Cerebral vasoconstriction in response to hypocapnia is maintained after ischemia/reperfusion injury in newborn pigs

Robert Mirro, Lisa Lowery-Smith, William M. Armstead, Masaaki Shibata, Samuel L. Zuckerman, Charles Leffler

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Background and Purpose: Hypocapnic cerebral vasoconstriction is used therapeutically to reduce elevated intracranial pressure caused by cerebral edema. Because cerebral ischemia/reperfusion injury causes a selective loss of prostanoid-dependent responses, including vasodilation to hypercapnia, we designed these experiments to examine the effect of ischemia/reperfusion on hypocapnic cerebral vasoconstriction. Methods: Microvascular responses were studied in 10 newborn pigs (closed cranial window) in response to hyperventilation-induced hypocapnia (PaCO2, 22±2 mm Hg) both before and 45 minutes after 20 minutes of global cerebral ischemia. Responses to hypercapnia (PaCO2, 63±3 mm Hg), topical isopro-terenol (10-7 M), and norepinephrine (10-4 M) were also studied before and after ischemia in the same animals for comparison. Results: Before ischemia/reperfusion, pial arterioles vasoconstricted to hypocapnia (-17±2%) and norepinephrine (-35±4%) and vasodilated to CO2 (37±7%) and isoproterenol (25±2%). After ischemia/ reperfusion, the constriction of pial arterioles to hypocapnia (-19±2%) was similar to that before ischemia. This is in contrast to the loss of dilation to hypercapnia. Dilation to isoproterenol and constriction to norepinephrine were not affected by ischemia. Conclusions: Hypocapnic cerebral vasoconstriction is maintained after ischemia/reperfusion. Since prostanoid-dependent responses, such as hypercapnic dilation, are lost following cerebral ischemia, these data suggest that hypocapnic constriction is not dependent on an intact prostanoid system and that cerebral vascular responses to CO2 involve multiple mechanisms, depending on whether CO2 is increasing or decreasing from baseline.

Original languageEnglish (US)
Pages (from-to)1613-1616
Number of pages4
JournalStroke
Volume23
Issue number11
DOIs
StatePublished - Jan 1 1992

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Hypocapnia
Vasoconstriction
Reperfusion Injury
Swine
Ischemia
Reperfusion
Hypercapnia
Brain Ischemia
Constriction
Prostaglandins
Dilatation
Norepinephrine
Arterioles
Isoproterenol
Intracranial Hypertension
Hyperventilation
Brain Edema
Vasodilation
Blood Vessels

All Science Journal Classification (ASJC) codes

  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine
  • Advanced and Specialized Nursing

Cite this

Cerebral vasoconstriction in response to hypocapnia is maintained after ischemia/reperfusion injury in newborn pigs. / Mirro, Robert; Lowery-Smith, Lisa; Armstead, William M.; Shibata, Masaaki; Zuckerman, Samuel L.; Leffler, Charles.

In: Stroke, Vol. 23, No. 11, 01.01.1992, p. 1613-1616.

Research output: Contribution to journalArticle

Mirro, Robert ; Lowery-Smith, Lisa ; Armstead, William M. ; Shibata, Masaaki ; Zuckerman, Samuel L. ; Leffler, Charles. / Cerebral vasoconstriction in response to hypocapnia is maintained after ischemia/reperfusion injury in newborn pigs. In: Stroke. 1992 ; Vol. 23, No. 11. pp. 1613-1616.
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abstract = "Background and Purpose: Hypocapnic cerebral vasoconstriction is used therapeutically to reduce elevated intracranial pressure caused by cerebral edema. Because cerebral ischemia/reperfusion injury causes a selective loss of prostanoid-dependent responses, including vasodilation to hypercapnia, we designed these experiments to examine the effect of ischemia/reperfusion on hypocapnic cerebral vasoconstriction. Methods: Microvascular responses were studied in 10 newborn pigs (closed cranial window) in response to hyperventilation-induced hypocapnia (PaCO2, 22±2 mm Hg) both before and 45 minutes after 20 minutes of global cerebral ischemia. Responses to hypercapnia (PaCO2, 63±3 mm Hg), topical isopro-terenol (10-7 M), and norepinephrine (10-4 M) were also studied before and after ischemia in the same animals for comparison. Results: Before ischemia/reperfusion, pial arterioles vasoconstricted to hypocapnia (-17±2{\%}) and norepinephrine (-35±4{\%}) and vasodilated to CO2 (37±7{\%}) and isoproterenol (25±2{\%}). After ischemia/ reperfusion, the constriction of pial arterioles to hypocapnia (-19±2{\%}) was similar to that before ischemia. This is in contrast to the loss of dilation to hypercapnia. Dilation to isoproterenol and constriction to norepinephrine were not affected by ischemia. Conclusions: Hypocapnic cerebral vasoconstriction is maintained after ischemia/reperfusion. Since prostanoid-dependent responses, such as hypercapnic dilation, are lost following cerebral ischemia, these data suggest that hypocapnic constriction is not dependent on an intact prostanoid system and that cerebral vascular responses to CO2 involve multiple mechanisms, depending on whether CO2 is increasing or decreasing from baseline.",
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AU - Lowery-Smith, Lisa

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AU - Shibata, Masaaki

AU - Zuckerman, Samuel L.

AU - Leffler, Charles

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