Comparisons of oxygen metabolism and tissue PO2 in cortex and hippocampus of gerbil brain.

Abstract

Recessed oxygen microelectrodes (tip diameter < 2 (j.m) were positioned stereotactically into either the cerebral cortex or the hippocampus of sodium pentobarbital anesthetized gerbils (n = 21). The mean tissue P02 levels (± SEM) were not significantly different between cortex (35.4 ± 1.7 torr) and hippocampus (33.6 ± 1.4 torr) although differences in the tissue P02 distributions were seen. The disappearance rate for oxygen ( -dPo^dt) was measured after brief (< 15 seconds) bilateral carotid artery (total brain blood flow) occlusion. The mean (±SEM) disappearance rate was significantly higher (p<0.05) in the cortex (Z3.8 ± 1.5 torr/sec, 160 locations in 21 gerbils) than In the hippocampus (17.0 ± 0.7 torr/sec, 119 locations in 16 gerbils). The maximum oxygen consumption rates (Vc^max) for Michaelis-Menten kinetics were calculated from the disappearance rates, correcting for gerbil oxyhemoglobin. The mean Vo^max was 8.28 ± 0.51 and 6.13 ± 0.25 ml O 2 /100 g/rain for the cortex and hippocampus, respectively. The apparent Michaelis-Menten kinetic constants (K_) for the 2 regions were not significantly different (overall mean 3.3 ± 0.4 torr The present study was undertaken to quantify oxygen metabolism at highly localized sites by the oxygen disappearance technique, correcting for the influence of oxyhemoglobin. Measurements were made in 2 regions of the gerbil brain, the cortex and the hippocampus, which are of interest due to marked differences in susceptibility to ischemic damage (selective vulnerability), even within a region. The gerbil model of ischemia was chosen because blood flow to the brain can be stopped completely with bilateral carotid artery occlusion since the circle of Willis has no connections to the basilar artery for a source of collateral blood flow. Materials and MethodsMongolian gerbils, aged 3-4 months, weighing 50-90 g, were maintained on standard laboratory food and water ad libitum. They were anesthetized with 30-40 mg/kg i.p. sodium pentobarbital, tracheotomized, and allowed to breathe spontaneously. Both common carotid arteries were exposed through ventral midline cervical incisions and isolated from the accompanying nerves and vein. Surgical sutures were placed around the arteries for causing occlusions. In by guest on May 9, 2018 http://stroke.ahajournals.org/ Downloaded from

Simultaneous recording of hippocampal oxygen and glucose in real time using constant potential amperometry in the freely-moving rat

“…In comparison, the oxygen levels found in the hippocampus (100.26 ± 5.76 M) in this study are quite high with hippocampal oxygen being 33.6 mm Hg (∼52.8 M) in the anaesthetised gerbil (Nair et al, 1987) and 20.3 mm Hg (∼31.9 M) in the anaesthetised rat (Cater et al, 1961). Compared to other regions in the rat brain, the hippocampal oxygen levels found here also appear to be higher with 50 M in the caudate nucleus (Zimmerman and Wightman, 1991) and 37 ± 16 M Calia et al, 2009) in the striatum.…”

Characterization in vitro and in vivo of the oxygen dependence of an enzyme/polymer biosensor for monitoring brain glucose

“…4. Thus, although the estimated concentration of brain extracellular O 2 is relatively low at approximately 50 mM (Nair et al, 1987;Murr et al, 1994), significant increases in its concentration did not affect the glucose current, supporting the O 2 interference analysis presented in Section 3.2.…”

“…Although O 2 ECF levels farthest from blood brain capillaries can be as low as 5 mM (Siesjo, 1978), electrodes the size of CPEs and Pt/PPD/GOx sensors sample the average tissue ECF concentration, estimated at Â/50 mM (Nair et al, 1987;Murr et al, 1994). We therefore calculated the percentage O 2 interference in the glucose signals at 50 mM O 2 per micromolar change in O 2 concentration (S % ), i.e., the tangential slope of plots similar to those in Fig.…”

Conditions for pharmacologic evaluation in the gerbil model of forebrain ischemia.

“…It is unlikely that the administration of hyperoxic gases (Fio 2 of 37% or 97%) significantly diminished the duration of tissue hypoxia after ischemia compared with normoxia. The rate of decrease of hippocampal and cortical Po 2 has been measured in the gerbil brain from the moment of carotid artery occlusion to the time tissue Po 2 reached 0 10 ; over a range of tissue Po 2 (20-50 mm Hg), the rate of decrease increased with increasing Po 2 so that brain Po 2 fell to 0 within 2-3 seconds of carotid artery occlusion. 10 This rapid rate of decrease of tissue Po 2 during ischemia makes it unlikely that increased brain Po 2 due to the administration of hyperoxic gases significantly diminished the duration of brain hypoxemia.…”