electrical conductive function. The best predictor of the onset and magnitude of the Cushing response in adult sheep is the decrease in CMRO2.

Efficacy of Cushing response during development in sheep

1991 ◽  
Vol 261 (2) ◽  
pp. H575-H582
Author(s):  
J. E. Backofen ◽  
R. C. Koehler ◽  
A. P. Harris ◽  
M. C. Rogers ◽  
R. J. Traystman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Metabolic Demand ◽  
O2 Uptake ◽  
Fetal Sheep ◽  
Cushing Response ◽  
Near Term

Mean aortic pressure (MAP) increases (Cushing response) when intracranial pressure (ICP) approaches MAP. We elevated ICP to levels equivalent to normal baseline MAP with infusion of mock cerebrospinal fluid (CSF) into the lateral cerebral ventricles and contrasted responses in near-term fetal sheep, 1-wk-old lambs, and adult sheep anesthetized with pentobarbital sodium. With CSF infusion 1-wk-old lambs and adults produced sustained increases in MAP of 16 +/- 1 and 22 +/- 2 mmHg, respectively, over a 40-min period. However, cerebral blood flow fell 66 and 57%, and cerebral O2 uptake fell 34 and 37%, respectively. In the near-term fetus, MAP increased by 11 +/- 1 mmHg and cerebral blood fell 49% at 3 min of elevated ICP. However, by 15 min MAP had increased further (+17 +/- 2 mmHg) and cerebral blood flow was nearly restored. In contrast to postnatal sheep, cerebral O2 uptake was maintained throughout in the fetus. The mechanism of increased MAP differed among groups. In adults total peripheral resistance fell significantly, whereas in the fetus and lamb it remained constant. Cardiac output increased in each group, but, because of the fall in peripheral resistance, increased cardiac output was relatively more important to the rise in MAP in adults. In addition, marked vasoconstriction occurred in intestines and skin in the fetus. The Cushing response is well-developed in near-term fetal sheep. After birth it may lose its effectiveness in providing for the basal metabolic demand of the brain.

Suctioning and Cerebral Blood Flow

PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 737-737
Author(s):  
JEFFREY M. PERLMAN ◽  
JOSEPH J. VOLPE
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Flow Velocity ◽  
Arterial Blood Pressure ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Base Line ◽  
Arterial Blood

In Reply.— Marshall misread a critical piece of information in the text. His interpretation of the data would be correct, if the intracranial pressure, arterial blood pressure, and cerebral blood flow velocity changes occurred simultaneously. However, as we stated in the text (see section on "Temporal Features of Changes with Suctioning"), the intracranial pressure fell to base-line values immediately following suctioning, whereas the changes in arterial blood pressure and cerebral blood flow velocity occurred more slowly over an approximately two-minute period.

Cerebral blood flow and evoked potentials during cushing response in sheep

1989 ◽  
Vol 4 (3) ◽  
pp. 232 ◽  
Author(s):  
R.C. Koehler ◽  
J.E. Backofen ◽  
R.W. McPherson
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Evoked Potentials ◽  
Cushing Response

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.

scholarly journals Local Cerebral Blood Flow and the Electrocorticogram during Sodium Nitroprusside Hypotension

1978 ◽  
Vol 6 (4) ◽  
pp. 290-296 ◽  
Author(s):  
C. L. Miller ◽  
D. G. Lampard ◽  
R. I. Griffiths ◽  
W. A. Brown
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Sodium Nitroprusside ◽  
Large Range ◽  
Local Cerebral Blood Flow ◽  
Hydrogen Electrode ◽  
Electrode Technique

Changes in local cerebral blood flow during sodium nitroprusside hypotension were measured using the hydrogen electrode technique. At mean arterial pressures from 90% to 50% of control values, local cerebral blood flow showed a significant decrease by 20%. When blood pressure was reduced below 50%, the local cerebral blood flow increased significantly and approached control levels. It is suggested that the flow increase may be due to local hypoxia. Associated with this increase were electrocorticogram changes indicative of hypoxia. The significant decrease in mean local cerebral blood flow and the large range of flows seen during mild hypotension indicate that autoregulation is impaired. During hypotension, intracranial pressure increased by, at most, 3 mm Hg. Cardiac output was usually unaffected and was never decreased by more than 20%.

scholarly journals Augmentation of Blood Flow through Cerebral Collaterals by Inhibition of Nitric Oxide Synthase

1994 ◽  
Vol 14 (5) ◽  
pp. 704-714 ◽  
Author(s):  
Michael G. Muhonen ◽  
Donald D. Heistad ◽  
Frank M. Faraci ◽  
Christopher M. Loftus
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Aortic Pressure ◽  
No Synthase ◽  
Artery Pressure ◽  
Pial Artery ◽  
Anesthetized Dogs ◽  
Oxide Synthase

We examined the influence of nitric oxide (NO) on normal and collateral cerebral blood flow after occlusion of the middle cerebral artery (MCA). Effects of NG-nitro-l-arginine (nitroarginine), an inhibitor of NO synthase, were examined during normotension and hypotension (arterial pressure, 50 mm Hg) in 49 anesthetized dogs. Following a craniotomy, a branch of the MCA was cannulated, and collateral-dependent tissue was identified using the shadow-flow technique. Regional cerebral blood flow was measured with microspheres, and pial artery pressure was measured with a micropipette. Intravenous nitroarginine reduced blood flow to normal cerebrum by approximately 40% (p < 0.05) during normotension and hypotension, with aortic pressure maintained constant after nitroarginine administration. Injection of nitroarginine during hypotension, without control of pressor effects, increased aortic and pial artery pressure approximately twofold. Concurrently, blood flow to normal cerebrum decreased (p < 0.05), while flow to collateral-dependent cerebrum increased (p < 0.05). Phenylephrine was infused during hypotension to increase arterial pressure to values similar to those achieved following nitroarginine. Blood flow to collateral-dependent cerebrum increased (p < 0.05), but flow to normal cerebrum was not altered during infusion of phenylephrine. Thus, inhibition of NO synthase during hypotension increases arterial pressure, decreases blood flow to normal cerebrum, and increases blood flow to collateral-dependent cerebrum. Phenylephrine also increases perfusion pressure and blood flow to collateral-dependent cerebrum, but in contrast to nitroarginine, it does not redistribute blood flow from normal cerebrum.

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