Cerebral ischemia alters cerebral microvascular reactivity in newborn pigs

Charles Leffler, D. G. Beasley, D. W. Busija

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

The effects of cerebral ischemia on cerebral microvascular reactivity and prostanoid synthesis were examined in chloralose-anesthetized newborn pigs. Microvascular responses and periarachnoid cerebrospinal fluid (CSF) prostanoid concentrations were determined between 10 and 140 min after a 20-min period of total cerebral ischemia, as well as in sham-control piglets without cerebral ischemia. After cerebral ischemia, the decrease in pial arteriolar diameter in response to topical norepinephrine (10-4 M) was similar in sham (-27 ± 6%) and postischemic (-25 ± 5%) piglets. However, the increase in pial arteriolar diameter in response to hypercapnia (10% CO2 ventilation) that was observed in sham piglets (+21 ± 5%) was absent after ischemia (-2 ± 3%). In contrast, dilations of pial arterioles in response to topical prostaglandin (PG)E2 (at 100 ng PGE2/ml: sham, +13 ± 3%; postischemia, +21 ± 4%) and topical isoproterenol (10-6 M) (sham, +29 ± 4%; postischemia, +23 ± 3%) were not decreased by prior cerebral ischemia. In sham piglets, norepinephrine and hypercapnia produced increases in cortical periarachnoid prostanoid concentrations, whereas after cerebral ischemia, neither stimulus increased cortical periarachnoid prostanoid concentrations. The results are consistent with the hypothesis that failure of hypercapnia to dilate pial arterioles after cerebral ischemia results from the inability of this stimulus to increase cerebral vasodilator prostanoid synthesis.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume257
Issue number1
StatePublished - Jan 1 1989

Fingerprint

Brain Ischemia
Swine
Prostaglandins
Hypercapnia
Arterioles
Dinoprostone
Norepinephrine
Chloralose
Vasodilator Agents
Isoproterenol
Ventilation
Cerebrospinal Fluid
Dilatation
Ischemia

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Cerebral ischemia alters cerebral microvascular reactivity in newborn pigs. / Leffler, Charles; Beasley, D. G.; Busija, D. W.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 257, No. 1, 01.01.1989.

Research output: Contribution to journalArticle

@article{63b8da9cc64a4108b16d97b549d17319,
title = "Cerebral ischemia alters cerebral microvascular reactivity in newborn pigs",
abstract = "The effects of cerebral ischemia on cerebral microvascular reactivity and prostanoid synthesis were examined in chloralose-anesthetized newborn pigs. Microvascular responses and periarachnoid cerebrospinal fluid (CSF) prostanoid concentrations were determined between 10 and 140 min after a 20-min period of total cerebral ischemia, as well as in sham-control piglets without cerebral ischemia. After cerebral ischemia, the decrease in pial arteriolar diameter in response to topical norepinephrine (10-4 M) was similar in sham (-27 ± 6{\%}) and postischemic (-25 ± 5{\%}) piglets. However, the increase in pial arteriolar diameter in response to hypercapnia (10{\%} CO2 ventilation) that was observed in sham piglets (+21 ± 5{\%}) was absent after ischemia (-2 ± 3{\%}). In contrast, dilations of pial arterioles in response to topical prostaglandin (PG)E2 (at 100 ng PGE2/ml: sham, +13 ± 3{\%}; postischemia, +21 ± 4{\%}) and topical isoproterenol (10-6 M) (sham, +29 ± 4{\%}; postischemia, +23 ± 3{\%}) were not decreased by prior cerebral ischemia. In sham piglets, norepinephrine and hypercapnia produced increases in cortical periarachnoid prostanoid concentrations, whereas after cerebral ischemia, neither stimulus increased cortical periarachnoid prostanoid concentrations. The results are consistent with the hypothesis that failure of hypercapnia to dilate pial arterioles after cerebral ischemia results from the inability of this stimulus to increase cerebral vasodilator prostanoid synthesis.",
author = "Charles Leffler and Beasley, {D. G.} and Busija, {D. W.}",
year = "1989",
month = "1",
day = "1",
language = "English (US)",
volume = "257",
journal = "American Journal of Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "1",

}

TY - JOUR

T1 - Cerebral ischemia alters cerebral microvascular reactivity in newborn pigs

AU - Leffler, Charles

AU - Beasley, D. G.

AU - Busija, D. W.

PY - 1989/1/1

Y1 - 1989/1/1

N2 - The effects of cerebral ischemia on cerebral microvascular reactivity and prostanoid synthesis were examined in chloralose-anesthetized newborn pigs. Microvascular responses and periarachnoid cerebrospinal fluid (CSF) prostanoid concentrations were determined between 10 and 140 min after a 20-min period of total cerebral ischemia, as well as in sham-control piglets without cerebral ischemia. After cerebral ischemia, the decrease in pial arteriolar diameter in response to topical norepinephrine (10-4 M) was similar in sham (-27 ± 6%) and postischemic (-25 ± 5%) piglets. However, the increase in pial arteriolar diameter in response to hypercapnia (10% CO2 ventilation) that was observed in sham piglets (+21 ± 5%) was absent after ischemia (-2 ± 3%). In contrast, dilations of pial arterioles in response to topical prostaglandin (PG)E2 (at 100 ng PGE2/ml: sham, +13 ± 3%; postischemia, +21 ± 4%) and topical isoproterenol (10-6 M) (sham, +29 ± 4%; postischemia, +23 ± 3%) were not decreased by prior cerebral ischemia. In sham piglets, norepinephrine and hypercapnia produced increases in cortical periarachnoid prostanoid concentrations, whereas after cerebral ischemia, neither stimulus increased cortical periarachnoid prostanoid concentrations. The results are consistent with the hypothesis that failure of hypercapnia to dilate pial arterioles after cerebral ischemia results from the inability of this stimulus to increase cerebral vasodilator prostanoid synthesis.

AB - The effects of cerebral ischemia on cerebral microvascular reactivity and prostanoid synthesis were examined in chloralose-anesthetized newborn pigs. Microvascular responses and periarachnoid cerebrospinal fluid (CSF) prostanoid concentrations were determined between 10 and 140 min after a 20-min period of total cerebral ischemia, as well as in sham-control piglets without cerebral ischemia. After cerebral ischemia, the decrease in pial arteriolar diameter in response to topical norepinephrine (10-4 M) was similar in sham (-27 ± 6%) and postischemic (-25 ± 5%) piglets. However, the increase in pial arteriolar diameter in response to hypercapnia (10% CO2 ventilation) that was observed in sham piglets (+21 ± 5%) was absent after ischemia (-2 ± 3%). In contrast, dilations of pial arterioles in response to topical prostaglandin (PG)E2 (at 100 ng PGE2/ml: sham, +13 ± 3%; postischemia, +21 ± 4%) and topical isoproterenol (10-6 M) (sham, +29 ± 4%; postischemia, +23 ± 3%) were not decreased by prior cerebral ischemia. In sham piglets, norepinephrine and hypercapnia produced increases in cortical periarachnoid prostanoid concentrations, whereas after cerebral ischemia, neither stimulus increased cortical periarachnoid prostanoid concentrations. The results are consistent with the hypothesis that failure of hypercapnia to dilate pial arterioles after cerebral ischemia results from the inability of this stimulus to increase cerebral vasodilator prostanoid synthesis.

UR - http://www.scopus.com/inward/record.url?scp=0024328919&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024328919&partnerID=8YFLogxK

M3 - Article

C2 - 2750942

AN - SCOPUS:0024328919

VL - 257

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6135

IS - 1

ER -