scholarly journals Local Cerebral Blood Flow during Hibernation, a Model of Natural Tolerance to “Cerebral Ischemia”

1994 ◽  
Vol 14 (2) ◽  
pp. 193-205 ◽  
Author(s):  
Kai U. Frerichs ◽  
Charles Kennedy ◽  
Louis Sokoloff ◽  
John M. Hallenbeck
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Body Temperature ◽  
Physiological State ◽  
Ground Squirrels ◽  
Control Group ◽  
Spermophilus Tridecemlineatus ◽  
Destructive Processes ◽  
Natural Tolerance

The breakdown of cellular homeostasis and progressive neuronal destruction in cerebral ischemia appears to be mediated by a complex network of causes that are intricately interrelated. We have investigated a physiological state existing normally in nature in which mammals appear to tolerate the ordinarily detrimental effects of ischemia with reduced oxygen availability and to resist activation of self-destructive processes, i.e., mammalian hibernation. Ground squirrels (Spermophilus tridecemlineatus) were chronically implanted with arterial and venous catheters and telemetry devices for electroencephalography, electrocardiography, and monitoring of body temperature. The animals were placed in an environmental chamber at an ambient temperature of 5°C. Entrance into hibernation was characterized by a drop in heart rate followed by a gradual decline in body temperature and an isoelectric electroencephalogram. Cold-adapted active animals that were not hibernating served as controls. Cerebral blood flow (CBF) was measured in both groups with the autoradiographic [14C]iodoantipyrine method. Mean (±SD) mass-weighted CBF in the brain as a whole was 62 ± 16 ml/100 g/min (n = 4) in the control group but was reduced to ischemic levels, 7 ± 4 ml/100 g/min (n = 4), in the hibernating animals (p < 0.001). No neuropathological changes were found in similarly hibernating animals aroused from hibernation. Hibernation appears to be actively regulated, and hormonal factors may be involved. The identification and characterization of such factors and of the mechanisms used by hibernating species to increase ischemic tolerance and to blunt the destructive effects of ischemia may enable us to prevent or minimize the loss of homeostatic control during and after cerebral ischemia in other species.

Erratum

1994 ◽  
Vol 14 (5) ◽  
pp. 884-884
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Ground Squirrel ◽  
Weighted Average ◽  
Ground Squirrels ◽  
Control Group ◽  
Local Cerebral Blood Flow ◽  
Correct Number ◽  
Natural Tolerance ◽  
The Brain

Local Cerebral Blood Flow During Hibernation, a Model of Natural Tolerance to “Cerebral Ischemia” Kai U. Frerichs, Charles Kennedy, Louis Sokoloff and John M. Hallenbeck [ originally published in Journal of Cerebral Blood Flow and Metabolism 1994;14(2):193–205] The weighted average cerebral blood flow in the brains of hibernating and nonhibernating ground squirrels appeared in three places in the article cited above. The numbers varied to some extent in each of the three places that they were displayed. The correct number for the active ground squirrel group was 62 ± 18 ml 100 g−1 min−1. The correct number for the hibernating group was 7 ± 4 ml 100 g−1 min−1. These numbers should be inserted on page 193 in the abstract so that the sentence would read, “Mean (± SD) mass-weighted CBF in the brain was 62 ± 18 ml 100 g−1 min−1 (n = 4) in the control group but was reduced to ischemic levels, 7 ± 4 ml 100 g−1 min−1 (n = 4), in the hibernating animals (p < 0.001).” The same numbers should be inserted into the sentence that begins at the bottom of page 198, “Average blood flow (± SD) in the brain as a whole in the hibernating animals was reduced to about 1/10 (7 ± 4 ml 100 g−1 min−1) of the level in active animals (62 ± 18 ml 100 g−1 min−1) (Table 4).” Finally, on page 201 at the bottom of Table 4 below “Weighted average in brain as a whole,” the readings should be 62 ± 18 for active and 7 ± 4 for hibernating.

Hypothermic cerebral reperfusion and recovery from ischemia

1991 ◽  
Vol 261 (3) ◽  
pp. H774-H781 ◽  
Author(s):  
W. A. Baldwin ◽  
J. R. Kirsch ◽  
P. D. Hurn ◽  
W. S. Toung ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Cerebral Ischemia ◽  
Control Group ◽  
Experimental Animals ◽  
Anesthetized Dogs ◽  
Group Recovery ◽  
Cerebral Reperfusion ◽  
Experimental Group

The effect of transient postischemic hypothermia (30 degrees C) on recovery of cerebral blood flow (CBF), oxygen consumption (CMRO2) and somatosensory-evoked potentials (SEPs) was determined in anesthetized dogs. Ischemia was produced for 20 min by intracranial pressure (ICP) elevation while core temperature was lowered by cooling externalized blood. Epidural temperature was controlled at 37.6 +/- 0.2 degrees C during ischemia, lowered to 30.0 +/- 0.1 degrees C during the first hour of reperfusion, and then rewarmed to 38.0 +/- 0.1 degrees C in experimental dogs (n = 8) and maintained at 38.0 +/- 0.1 degrees C in control dogs (n = 8). ICP was lower throughout reperfusion in experimental as compared with control animals. By 240 min of reperfusion, CBF was approximately 70% of control in both groups. CMRO2 was 60% of preischemic values in control animals and 74% in experimental animals (P = 0.077). A persistent uncoupling of CBF and CMRO2 was observed throughout reperfusion only in the control group. Recovery of SEP amplitude was significantly improved in the experimental group (26 vs. 11% of preischemic values). These data suggest that transient hypothermia reduces ICP and facilitates recovery of electrophysiological function after cerebral ischemia.

scholarly journals Kidney proteome changes provide evidence for a dynamic metabolism and regional redistribution of plasma proteins during torpor-arousal cycles of hibernation

2012 ◽  
Vol 44 (14) ◽  
pp. 717-727 ◽  
Author(s):  
Alkesh Jani ◽  
David J. Orlicky ◽  
Anis Karimpour-Fard ◽  
L. Elaine Epperson ◽  
Rae L. Russell ◽  
...  
Keyword(s):  
Blood Flow ◽  
Body Temperature ◽  
Plasma Proteins ◽  
Physiological State ◽  
Ground Squirrels ◽  
Endocytic Pathway ◽  
Protein Abundance ◽  
Regional Heterogeneity ◽  
Physiological Demands ◽  
Proteome Changes

Hibernating ground squirrels maintain homeostasis despite extreme physiological challenges. In winter, these circannual hibernators fast for months while cycling between prolonged periods of low blood flow and body temperature, known as torpor, and short interbout arousals (IBA), where more typical mammalian parameters are rapidly restored. Here we examined the kidney proteome for changes that support the dramatically different physiological demands of the hibernator's year. We identified proteins in 150 two-dimensional gel spots that altered by at least 1.5-fold using liquid chromatography and tandem mass spectrometry. These data successfully classified individuals by physiological state and revealed three dynamic patterns of relative protein abundance that dominated the hibernating kidney: 1) a large group of proteins generally involved with capturing and storing energy were most abundant in summer; 2) a select subset of these also increased during each arousal from torpor; and 3) 14 spots increased in torpor and early arousal were enriched for plasma proteins that enter cells via the endocytic pathway. Immunohistochemistry identified α2-macroglobulin and albumin in kidney blood vessels during late torpor and early arousal; both exhibited regional heterogeneity consistent with highly localized control of blood flow in the glomeruli. Furthermore, albumin, but not α2-macroglobulin, was detected in the proximal tubules during torpor and early arousal but not in IBA or summer animals. Taken together, our findings indicate that normal glomerular filtration barriers remain intact throughout torpor-arousal cycles but endocytosis, and hence renal function, is compromised at low body temperature during torpor and then recovers with rewarming during arousal.

Regional cerebral blood flow in cats with cross-linked hemoglobin transfusion during focal cerebral ischemia

2002 ◽  
Vol 282 (3) ◽  
pp. H832-H841 ◽  
Author(s):  
Annette Rebel ◽  
John A. Ulatowski ◽  
Karena Joung ◽  
Enrico Bucci ◽  
Richard J. Traystman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Caudate Nucleus ◽  
Oxygen Transport ◽  
Focal Cerebral Ischemia ◽  
Acute Injury ◽  
Arterial Oxygen ◽  
Control Group ◽  
Large Animal

841, 2002. First published November 8, 2001; 10.1152/ajpheart. 00880.2001.—The beneficial effect of hemodilution on cerebral blood flow (CBF) during focal cerebral ischemia is mitigated by reduced arterial oxygen content (CaO2 ). In anesthetized cats subjected to permanent middle cerebral artery occlusion, the time course of regional CBF was evaluated after isovolemic exchange transfusion with either albumin or a tetrameric hemoglobin-based oxygen carrier. The transfusion started 30 min after arterial occlusion. We tested the hypothesis that bulk oxygen transport (CBF × CaO2 ) to ischemic tissue is increased by hemoglobin transfusion at a hematocrit of 18% compared with albumin-transfused cats at a hematocrit of 18% or control cats at a hematocrit of 30% and equivalent arterial pressure. In the nonischemic hemisphere, CBF increased selectively after albumin transfusion, and oxygen transport was similar among groups. In the ischemic cortex, albumin transfusion increased CBF, but oxygen transport was not increased above that of the control group. Hemoglobin transfusion increased both CBF and oxygen transport in the ischemic cortex above values in the control group, but the increase was delayed until 4 h of ischemia. Consequently, acute injury volume measured at 6 h of ischemia was not significantly attenuated. In contrast to the cortex, CBF in the ischemic caudate nucleus was not substantially increased by either albumin or hemoglobin transfusion. Therefore, in a large animal model of permanent focal ischemia in which transfusion starts 30 min after ischemia, tetrameric cross-linked hemoglobin transfusion can augment oxygen transport to the ischemic cortex, but the increase can be delayed and not necessarily provide protection. Moreover, an end-artery region such as the caudate nucleus is less likely to benefit from hemodilution.

Effect of mannitol on local cerebral blood flow after temporary complete cerebral ischemia in rats

1992 ◽  
Vol 76 (3) ◽  
pp. 486-492 ◽  
Author(s):  
Reizo Shirane ◽  
Philip R. Weinstein
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
External Carotid ◽  
Control Group ◽  
Local Cerebral Blood Flow ◽  
Content Type ◽  
Arterial Blood ◽  
Permanent Occlusion ◽  
Fine Print

✓ The effects of pretreatment with mannitol on local cerebral blood flow (CBF) after permanent or temporary global cerebral ischemia were evaluated with 14C-iodoantipyrine autoradiography in rats under halothane-N2O endotracheal anesthesia. Blood pressure, pulse rate, arterial blood gas levels, and electroencephalographic (EEG) tracings were monitored throughout the experiments. After permanent occlusion of the basilar artery and both external carotid and pterygopalatine arteries, severe global ischemia was induced by permanent occlusion of the common carotid arteries (CCA's) or by a 30-minute temporary CCA occlusion followed by 5 minutes of reperfusion. Intravenous mannitol (25%, 1 gm/kg) or saline solution was administered 5 minutes before occlusion of the CCA's. Cerebral blood flow was measured in 24 anatomical regions. The EEG tracings flattened within 2 to 3 minutes after the onset of ischemia, and no recovery was observed during reperfusion. In the mannitol-treated rats and the saline-treated controls, autoradiographic studies after permanent occlusion showed no CBF in the forebrain or cerebellum, although brain-stem and spinal cord CBF values were normal. After 5 minutes of reperfusion, CBF in the cortex, basal ganglia, and white matter was 100% to 200% higher in mannitol-treated rats and 50% to 100% higher in saline-injected rats than in the nonischemic anesthetized control group. Heterogeneously distributed areas of no-reflow were seen in all saline-injected rats but were observed in none of the mannitol-treated rats. Pretreatment with mannitol prevented postischemic obstruction of the microcirculation during 5 minutes of recirculation after 30 minutes of severe temporary ischemia, but the EEG signals did not recover. Further studies of the functional and morphological responses to longer periods of postischemic recirculation are needed to verify the extent to which these mannitol-induced effects are protective.

New display methods of combined topographic EEG and cerebral blood flow images in the evaluation of cerebral ischemia

1996 ◽  
Vol 8 (3) ◽  
pp. 275-278 ◽  
Author(s):  
Akifumi Suzuki ◽  
Hiromi Nishimura ◽  
Kimio Yoshioka ◽  
Masaaki Lwase ◽  
Nobuyuki Yasui ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Topographic Eeg

The Study of Electroacupuncture on Cerebral Blood Flow in Rats With and Without Cerebral Ischemia

2006 ◽  
Vol 34 (02) ◽  
pp. 351-361 ◽  
Author(s):  
Ching-Liang Hsieh ◽  
Qwang-Yuen Chang ◽  
I-hsin Lin ◽  
Jaung-Geng Lin ◽  
Chung-Hsiang Liu ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Cortex ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Peripheral Blood ◽  
Sprague Dawley ◽  
Calcitonin Gene ◽  
Cerebral Ischemic ◽  
Induced Changes ◽  
Common Carotid Arteries

Electroacupuncture (EA) is widely used to treat disorders of the nervous system, such as stroke. The aim of the present study was to investigate the effect of EA on cerebral blood flow (CBF) in cerebral ischemic rats. We developed an animal model of cerebral ischemia (CI) by occluding the blood flow of both common carotid arteries in Sprague-Dawley (SD) rats; 2 or 15 Hz EA was applied to both Zusanli acupoints. The levels of nitric oxide (NO) in the peripheral blood and amounts of calcitonin gene-related peptide (CGRP) in the cerebral cortex and thalamus were measured. In addition, L-N (G)-nitro arginine methyl ester (L-NAME) was used to measure the changes in CBF induced by EA in rats with and without CI. The results indicated that both 2 and 15 Hz EA increase the mean CBF in rats with and without CI. However, neither 2 nor 15 Hz EA induced changes in levels of NO in peripheral blood or changes in CGRP levels in cerebral cortex and thalamus. In addition, L-NAME did not change the increase in CBF. We concluded that both 2 and 15 Hz EA at both Zusanli acupoints induced the increase of CBF in rats with and without CI. Whether the effect of EA is related to NO or CGRP will be investigated in a future study.

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