scholarly journals Infarct Rim: Effect of Hyperglycemia on Direct Current Potential and [14C]2-Deoxyglucose Phosphorylation

1986 ◽  
Vol 6 (5) ◽  
pp. 607-615 ◽  
Author(s):  
Maiken Nedergaard ◽  
Jens Astrup

Focal ischemia was produced by occlusion of the right middle cerebral artery (MCA) in normo- and hyperglycemic rats. In the cortical infarct rim, regional [14C]2-deoxyglucose ([14C]2-DG) phosphorylation was correlated to spontaneous transient changes in extracellular potassium recorded as direct current (DC) potential deflections. In normoglycemic rats the DC potential showed transient but recurrent deflections in the first hours following MCA occlusion. The 2-DG phosphorylation was elevated by 200% in the same area. In contrast, hyperglycemic rats had no, or a single, deflection of the DC potential in the rim, and the 2-DG phosphorylation remained normal. The same pattern was obtained by application of 3 M KCl to the exposed cortex. In normoglycemia potassium application resulted in recurrent deflections of the DC potential, and 2-DG phosphorylation increased in most parts of the hemisphere. Hyperglycemic animals had a nearly stable DC potential, and 2-DG phosphorylation increased only in the tissue area situated directly below the site of potassium application. The results indicate that metabolism in the cortical infarct rim is stimulated by spontaneous and recurrent changes in extracellular potassium—a phenomenon that may be related to spreading depression—and that the metabolism remained normal in the same area in hyperglycemic animals owing to an inhibition of transient increases of extracellular potassium.

1991 ◽  
Vol 260 (5) ◽  
pp. R911-R915 ◽  
Author(s):  
N. Mori ◽  
N. Uozumi

Our recent study has revealed that catecholamines depress the endolymphatic sac direct current potential (ESP) by the beta-adrenergic action [Mori et al., Am. J. Physiol. 259 (regulatory Integrative Comp. Physiol. 28): R921-R924, 1990]. Beta-Adrenergic receptors have been subclassified into beta 1- and beta 2-receptors. Using beta 1-selective (dobutamine) and beta 2-selective (salbutamol) agonists and a beta 1-selective antagonist (atenolol), we determined the subtype of beta-adrenergic receptors that mediate the action of catecholamines on the ESP. Salbutamol depressed the ESP to a larger degree than dobutamine [34.0 +/- 2.6 (n = 7) vs. 13.0 +/- 2.0% (n = 8)] with a much lower dose (100 vs. 1,000 micrograms/kg). Atenolol failed to block the action of salbutamol on the ESP at a dose of 1 mg/kg, whereas propranolol inhibited it at the same dose. The results indicate that beta 2-receptors mediate the action of catecholamines on the ESP.


2002 ◽  
Vol 22 (1) ◽  
pp. 71-79 ◽  
Author(s):  
Tomoyasu Higuchi ◽  
Yoshimasa Takeda ◽  
Megumi Hashimoto ◽  
Osamu Nagano ◽  
Masahisa Hirakawa

Forty rats were subjected to 3 hours of focal ischemia by occluding the left middle cerebral and left common carotid arteries. The propagation of recurrent depolarization around the ischemic core was analyzed using direct-current potential and NADH (reduced nicotinamide adenine dinucleotide) fluorescence images by irradiating the parietal-temporal cortex with ultraviolet light. Based on histological evaluation at direct-current recording sites, the total time of depolarization causing 50% neuronal injury was estimated to be 18.2 minutes. The sites showing recurrent depolarizations resulted in 23 ± 29% neuronal injury due to the short depolarization time, whereas the sites showing recurrent depolarizations and eventually persistent depolarization resulted in infarction. The NADH fluorescence images showed that recurrent depolarizations propagated along the margin of the ischemic core. In 85.9% of the recurrent depolarizations, the fluorescence disappeared without leaving any traces and did not affect the area of the ischemic core. However, in 47.5% of the animals, 14.1% of recurrent depolarizations merged with the ischemic core and increased the area by 6 ± 4 mm2. These findings suggest that recurrent depolarization increases the severity of neuronal injury but does not cause infarction by itself if persistent depolarization does not follow, and that the area of persistent depolarization is enlarged with 14.1% of recurrent depolarizations.


1980 ◽  
Vol 88 (2) ◽  
pp. 188-193 ◽  
Author(s):  
Shinichiro Asakuma ◽  
James B. Snow

The effects of loop diuretics on the endocochlear direct current (DC) potential and the effective electrical resistance of the cochlear partition were studied. The effective electrical resistance was increased, and the endocohlear DC potential was decreased. The decrease in the endocohlear DC potential must not be caused by breaks in the electrical insulation of the cochlear partition. With loop diuretics the endocochlear DC potential decreased less in guinea pigs treated with kanamycin sulfate than it did in the control group. Two interpretations of these phenomena are presented.


2021 ◽  
Vol 6 (1) ◽  
pp. 94-100
Author(s):  
O. I. Shevchenko ◽  
O. L. Lakhman

The aim of the study was to identify the peculiarities of neuropsychological indices disorders depending on changes in the level of constant potential in patients with occupational diseases as a result of physical factors.Materials and methods. The study involved 60 patients with vibration disease caused by local vibration (group I), 106 patients with vibration disease caused by combined exposure to local and general vibration (group II), 101 civil aviation pilots with an established diagnosis of professional sensorineural hearing loss (group III), and 50 healthy men (group IV, comparison group) who were not exposed to vibration and noise due to the specifics of their professional activities. Methods of neuro-energy mapping and neuropsychological testing were used.Results. In groups I–II, compared with group IV, an increase in local levels of constant potential (DC-potential level) in the central, right temporal, and central frontal parts of the brain (2.3 (6.5–3.8) mV; –0.3 (–2.1–2.1); 2.1 (–3.4–6.8) and –0.3 (–3.1–4.3); –2.24 (–6.4–3.8); 0.9 (–3.1–8.5) mV at p = 0.005, 0.007 and 0.004 respectively). Differences in the values of DC-potential level gradients in individuals of group III when compared with group IV reached the level of significance in the central, temporal, occipital leads relative to the central frontal (–5.0 (–13.1–3.8); –4.1 (–9.4–5.1); –2.1 (–10.9–6.6); –6.3 (–15.3–1.8) and 2.9 (–3.0–10.6); 2.2 (–4.5–13.8); 5.6 (–7.6–14.1); –1.4 (–7.5–3.9) mV at p = 0.008; 0.009; 0.009, and 0.007 respectively). Cognitive disorders in patients of groups I–III when compared with group IV correspond to a mild disorder of dynamic, constructive praxis and expressive speech (1.40 (0–1,6); 1.43 (0–1,7); 1.2 (0–1,5) and 0.3 (0–1); 0.2 (0–1); 0.06 (0–1) points at p = 0.008, 0.008 and 0.009 respectively).Conclusions. A common neurofunctional sign of a mild impairment of the cognitive sphere in occupational diseases caused by physical factors is an increase in direct current potential level in the frontal-central and parieto-occipital regions, predominantly of the left hemisphere of the brain.


1998 ◽  
Vol 18 (10) ◽  
pp. 1114-1120 ◽  
Author(s):  
Thomas J. Sick ◽  
Zi-Cai Feng ◽  
Myron Rosenthal

Extracellular potassium ion activity ([K+]o) increases precipitously during brain ischemia when blood flow falls below threshold values less than approximately 15 mL/100 g/min. This flow threshold for increase of [K+]o occurs also in focal ischemia producing gradient from ischemic core to adjacent normally perfused brain. In this study we investigated the spatial and temporal stability of extracellular potassium ion and blood flow gradients after permanent middle cerebral artery occlusion (MCAO) in rats. [K+]o and regional CBF were measured, respectively, with K+-sensitive and polarographic hydrogen-sensitive microelectrodes at different cortical locations in the middle cerebral artery distribution region. Spatial assessment of [K+]o and regional CBF was conducted at 30, 90, and 180 minutes after MCAO. [K+]o in the more lateral cortex (core) increased from near 3 mmol/L before MCAO to greater than 50 mmol/L and was associated with flow values less than 25% of pre-ischemic levels. Measurements medial to the core (penumbra) indicated progressively decreasing levels of [K+]o and improvement of CBF. There was a tendency for [K+]o in penumbral zones to decrease toward normal levels with time, but there was little dissipation of [K+]o in core regions. In contrast, the spatial CBF profile remained remarkably constant for the entire recording period. Thus, unlike infarction which has been reported to expand with time after focal ischemia, the spatial [K+]o disturbance tends to contract primarily due to decreasing [K+]o with time in the penumbra. Thus, steady state levels of [K+]o after focal ischemia may not be a valuable predictor of cell viability.


Author(s):  
Z. Gao Huang ◽  
Dong Xue ◽  
Hasneen Karbalai ◽  
Alastair M. Buchan ◽  
Z. Gao Huang ◽  
...  

Objective:Tracer constants (Ki) for blood-to-brain diffusion of sucrose were measured in the rat to profile the time course of blood-brain barrier injury after temporary focal ischemia, and to determine the influence of post-ischemic hypothermia.Methods:Spontaneously hypertensive rats were subjected to transient (2 hours) clip occlusion of the right middle cerebral artery. Reperfusion times ranged from 1.5 min to 46 hours, and i.v. 3H-sucrose was circulated for 30 min prior to each time point (1h, 4h, 22h, and 46h; n=5-7 per time point). Ki was calculated from the ratio of parenchymal tracer uptake and the time-integrated plasma concentration. Additional groups of rats (n=7-8) were maintained either normothermic (37.5oC) or hypothermic (32.5oC or 28.5oC) for the first 6 hours of reperfusion, and Ki was measured at 46 hours.Results:Rats injected after 1.5 - 2 min exhibited a 10-fold increase in Ki for cortical regions supplied by the right middle cerebral artery (p<0.01). This barrier opening had closed within 1 to 4 hours post-reperfusion. By 22 hours, the blood-brain barrier had re-opened, with further opening 22 and 46 hours (p<0.01), resulting in edema. Whole body hypothermia (28oC-29oC) during the first six hours of reperfusion prevented opening, reducing Ki by over 50% (p<0.05).Conclusion:Transient middle cerebral artery occlusion evokes a marked biphasic opening of the cortical blood-brain barrier, the second phase of which causes vasogenic edema. Hypothermic treatment reduced infarct volume and the late opening of the blood-brain barrier. This opening of the blood-brain barrier may enhance delivery of low permeability neuroprotective agents.


1980 ◽  
Vol 88 (2) ◽  
pp. 188-193 ◽  
Author(s):  
Shinichiro Asakuma ◽  
James B. Snow

The effects of loop diuretics on the endocochlear direct current (DC) potential and the effective electrical resistance of the cochlear partition were studied. The effective electrical resistance was increased, and the endocohlear DC potential was decreased. The decrease in the endocohlear DC potential must not be caused by breaks in the electrical insulation of the cochlear partition. With loop diuretics the endocochlear DC potential decreased less in guinea pigs treated with kanamycin sulfate than it did in the control group. Two interpretations of these phenomena are presented.


1992 ◽  
Vol 12 (2) ◽  
pp. 230-237 ◽  
Author(s):  
Marleen J. Verhaegen ◽  
Michael M. Todd ◽  
David S. Warner ◽  
Bruce James ◽  
Julie B. Weeks

Cerebral blood flow was measured by the H2 clearance method 30 and 60 min after the implantation of 300, 250, 125, or 50 μm diameter platinum–iridium electrodes 2 mm deep into the right parietal cortex of normothermic, normocarbic halothane-anesthetized rats. Another group of animals had 50 μm electrodes inserted 1 mm. In all animals, the presence or absence of a wave of spreading depression (SD) was noted at the time of implantation, with recordings made with glass micropipettes. H2 flow values were compared with those measured in gray matter from the same anatomical region (but from different rats), using [3H]nicotine. The incidence of SD ranged from 60% following insertion of 300 μm electrodes to 0% with 50 μm electrodes. H2 clearance flows also varied with electrode size, from 77 ± 21 ml 100 g−1 min−1 (mean ± standard deviation) with 300 μm electrodes to 110 ± 31 and 111 ± 16 ml 100 g−1 min−1 with 125 and 50 μm electrodes, respectively (insertion depth of 2 mm). A CBF value of 155 ± 60 ml 100 g−1 min−1 was obtained with 50 μm electrodes inserted only 1 mm. Cortical gray matter blood flow measured with [3H]nicotine was 154 ± 35 ml 100 g−1 min−1. When the role of SD in subsequent flow measurements was examined, there was a gradual increase in CBF between 30 and 60 min after electrode insertion in those animals with SD, while no such change was seen in rats without SD. These results indicate that the choice of electrode size and implantation depth influences the measurement of CBF by H2 clearance. CBF values equivalent to those obtained with isotopic techniques can be acutely obtained with small (50 μm diameter) electrodes inserted 1 mm into the cortex. While the occurrence of SD does influence CBF in the period immediately after implantation, a relationship between electrode size and measured flow is present that is independent of SD.


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