Effects of Moderate Hypoxemia and Unilateral Carotid Ligation on Cerebral Glucose Metabolism and Acid-Base Balance in the Rat

Lockwood, Alan H.; Peek, Kathryn E.; Izumiyama, Masahiro; Yap, Eddy W. H.; Labove, Jocelyn

doi:10.1038/jcbfm.1989.52

Cited by 8 publications

(3 citation statements)

References 27 publications

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“…occipital cortex, frontal cortex, lateral and medial temporal lobes, showed less of an increase at high altitude than in the cerebellum and hypothalamus. Regions primarily responsible for autonomic function are perfused by branches of the VA and are influenced by regional changes in pH during hypercapnia (Kuschinsky et al 1981) and hypoxia (Lockwood et al 1989). Cerebral CO 2 reactivity in the VA is lower than that in ICA (Sato et al 2012).…”

Section: Discussionmentioning

confidence: 99%

Effect of acute hypoxia on blood flow in vertebral and internal carotid arteries

Ogoh

Sato

Nakahara

et al. 2012

Experimental Physiology

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New Findings r What is the central question of this study? Does hypoxia enhance blood flow to all parts of the brain uniformly? r What is the main finding and its importance?During hypoxia, internal carotid artery flow is maintained despite a reduction in (end-tidal) carbon dioxide tension, while vertebral artery blood flow increases. Only with maintained end-tidal carbon dioxide tension is there an increase in both vertebral and internal carotid blood flow during hypoxia.Hypoxia changes the regional distribution of cerebral blood flow and stimulates the ventilatory chemoreflex, thereby reducing CO 2 tension. We examined the effects of both hypoxia and isocapnic hypoxia on acute changes in internal carotid (ICA) and vertebral artery (VA) blood flow. Ten healthy male subjects underwent the following two randomly assigned respiratory interventions after a resting baseline period with room air: (i) hypoxia; and (ii) isocapnic hypoxia with a controlled gas mixture (12% O 2 ; inspiratory P O 2 = 86 mmHg). In the isocapnic hypoxia intervention, subjects were instructed to maintain the rate and depth of breathing to maintain the level of end-tidal partial pressure of CO 2 (P ET,CO 2 ) during the resting baseline period. The ICA and VA blood flow (velocity × cross-sectional area) were measured using Doppler ultrasonography. The P ET,CO 2 was decreased (−6.3 ± 0.9%, P < 0.001) during hypoxia by hyperventilation (minute ventilation +12.9 ± 2.2%, P < 0.001), while P ET,CO 2 was unchanged during isocapnic hypoxia. The ICA blood flow was unchanged (P = 0.429), while VA blood flow increased (+10.3 ± 3.1%, P = 0.010) during hypoxia. In contrast, isocapnic hypoxia increased both ICA (+14.5 ± 1.4%, P < 0.001) and VA blood flows (+10.9 ± 2.4%, P < 0.001). Thus, hypoxic vasodilatation outweighed hypocapnic vasoconstriction in the VA, but not in the ICA. These findings suggest that acute hypoxia elicits an increase in posterior cerebral blood flow, possibly to maintain essential homeostatic functions of the brainstem.

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Section: Discussionmentioning

confidence: 99%

Effect of acute hypoxia on blood flow in vertebral and internal carotid arteries

Ogoh

Sato

Nakahara

et al. 2012

Experimental Physiology

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“…Hypoxia and hypercapnia-induced changes in CBF may share common mediators and/or pathways, although an obvious candidate, the peripheral chemoreceptor, does not appear to be involved with CBF control (31). Regional changes in pH can also influence local blood flow during both hypercapnia (25) and hypoxia (27). Hypoxic and hypercapnic changes in vascular tone may both be mediated by adenosine (35) or nitric oxide (34), although the direct role of the latter is less clear (13).…”

Section: Discussionmentioning

confidence: 99%

Gray matter blood flow change is unevenly distributed during moderate isocapnic hypoxia in humans

Binks¹,

Cunningham²,

Adams³

et al. 2008

Journal of Applied Physiology

106

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Hypoxia increases cerebral blood flow (CBF), but it is unknown whether this increase is uniform across all brain regions. We used H(2)(15)O positron emission tomography imaging to measure absolute blood flow in 50 regions of interest across the human brain (n = 5) during normoxia and moderate hypoxia. Pco(2) was kept constant ( approximately 44 Torr) throughout the study to avoid decreases in CBF associated with the hypocapnia that normally occurs with hypoxia. Breathing was controlled by mechanical ventilation. During hypoxia (inspired Po(2) = 70 Torr), mean end-tidal Po(2) fell to 45 +/- 6.3 Torr (means +/- SD). Mean global CBF increased from normoxic levels of 0.39 +/- 0.13 to 0.45 +/- 0.13 ml/g during hypoxia. Increases in regional CBF were not uniform and ranged from 9.9 +/- 8.6% in the occipital lobe to 28.9 +/- 10.3% in the nucleus accumbens. Regions of interest that were better perfused during normoxia generally showed a greater regional CBF response. Phylogenetically older regions of the brain tended to show larger vascular responses to hypoxia than evolutionary younger regions, e.g., the putamen, brain stem, thalamus, caudate nucleus, nucleus accumbens, and pallidum received greater than average increases in blood flow, while cortical regions generally received below average increases. The heterogeneous blood flow distribution during hypoxia may serve to protect regions of the brain with essential homeostatic roles. This may be relevant to conditions such as altitude, breath-hold diving, and obstructive sleep apnea, and may have implications for functional brain imaging studies that involve hypoxia.

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“…Moderate decreases (50%) of glucose metabolism and blood flow (Shiraishi et aI., 1989), as well as increases of metabolism (Levy and Duffy, 1977;Lockwood et a!., 1989) have been observed in hippocampus following MCA occlusions. In addition, all animals in this study demonstrated evidence of a marked midline shift at death, indicative of edema, which could affect blood flow to hippocampus.…”

Section: Previous Evidence For Hippocampal Injury and Cell Death Follmentioning

confidence: 99%

DNA Fragmentation and HSP70 Protein Induction in Hippocampus and Cortex Occurs in Separate Neurons following Permanent Middle Cerebral Artery Occlusions

States

Honkaniemi

Weinstein

et al. 1996

J Cereb Blood Flow Metab

106

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DNA nick end-labeling (TUNEL) and heat shock protein (HSP)70 immunocytochemistry were performed on the same brain sections 1 (n = 6), 3 (n = 12), and 7 (n = 7) days following permanent middle cerebral artery (MCA) occlusions produced in adult rats using the endovascular carotid suture method. In the cortex at 1 and 3 days following MCA occlusions, HSP70 immunoreactive neurons were located outside areas of infarction and showed little evidence of DNA fragmentation. HSP70-stained cortical neurons were intermingled with TUNEL cells near the infarct, but extended for greater distances away from the infarct. DNA fragmentation occurred in CA1 hippocampal neurons in 39% of the animals at 1 and 3 days following ipsilateral MCA occlusion. Bilateral DNA fragmentation occurred in CA1 neurons in one subject. HSP70 protein was expressed in CA1 hippocampal neurons in nine of 18 (50%) animals at 1 and 3 days following MCA occlusions, including all animals that exhibited hippocampal DNA fragmentation. Three animals had bilateral expression of HSP70 in CA1 neurons. Cells that stained for either HSP70 protein or DNA fragmentation existed in close proximity to one another. Approximately 5-7% of HSP70-stained cells were TUNEL stained and 3% of TUNEL-positive cells also stained for HSP70. There was no HSP70 staining or DNA fragmentation in the brains of sham-operated controls (n = 4) or in the brains of animals 7 days following MCA occlusions. These data suggest that ischemic cells capable of translating HSP70 protein generally do not undergo DNA fragmentation. These data support the concept that most HSP70 protein-containing neurons in the cortical "penumbra" and hippocampus survive ischemic injury and are "reversibly injured." It is shown that CA1 hippocampal pyramidal neurons die or are reversibly injured in approximately 50% of animals following permanent MCA occlusions. Although the mechanism of this hippocampal injury is unknown, it could relate to transynaptic activation of N-methyl-D-aspartate (NMDA) receptors that mediate induction of early genes in hippocampus.

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Effects of Moderate Hypoxemia and Unilateral Carotid Ligation on Cerebral Glucose Metabolism and Acid-Base Balance in the Rat

Cited by 8 publications

References 27 publications

Effect of acute hypoxia on blood flow in vertebral and internal carotid arteries

Effect of acute hypoxia on blood flow in vertebral and internal carotid arteries

Gray matter blood flow change is unevenly distributed during moderate isocapnic hypoxia in humans

DNA Fragmentation and HSP70 Protein Induction in Hippocampus and Cortex Occurs in Separate Neurons following Permanent Middle Cerebral Artery Occlusions

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