Arterial pCO2 and Blood Flow in Different Parts of the Central Nervous System of the Anesthetized Cat

Flohr, H.; Brock, M.; Christ, Ryan; Heipertz, R.; Pöll, W.

doi:10.1007/978-3-642-85860-4_28

Cited by 27 publications

(10 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…They found the responsiveness to blood pressure, arterial Po 2 and Pco 2 was similar in the spinal cord and in the brain. Similar results were obtained by Wiillenweber 6 in man, by Flohr et al 6 in cats, and by Tschetter et al 7 in dogs. In this report we wish to present some physiological observations concerning the oxygen supply of the cerebral cortex and the spinal cord of rats based on measurements with ultramicro-oxygen electrodes.…”

Section: Introductionsupporting

confidence: 86%

Comparison of vascular reactivity in spinal cord and brain.

Nix¹,

Capra²,

Erdmann³

et al. 1976

Stroke

View full text Add to dashboard Cite

SUMMARYThe local tissue Po 2 in the brain cortex and in the spinal cord of rats was examined with ultramicroelectrodes. In the spinal cord the Po 2 was highest in white matter, intermediate in dorsal horn gray matter, and lowest in the ventral horn gray matter. In the gray matter of the cord, as well as in the brain, the Po 2 at a fixed locus was found normally to oscillate. CO 2 responses were more brisk in the cord than in the brain while the responses to hypoxia were similar. Therefore, it appears that the physiological regulation of blood flow in the spinal cord is qualitatively similar to that of the brain.

show abstract

Section: Introductionsupporting

confidence: 86%

Comparison of vascular reactivity in spinal cord and brain.

Nix¹,

Capra²,

Erdmann³

et al. 1976

Stroke

View full text Add to dashboard Cite

show abstract

“…Areas with high capillary density also have a greater reactivity to CO 2 . 30 Our results show that different brain regions are reoxygenated at different CPPs after global brain ischemia. We attribute the difference in reoxygenation to regional variations in critical perfusion pressure (i.e., that perfusion pressure required to reperfuse a given area of the brain after an ischemic insult).…”

Section: Discussionmentioning

confidence: 73%

Regional brain PO2 after global ischemia in monkeys: evidence for regional differences in critical perfusion pressures.

Nemoto¹,

Erdmann²,

Strong³

et al. 1979

Stroke

View full text Add to dashboard Cite

SUMMARY We measured brain tissue Po 2 in the frontal and occipital cortices, mid-brain and basal ganglia in monkeys for up to 5 hours after 16 min global brain ischemia to gain some insight into those factors responsible for the selective vulnerability of the brain to ischemic anoxia. Brain tissue Po 2 measurements were made with gold microelectrodes with tip diameters of 5 to 10 nm. Reoxygenation of the different brain regions occurred at different "apparent" cerebral perfusion pressures and times postischemia. Areas of low susceptibility to ischemic brain damage, such as the frontal cortex, were not consistently reoxygenated at lower perfusion pressures or earlier postischemia than were areas of high susceptibility such as the occipital cortex, basal ganglia and midbrain. These findings support earlier observations that perfusion defects and brain histologic changes are multifocal in nature after global brain ischemia. We suggest that the selective vulnerability of the brain to ischemia is attributable to the development of regional edema and a local increase in tissue pressure during ischemia thereby decreasing cerebral perfusion pressure and leading to local perfusion defects after restoration of circulation. Also, that the selective vulnerability of the brain is attributable to variable degrees of neuronal-glial edema and regional shifts in brain water during ischemia leading to the development of local perfusion defects and the expansion of lesions from areas of high to low vulnerability.Stroke, Vol. 10, No. 1, 1979THE SELECTIVE vulnerability of the brain to ischemia-anoxia was recognized as early as 1858 by Brown-Sequard. 1 To explain this phenomenon, O. Vogt 2 and C. Vogt 3 hypothesized a greater sensitivity of neurons to "toxic factors" (i.e., pathoclisis) while Spielmeyer 4 suggested a major role of "vascular factors" such as arterial compression and vascular obstruction. Scholz 6 proposed that the selective vulnerability of the brain was due to a combination of both toxic and vascular factors.Present-day proponents of these earlier hypotheses are Ames and associates 68 (vascular factors) and Brierley and associates 9 (pathoclisis). Chiang et al. 7 showed that vascular obstruction occurred as a result of endothelial "bleb" formation, capillary "pinching" due to swollen astrocytic foot processes, and red blood cell and platelet aggregation. Brierley argued that the "no-reflow phenomenon" does not explain the selective vulnerability of the brain because so anatomically diffuse a process as vascular obstruction does not account for the frequently observed laminar destruction of cortical layers or viable neurons adjacent to dead neurons. There is little doubt that neuronal death after ischemia can occur without the no-reflow phenomenon as shown by Levy and Plum 10 but this does not preclude some role for perfusion defects in the pathogenesis of ischemic brain damage. Indeed, we" and Hossmann et al. 12 have clearly demonstrated delayed development of brain hypoperfusion within 1 hour after global brain...

show abstract

“…This cannot be answered with confidence since vessels within various parts of the brain cannot be examined directly. It is known, however, that the responses of the pial vessels are qualitatively similar to what one might expect of the blood vessels of the brain as a whole, as judged by indirect studies based on measurements of pressure and flow (6), but it is also known that there are regional quantitative differences in the responsiveness of brain blood vessels to CO 2 (7).…”

Section: Raper Kontos Pattersonmentioning

confidence: 99%

Response of Pial Precapillary Vessels to Changes in Arterial Carbon Dioxide Tension

1971

View full text Add to dashboard Cite

A quantitative study of responses of pial precapillary vessels to changes in arterial blood carbon dioxide tension was made in anesthetized cats. All vessels examined ranging in diameter from 13 to 90/ x responded to hypercapnia with increases in diameter and to hypocapnia with decreases in diameter. The onset of the response to hypercapnia was earlier, its speed was faster, and its magnitude greater with higher concentrations of CO 2 . In response to the same increase in arterial blood Pco 2l smaller vessels (13 to 40/i) increased in diameter by 47.7 ± 10.8% of the control value while the increase in diameter of larger vessels (41 to 90/x) was significantly lower and equal to 29.5 ± 6.3% of the control value. In the steady state the relation between pial vessel diameter expressed as percent of the control value (Y) and arterial blood Pco 2 (X) was given by the equation Y = 53.07 + 1.587X -0.00715X 2 . The relatively large magnitude of the response of pial arteries and arterioles to CO 2 and the fact that it was dependent on vessel size show that there must be significant readjustments in the pressure gradients in these vessels when CO 2 tension is changed. KEY WOKDScat hypercapnia cerebral blood vessels hypocapnia arterioles B In view of the generally acknowledged importance of the action of carbon dioxide on cerebral blood vessels in the regulation of blood flow to this vascular bed, and because of the well-recognized principle that normal adjustments in the vascular resistance in most vascular beds are usually carried out by alterations in the caliber of the small precapillary blood vessels, it appeared important to study the effect of CO 2 on small precapillary cerebral blood vessels. There are only two previous studies in which this aspect of the cerebral vascular action of CO 2 was From the Department of Medicine, Medical College of Virginia, Health Sciences Division, Virginia Commonwealth University, Richmond, Virginia 23219. This work was supported by Contract NGL 47-002-001 from the National Aeronautics and Space Administration, by Grant HE-11077 from the National Heart and Lung Institute, and by a grant from the Virginia Heart Association. Dr. Kontos is the recipient of a Research Career Development Award from the National Heart and Lung Institute, and Markle Scholar in Academic Medicine. Dr. Patterson is the recipient of a Research Career Award from the National Heart and Lung Institute.Received October 27, 1970. Accepted for publication February 23, 1971. examined systematically. In one study (1) it was found that the inhalation of the CO 2 by anesthetized or unanesthetized cats and monkeys produced vasodilation, but the results were reported only qualitatively. In the other study (2) quantitative results were presented, but only arteries larger than 150/JL in diameter were examined. Furthermore, methods presently available allow more accurate and complete studies than were possible in the past. The present study was undertaken to investigate the effect of changes in blood CO 2 tension on ...

show abstract

Arterial pCO2 and Blood Flow in Different Parts of the Central Nervous System of the Anesthetized Cat

Cited by 27 publications

References 6 publications

Comparison of vascular reactivity in spinal cord and brain.

Comparison of vascular reactivity in spinal cord and brain.

Regional brain PO2 after global ischemia in monkeys: evidence for regional differences in critical perfusion pressures.

Response of Pial Precapillary Vessels to Changes in Arterial Carbon Dioxide Tension

Contact Info

Product

Resources

About