Effect of Histamine on Regional Cerebral Blood Flow in Man

Cephalalgia ◽  
1982 ◽  
Vol 2 (1) ◽  
pp. 15-18 ◽  
Author(s):  
Annette Æbelholt Krabbe ◽  
Jes Olesen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Resting State ◽  
Regional Cerebral Blood Flow ◽  
Regional Distribution ◽  
Regional Cerebral Blood ◽  
Arterial Blood ◽  
Significant Change ◽  
Change In Mean

Regional cerebral blood flow (rCBF) was measured using the intra-arterial 133Xe technique in 35 or 256 areas of a hemisphere. In seven patients rCBF was measured in the resting state and following intracarotid (i.c.) infusion of histamine 10–50 μg/min. In four patients histamine was infused intravenously in a dose of 25–40 μg/min. Histamine caused no significant change in mean arterial blood pressure or arterial PCO2. There was no significant change in mean hemispheric blood flow during i.v. or i.c. histamine infusion. No change in the regional distribution of hemispheric blood flow was observed. Experimental histamine headache is most likely of extracranial origin.

scholarly journals Regional Cerebral Blood Flow in Patients with Aneurysms: Estimation by Xenon 133 Inhalation

1978 ◽  
Vol 5 (3) ◽  
pp. 301-305 ◽  
Author(s):  
Bryce Weir ◽  
Devidas Menon ◽  
Thomas Overton
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Normal Values ◽  
Regional Distribution ◽  
Progressive Increase ◽  
Control Group ◽  
Regional Cerebral Blood ◽  
Progressive Reduction ◽  
Distribution Of Flow

SUMMARY:Seventy six regional cerebral blood flow (rCBF) studies were conducted on 32 patients who had a total of 39 aneurysms. Twenty three of these patients were studied pre- and post-operatively. Normal values were obtained from a control group of 33 subjects, each of whom underwent one rCBF study. Flow was reduced following subarachnoid hemorrhage (SAH); it increased significantly postoperatively. Lower flows were associated with poorer clinical grades. There was a greater variation in regional distribution of flow immediately following SAH than in normals or in patients who had recovered from the acute phase. rCBF studies correlated with CT scans demonstrated that a progressive increase in ventricular size was accompanied by a progressive reduction in flow. In addition, intraventricular hemorrhage (IVH) was associated with a significant reduction in cerebral blood flow (CBF). No significant correlation between CBF and spasm was demonstrable.

scholarly journals Effect of the Calcium Antagonist, Nimodipine, on Cerebral Blood Flow and Metabolism in the Primate

1981 ◽  
Vol 1 (3) ◽  
pp. 349-356 ◽  
Author(s):  
A. M. Harper ◽  
L. Craigen ◽  
S. Kazda
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Calcium Antagonist ◽  
Arterial Blood Pressure ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Arterial Blood ◽  
Blood Brain ◽  
Significant Change

The effect of the calcium antagonist nimodipine was tested in anaesthetised primates. A rapid intravenous injection of 3 or 10 μg kg−1 produced a transient rise in end-tidal Pco2 and a fall in arterial blood pressure, but 10 min after the injection there was no significant change in CBF. A continuous intravenous infusion of 2 μg kg−1 min−1 caused a modest fall in mean arterial blood pressure and an increase in cerebral blood flow (CBF), which gradually increased to 27% above control after 50 min infusion. There was no significant change in CMRO2. A continuous intracarotid infusion of 0.67 μg kg−1 min−1 caused an increase in CBF of between 46 and 57%. This was further increased to 87% above control after disruption of the blood-brain barrier with hyperosmolar urea. Thirty minutes after the urea, the CBF returned to 43% above control. Twenty minutes after the infusion of nimodipine had been stopped, the CBF had returned to control values. EEG studies in this group showed no obvious increase in electrocortical activity. This evidence suggests that nimodipine has no effect on cerebral metabolism but increases CBF, particularly after disruption of the blood-brain barrier.

Chronic whiplash symptoms are related to altered regional cerebral blood flow in the resting state

2009 ◽  
Vol 13 (1) ◽  
pp. 65-70 ◽  
Author(s):  
Clas Linnman ◽  
Lieuwe Appel ◽  
Anne Söderlund ◽  
Örjan Frans ◽  
Henry Engler ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Resting State ◽  
Regional Cerebral Blood Flow ◽  
Regional Cerebral Blood ◽  
Chronic Whiplash

scholarly journals Relations of blood pressure and head injury to regional cerebral blood flow

2016 ◽  
Vol 365 ◽  
pp. 9-14 ◽  
Author(s):  
Jason E. Kisser ◽  
Allyssa J. Allen ◽  
Leslie I. Katzel ◽  
Carrington R. Wendell ◽  
Eliot L. Siegel ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Regional Cerebral Blood Flow ◽  
Regional Cerebral Blood

Effect of hypoxia and hypercapnia on neurohypophyseal blood flow

1986 ◽  
Vol 250 (1) ◽  
pp. H7-H15
Author(s):  
D. F. Hanley ◽  
D. A. Wilson ◽  
R. J. Traystman
Keyword(s):  
Blood Pressure ◽  
Carbon Monoxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Brain Regions ◽  
Regulatory Mechanisms ◽  
Similar Increase ◽  
Regional Cerebral Blood ◽  
Pressure Controlled

Neurohypophyseal blood flow responses to hypoxia and hypercapnia were studied in pentobarbital anesthetized, paralyzed dogs. Arterial O2 content was lowered from control (18 +/- 2 vol%) to 8 +/- 1 vol% by either decreasing O2 tension (hypoxic hypoxia, HH) or by increasing carboxyhemoglobin saturation (carbon monoxide hypoxia, COH) at normal O2 tension. In all animals HH and COH resulted in similar increases in total cerebral blood flow (239 and 300%, respectively). Regional cerebral blood flow showed a similar increase for all brain regions except the neurohypophysis (NH). The NH increased its blood flow with HH (approximately 320% of control) but was unchanged with COH (117% of control). The responsiveness of NH blood vessels was tested under conditions of hypercapnia (10% CO2) and HH with blood pressure controlled by concurrent hemorrhage. The response of NH vessels to altered arterial O2 tension occurs independently of blood pressure. Systemic [H+] or CO2 tension produce only small changes in NH blood flow. These data suggest that hypoxic and hypercapnic regulatory mechanisms for the NH are different from those of other brain regions. The precise mechanism by which the NH hypoxic response occurs remains unclear, but our data suggest an important role for systemic arterial O2 tension and chemoreceptors.

Sign in / Sign up

Export Citation Format

Share Document