Pial arteriolar vessel diameter and CO2 reactivity during prolonged hyperventilation in the rabbit

Jan Paul Muizelaar, H. G. Van Der Poel, Z. Li, H. A. Kontos, J. E. Levasseur

Research output: Contribution to journalArticle

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Abstract

Hyperventilation reduces intracranial pressure (ICP) acutely through vasoconstriction, but its long-term effect on vessel diameter is unknown. In seven rabbits with a cranial window implanted 3 weeks earlier, the effect of prolonged hyperventilation on vessel diameter was studied. Anesthesia was maintained for 54 hours with a pentobarbital drip (1 mg/kg/hr). The pH, CO2, and HCO3̄ levels were measured in arterial blood and cisterna magna cerebrospinal fluid (CSF). The diameter of 31 pial arterioles was measured with an image splitter. After baseline measurements, pCO2 was reduced from 38 to 25 mm Hg and allowed to return to 38 mm Hg for 10 minutes every 4 hours. There was an initial vasoconstriction of 13%, which progressively diminished by 3% every 4 hours. Thus, by the 20th hour, vessel diameters at a pCO2 of 25 mm Hg had returned to slightly above baseline values obtained at a pCO2 of 38 mm Hg. The temporary return of pCO2 to 38 mm Hg every 4 hours caused vasodilation: 12% at 4 hours, gradually increasing to 16% at 52 hours. Thus, at 52 hours, the vessel diameters were 105% of baseline at pCO2 of 25 mm Hg and increased to 122% at a pCO2 of 38 mm Hg. Arterial pH had returned to baseline at 20 hours, and CSF pH had returned at 24 hours. Bicarbonate in blood and CSF remained decreased throughout the experiments. In three control experiments during which normocapnia was maintained, vessel diameter and pH and bicarbonate levels remained unaltered over the same period. The CO2 reactivity, tested by brief periods of hyperventilation every 4 hours, also did not change. These results indicate that hyperventilation is effective in reducing cerebral blood volume for less than 24 hours and that it should be used only during actual ICP elevations. If used preventively, its effect may have worn off by the time ICP starts to rise for other reasons, and further decreases in pCO2 cannot be obtained. Moreover, the reduction in buffer capacity with lower bicarbonate renders the vessels more sensitive to changes in PaCO2. This could lead to more pronounced elevations in ICP during transient rises in PaCO2, such as during endotracheal suctioning in head-injured patients.

Original languageEnglish (US)
Pages (from-to)923-927
Number of pages5
JournalJournal of Neurosurgery
Volume69
Issue number6
StatePublished - 1988
Externally publishedYes

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Hyperventilation
Bicarbonates
Rabbits
Cerebrospinal Fluid
Intracranial Hypertension
Intracranial Pressure
Vasoconstriction
Cisterna Magna
Arterioles
Pentobarbital
Vasodilation
Buffers
Anesthesia
Head

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Muizelaar, J. P., Van Der Poel, H. G., Li, Z., Kontos, H. A., & Levasseur, J. E. (1988). Pial arteriolar vessel diameter and CO2 reactivity during prolonged hyperventilation in the rabbit. Journal of Neurosurgery, 69(6), 923-927.

Pial arteriolar vessel diameter and CO2 reactivity during prolonged hyperventilation in the rabbit. / Muizelaar, Jan Paul; Van Der Poel, H. G.; Li, Z.; Kontos, H. A.; Levasseur, J. E.

In: Journal of Neurosurgery, Vol. 69, No. 6, 1988, p. 923-927.

Research output: Contribution to journalArticle

Muizelaar, JP, Van Der Poel, HG, Li, Z, Kontos, HA & Levasseur, JE 1988, 'Pial arteriolar vessel diameter and CO2 reactivity during prolonged hyperventilation in the rabbit', Journal of Neurosurgery, vol. 69, no. 6, pp. 923-927.
Muizelaar, Jan Paul ; Van Der Poel, H. G. ; Li, Z. ; Kontos, H. A. ; Levasseur, J. E. / Pial arteriolar vessel diameter and CO2 reactivity during prolonged hyperventilation in the rabbit. In: Journal of Neurosurgery. 1988 ; Vol. 69, No. 6. pp. 923-927.
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title = "Pial arteriolar vessel diameter and CO2 reactivity during prolonged hyperventilation in the rabbit",
abstract = "Hyperventilation reduces intracranial pressure (ICP) acutely through vasoconstriction, but its long-term effect on vessel diameter is unknown. In seven rabbits with a cranial window implanted 3 weeks earlier, the effect of prolonged hyperventilation on vessel diameter was studied. Anesthesia was maintained for 54 hours with a pentobarbital drip (1 mg/kg/hr). The pH, CO2, and HCO3̄ levels were measured in arterial blood and cisterna magna cerebrospinal fluid (CSF). The diameter of 31 pial arterioles was measured with an image splitter. After baseline measurements, pCO2 was reduced from 38 to 25 mm Hg and allowed to return to 38 mm Hg for 10 minutes every 4 hours. There was an initial vasoconstriction of 13{\%}, which progressively diminished by 3{\%} every 4 hours. Thus, by the 20th hour, vessel diameters at a pCO2 of 25 mm Hg had returned to slightly above baseline values obtained at a pCO2 of 38 mm Hg. The temporary return of pCO2 to 38 mm Hg every 4 hours caused vasodilation: 12{\%} at 4 hours, gradually increasing to 16{\%} at 52 hours. Thus, at 52 hours, the vessel diameters were 105{\%} of baseline at pCO2 of 25 mm Hg and increased to 122{\%} at a pCO2 of 38 mm Hg. Arterial pH had returned to baseline at 20 hours, and CSF pH had returned at 24 hours. Bicarbonate in blood and CSF remained decreased throughout the experiments. In three control experiments during which normocapnia was maintained, vessel diameter and pH and bicarbonate levels remained unaltered over the same period. The CO2 reactivity, tested by brief periods of hyperventilation every 4 hours, also did not change. These results indicate that hyperventilation is effective in reducing cerebral blood volume for less than 24 hours and that it should be used only during actual ICP elevations. If used preventively, its effect may have worn off by the time ICP starts to rise for other reasons, and further decreases in pCO2 cannot be obtained. Moreover, the reduction in buffer capacity with lower bicarbonate renders the vessels more sensitive to changes in PaCO2. This could lead to more pronounced elevations in ICP during transient rises in PaCO2, such as during endotracheal suctioning in head-injured patients.",
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AU - Levasseur, J. E.

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N2 - Hyperventilation reduces intracranial pressure (ICP) acutely through vasoconstriction, but its long-term effect on vessel diameter is unknown. In seven rabbits with a cranial window implanted 3 weeks earlier, the effect of prolonged hyperventilation on vessel diameter was studied. Anesthesia was maintained for 54 hours with a pentobarbital drip (1 mg/kg/hr). The pH, CO2, and HCO3̄ levels were measured in arterial blood and cisterna magna cerebrospinal fluid (CSF). The diameter of 31 pial arterioles was measured with an image splitter. After baseline measurements, pCO2 was reduced from 38 to 25 mm Hg and allowed to return to 38 mm Hg for 10 minutes every 4 hours. There was an initial vasoconstriction of 13%, which progressively diminished by 3% every 4 hours. Thus, by the 20th hour, vessel diameters at a pCO2 of 25 mm Hg had returned to slightly above baseline values obtained at a pCO2 of 38 mm Hg. The temporary return of pCO2 to 38 mm Hg every 4 hours caused vasodilation: 12% at 4 hours, gradually increasing to 16% at 52 hours. Thus, at 52 hours, the vessel diameters were 105% of baseline at pCO2 of 25 mm Hg and increased to 122% at a pCO2 of 38 mm Hg. Arterial pH had returned to baseline at 20 hours, and CSF pH had returned at 24 hours. Bicarbonate in blood and CSF remained decreased throughout the experiments. In three control experiments during which normocapnia was maintained, vessel diameter and pH and bicarbonate levels remained unaltered over the same period. The CO2 reactivity, tested by brief periods of hyperventilation every 4 hours, also did not change. These results indicate that hyperventilation is effective in reducing cerebral blood volume for less than 24 hours and that it should be used only during actual ICP elevations. If used preventively, its effect may have worn off by the time ICP starts to rise for other reasons, and further decreases in pCO2 cannot be obtained. Moreover, the reduction in buffer capacity with lower bicarbonate renders the vessels more sensitive to changes in PaCO2. This could lead to more pronounced elevations in ICP during transient rises in PaCO2, such as during endotracheal suctioning in head-injured patients.

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