scholarly journals Effect of Thyrotropin-Releasing Hormone on Cerebral Blood Flow in Conscious Rat

1989 ◽  
Vol 9 (2) ◽  
pp. 196-203 ◽  
Author(s):  
Yasushi Kondoh ◽  
Shigenori Mizusawa ◽  
Matsutaro Murakami ◽  
Ken Nagata ◽  
Hiroshi Sasaki ◽  
...  

The effect of thyrotropin-releasing hormone (TRH) was studied on local CBF (LCBF) in normal conscious rats. LCBF was measured by the autoradiographic [14C]iodoantipyrine method 5 min after TRH (5 mg/kg, i.v.) administration. TRH significantly increased LCBF in 22 of 33 brain regions. This increase of LCBF exceeded 100% of the control values in the cerebral cortices, whereas there was no significant increase in white matter or in some gray matter structures. The increase of CBF following TRH administration was abolished by pretreatment with indomethacin (5 mg/kg, i.v.). The mechanisms underlying the increase of CBF following TRH administration are discussed in relation to prostaglandin metabolism.

1987 ◽  
Vol 253 (5) ◽  
pp. H1289-H1297
Author(s):  
F. J. Schuier ◽  
S. C. Jones ◽  
T. Fedora ◽  
M. Reivich

A comparison of local cerebral blood flow estimates with the microsphere and the 4-[N-methyl-14C]iodoantipyrine ([14C]IAP) techniques has been performed in cats. Good correlation of [14C]IAP with microsphere flow estimates in the gray matter was found. In the white matter, however, [14C]IAP flow estimates were consistently lower than microsphere flow estimates. Error analysis of both techniques and comparison with previous studies suggest that peculiarities of white matter arterial vasculature with preferential microsphere accumulation may lead to this discrepancy. Microspheres did not interfere with flow as shown by the normal appearance of subsequent [14C]IAP autoradiograms. The number of microspheres seen on autoradiograms was used for an estimate of microvessels blocked by spheres and found to be negligible. The study also demonstrates that [14C]IAP is not diffusion limited up to the observed flow values of 2 ml.g-1.min-1. Both techniques might be used together for a combination of their respective advantages, which are temporal and spatial resolution for microsphere and [14C]IAP, respectively.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Chie Suzuki ◽  
Mutsumi Kosugi ◽  
Yasuhiro Magata

Abstract Background Animal brain functions evaluated by in vivo imaging under anesthesia can be affected by anesthetic agents, resulting in incorrect assessment of physiological brain function. We therefore performed dynamic positron emission tomography (PET) imaging of conscious rats using recently reported soft immobilization to validate the efficacy of the immobilization for brain function assessments. We also determined the effects of six anesthetic agents—a mixed anesthetic agent (MMB), ketamine + xylazine (KX), chloral hydrate (Chloral), pentobarbital (PTB), propofol (PF), and isoflurane (IFL)—on brain function by comparison with conscious rats. Results The immobilization enabled 45-min dynamic [18F]FDG-PET acquisition with arterial blood sampling using conscious rats without the use of special techniques or invasive surgery. The spatial resolution and quantitativity of [18F]FDG-PET were not significantly lower for conscious rats than for anesthetized rats. While MMB, Chloral, PTB, and PF showed ubiquitous reduction in the cerebral metabolic rates of glucose (CMRglu) in brain regions, KX and IFL showed higher reductions in cerebellum and interbrain, and cerebellum, respectively. Cerebral blood flow (CBF) was reduced by MMB, KX, PTB, and PF; increased by IFL; and unaltered by Chloral. The magnitude of decrease in CMRglu and CBF for MMB were not larger than for other five anesthetic agents, although blood glucose levels and body temperature can be easily affected by MMB. Conclusion The six anesthetic agents induced various effects on CMRglu and CBF. The immobilization technique presented here is a promising tool for noninvasive brain functional imaging using conscious rats to avoid the effects of anesthetic agents.


2010 ◽  
Vol 112 (1) ◽  
pp. 50-56 ◽  
Author(s):  
Mads Rasmussen ◽  
Niels Juul ◽  
Søren M. Christensen ◽  
Kristjana Y. Jónsdóttir ◽  
Carsten Gyldensted ◽  
...  

Background The regional cerebral blood flow (CBF) response to propofol and indomethacin may be abnormal in patients with brain tumors. First, the authors tested the hypothesis that during propofol anesthesia alone and combined with indomethacin, changes in CBF, cerebral blood volume (CBV), and plasma mean transit time (MTT) differ in the peritumoral tissue compared with the contralateral normal brain region. Second, the authors tested the hypothesis that CBF and CBV are reduced and MTT is prolonged, in both regions during propofol anesthesia and indomethacin administration compared with propofol alone. Methods The authors studied eight patients subjected to craniotomy under propofol-fentanyl anesthesia for supratentorial brain tumors. Magnetic resonance imaging, including perfusion- and diffusion-weighted and structural sequences, was performed (1) on the day before surgery, (2) before and (3) after administration of indomethacin in the propofol-fentanyl anesthetized patient, and (4) 2 days after surgery. Maps of CBF, CBV, and MTT were calculated. The regions of interest were peritumoral gray matter and opposite contralateral gray matter. Analysis of variance was used to analyze flow data. Results Propofol anesthesia was associated with a median 32% (range, 3-61%) and 47% (range, 17-67%) reduction in CBF in the peritumoral and contralateral regions, respectively.The interaction between intervention with propofol and indomethacin and region of interest was not significant for any flow modalities. Neither intervention nor region was significant for MTT, CBF, and CBV (P > 0.05). Conclusion The CBF, CBV, and MTT responses to propofol and indomethacin are not different in the peritumoral region compared with contralateral brain tissue. Indomethacin did not further influence regional CBF, CBV, and MTT during propofol anesthesia.


1981 ◽  
Vol 1 (2) ◽  
pp. 187-194 ◽  
Author(s):  
M. Ohata ◽  
W. R. Fredericks ◽  
U. Sundaram ◽  
S. I. Rapoport

Immobilization stress of conscious, normotensive, freely breathing 10-month-old Wistar-Kyoto rats produced an overall decline in regional cerebral blood flow (rCBF), as measured with [14C]iodoantipyrine, except at the frontal lobe. In 14 brain regions, rCBF fell by an average of 14.3% after 5 min of immobilization and by 11.9% after 15 min. Immobilization stress also stimulated hyperventilation and thereby reduced Paco2. The slope relating rCBF to Paco2 averaged 1.5 ml 100 g−1 min−1 mm Hg−1 in 9 significantly affected regions. The findings suggest that rCBF declines during immobilization stress because of cerebrovascular constriction caused by a reduction in Paco2. Comparison of the average slope with published values indicates furthermore that were Paco2 to remain unchanged during immobilization, rCBF would increase by at most 20%.


1992 ◽  
Vol 126 (3) ◽  
pp. 243-246 ◽  
Author(s):  
Peter S Oturai ◽  
Lars Friberg ◽  
Ian Sam ◽  
Hans Perrild

To assess the regional changes in cerebral blood flow, 10 healthy volunteers were given 400 μg thyrotropin-releasing hormone iv in a double-blind, randomized, cross-over study. Regional cerebral blood flow was determined simultaneously in two slices of the brain, using a single photon emission computerized tomograph and inhalation of 133Xe. Thyrotropin-releasing hormone caused a significant mean increase of 3.7% (range −8.8–22.7) in blood flow in a region consistent with the left thalamus compared to placebo (3.2% decrease). In 25 other regions no significant change was detected. The thalamic region has previously been shown to be a region especially affected by thyrotropin-releasing hormone in animal studies. The thyrotropin-releasing hormone injection was followed by a minor rise in systemic blood pressure, but not a rise that could affect the cerebral blood flow. The effect of thyrotropin-releasing hormone on the regional cerebral blood flow in the thalamic region was much lower compared to changes found in sedated animals given a hundredfold higher dose of thyrotropin-releasing hormone.


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