scholarly journals Effects of Indomethacin and Ibuprofen on Cerebral Metabolism and Blood Flow in Traumatized Brain

1983 ◽  
Vol 3 (4) ◽  
pp. 448-459 ◽  
Author(s):  
Hanna M. Pappius ◽  
Leonhard S. Wolfe

Local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) were studied by autoradiographic techniques in indomethacin- and ibuprofen-treated rats with focal cortical freezing lesions. Widespread depression of LCGU, which developed with time after the lesion in untreated animals was significantly diminished by the prostaglandin synthetase inhibitors indomethacin (single injection 7.5 mg/kg) and ibuprofen (36 mg/kg/day). Both drugs were effective when given 6 h before or up to 24 h after the lesion was made. The effect of the drugs was most striking in cortical areas of the traumatized hemisphere, where the depression was most profound in untreated animals. Thus, 3 days afer the lesion, average LCGU in these regions was 46%, 86%, and 98% of normal in untreated, indomethacin-pretreated, and ibuprofen-pretreated rats, respectively. Prostaglandin formation was completely inhibited in the lesion area in the indomethacin-treated rats (PGF2α 1.8 ng/g, compared to 57.5 ng/g in untreated and 1.4 ng/g in nonlesioned animals). The results suggest that some components of the prostaglandin system are involved in mechanisms underlying a widespread depression in functional state of the rat brain that develops in response to injury. In control animals, indomethacin was shown to have a biphasic effect on LCBF, an early depression shown previously by others followed at 24 h by a considerable increase.

1985 ◽  
Vol 5 (1) ◽  
pp. 58-64 ◽  
Author(s):  
W. Kuschinsky ◽  
S. Suda ◽  
L. Sokoloff

The relationship between local cerebral glucose utilization (LCGU) and local CBF (LCBF) was examined during the action of γ-hydroxybutyrate (GHB) (900 mg/kg i.v.) in conscious rats. GHB induced discrepant effects on blood flow and metabolism. LCGU was markedly depressed in all structures examined, whereas LCBF was differently affected in that no related changes were observed. Global glucose utilization was markedly depressed (- 51%), whereas global blood flow was not significantly altered. The marked dissociation between the changes in global glucose utilization and global blood flow induced by GHB is reflected only to a minor degree in the local values inasmuch as the correlation between LCGU and LCBF was only slightly weakened and its heterogeneity was increased.


1983 ◽  
Vol 3 (1) ◽  
pp. 62-66 ◽  
Author(s):  
Thomas W. Furlow ◽  
Lynn E. Harrison

A simplified technique that uses two radionuclide tracers has been devised to measure local cerebral glucose utilization (lCGU) and local cerebral blood flow (lCBF) in the same rat. The method employs [14C]-2-deoxyglucose and [14C]iodoantipyrine to produce an autoradiogram before and another after extraction into chloroform of the [14C]iodoantipyrine from the brain sections. The chloroform-extracted autoradiogram yields lCGU, and the difference in tissue carbon-14 concentration between the two autoradiograms permits calculation of lCBF. The double-isotope technique provides values of lCGU and lCBF that are statistically indistinguishable from those derived from conventional single-isotope methods.


1998 ◽  
Vol 89 (6) ◽  
pp. 1480-1488 ◽  
Author(s):  
Christian Lenz ◽  
Annette Rebel ◽  
Klaus van Ackern ◽  
Wolfgang Kuschinsky ◽  
Klaus F. Waschke

Background Compared to isoflurane, knowledge of local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF) during sevoflurane anesthesia is limited. Methods LCGU, LCBF, and their overall means were measured in Sprague-Dawley rats (8 groups, n=6 each) during sevoflurane and isoflurane anesthesia, 1 and 2 MAC, and in conscious control animals (2 groups, n=6 each) using the autoradiographic 2-[14C]deoxy-D-glucose and 4-iodo-N-methyl-[14C]antipyrine methods. Results During anesthesia, mean cerebral glucose utilization was decreased: control, 56+/-5 micronmol x 100 g(-1) x min(-1); 1 MAC isoflurane, 32+/-4 micromol x 100 g(-1) x min(-1) (-43%); 1 MAC sevoflurane, 37+/-5 micromol x 100 g(-1) x min(-1) (-34%); 2 MAC isoflurane, 23+/-3 micromol x 100 g(-1) x min(-1) (-58%); 2 MAC sevoflurane, 23+/-5 micromol x 100 g(-1) x min(-1) (-59%). Local analysis showed a reduction in LCGU in the majority of the 40 brain regions analyzed. Mean cerebral blood flow was increased as follows: control 93+/-8 ml x 100 g(-1) x min(-1); 1 MAC isofurane, 119+/-19 ml x 100 g(-1) x min(-1) (+28%); 1 MAC sevoflurane, 104+/-15 ml x 100 g(-1) x min(-1) (+12%); 2 MAC isoflurane, 149+/-17 ml x 100 g(-1) x min(-1) (+60%); 2 MAC sevoflurane, 118+/-21 ml x 100 g(-1) min(-1) (+27%). LCBF was increased in most brain structures investigated. Correlation coefficients obtained for the relationship between LCGU and LCBF were as follows: control 0.93; 1 MAC isoflurane, 0.89; 2 MAC isoflurane, 0.71; 1 MAC sevoflurane, 0.83; 2 MAC sevoflurane, 0.59). Conclusion Mean and local cerebral blood flows were lower during sevoflurane than during isoflurane anesthesia. This difference cannot be explained by differing changes in glucose utilization because glucose utilization was decreased to the same extent in both groups.


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