Activated oxygen and arachidonate effects on newborn cerebral arterioles

Charles Leffler, D. W. Busija, W. M. Armstead, D. R. Shanklin, R. Mirro, O. Thelin

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

We have observed that pial arteriolar dilation in response to hypercapnia and hypotension is abolished after cerebral ischemia in newborn pigs. We determined whether direct generation of activated oxygen on the brain surface (OX: xanthine oxidase, hypoxanthine, FeCl3, and FeSO4) or topical arachidonate altered pial arteriolar responsiveness in a manner similarly to cerebral ischemia. OX, which generated more brain surface superoxide than reperfusion after ischemia, dilated pial arterioles. This dilation was reversed within 10 min of the end of exposure. OX produced ultrastructural changes in pial vessel endothelium and appeared to cause intravascular aggregation of granulocytes. After OX, prostanoid-dependent pial arteriolar dilations in response to hypercapnia and hypotension were attenuated, whereas constrictor responses to norepinephrine and acetylcholine and dilator responses to prostaglandin E2 and isoproterenol were not affected. After OX, hypercapnia increased cortical periarachnoid cerebrospinal fluid prostanoids modestly, whereas acetylcholine produced the normal strong stimulation of prostanoid synthesis. Arachidonate (10-4 M and 7 x 10-4 M) also caused reversible pial arteriolar dilation but did not alter subsequent pial arteriolar responses. Therefore, although arachidonate did not mimic the effects of ischemia-reperfusion on pial arteriolar reactivity, OX produced alterations that are qualitatively similar, although quantitatively less, than those produced by ischemia.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume259
Issue number4 28-4
StatePublished - Jan 1 1990

Fingerprint

Arterioles
Hypercapnia
Dilatation
Oxygen
Prostaglandins
Ischemia
Brain Ischemia
Hypotension
Acetylcholine
Reperfusion
Xanthine Oxidase
Brain
Isoproterenol
Dinoprostone
Granulocytes
Superoxides
Endothelium
Cerebrospinal Fluid
Norepinephrine
Swine

All Science Journal Classification (ASJC) codes

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

Cite this

Leffler, C., Busija, D. W., Armstead, W. M., Shanklin, D. R., Mirro, R., & Thelin, O. (1990). Activated oxygen and arachidonate effects on newborn cerebral arterioles. American Journal of Physiology - Heart and Circulatory Physiology, 259(4 28-4).

Activated oxygen and arachidonate effects on newborn cerebral arterioles. / Leffler, Charles; Busija, D. W.; Armstead, W. M.; Shanklin, D. R.; Mirro, R.; Thelin, O.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 259, No. 4 28-4, 01.01.1990.

Research output: Contribution to journalArticle

Leffler, Charles ; Busija, D. W. ; Armstead, W. M. ; Shanklin, D. R. ; Mirro, R. ; Thelin, O. / Activated oxygen and arachidonate effects on newborn cerebral arterioles. In: American Journal of Physiology - Heart and Circulatory Physiology. 1990 ; Vol. 259, No. 4 28-4.
@article{37b38447b33f4a91b016c5b8421cfcb1,
title = "Activated oxygen and arachidonate effects on newborn cerebral arterioles",
abstract = "We have observed that pial arteriolar dilation in response to hypercapnia and hypotension is abolished after cerebral ischemia in newborn pigs. We determined whether direct generation of activated oxygen on the brain surface (OX: xanthine oxidase, hypoxanthine, FeCl3, and FeSO4) or topical arachidonate altered pial arteriolar responsiveness in a manner similarly to cerebral ischemia. OX, which generated more brain surface superoxide than reperfusion after ischemia, dilated pial arterioles. This dilation was reversed within 10 min of the end of exposure. OX produced ultrastructural changes in pial vessel endothelium and appeared to cause intravascular aggregation of granulocytes. After OX, prostanoid-dependent pial arteriolar dilations in response to hypercapnia and hypotension were attenuated, whereas constrictor responses to norepinephrine and acetylcholine and dilator responses to prostaglandin E2 and isoproterenol were not affected. After OX, hypercapnia increased cortical periarachnoid cerebrospinal fluid prostanoids modestly, whereas acetylcholine produced the normal strong stimulation of prostanoid synthesis. Arachidonate (10-4 M and 7 x 10-4 M) also caused reversible pial arteriolar dilation but did not alter subsequent pial arteriolar responses. Therefore, although arachidonate did not mimic the effects of ischemia-reperfusion on pial arteriolar reactivity, OX produced alterations that are qualitatively similar, although quantitatively less, than those produced by ischemia.",
author = "Charles Leffler and Busija, {D. W.} and Armstead, {W. M.} and Shanklin, {D. R.} and R. Mirro and O. Thelin",
year = "1990",
month = "1",
day = "1",
language = "English (US)",
volume = "259",
journal = "American Journal of Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "4 28-4",

}

TY - JOUR

T1 - Activated oxygen and arachidonate effects on newborn cerebral arterioles

AU - Leffler, Charles

AU - Busija, D. W.

AU - Armstead, W. M.

AU - Shanklin, D. R.

AU - Mirro, R.

AU - Thelin, O.

PY - 1990/1/1

Y1 - 1990/1/1

N2 - We have observed that pial arteriolar dilation in response to hypercapnia and hypotension is abolished after cerebral ischemia in newborn pigs. We determined whether direct generation of activated oxygen on the brain surface (OX: xanthine oxidase, hypoxanthine, FeCl3, and FeSO4) or topical arachidonate altered pial arteriolar responsiveness in a manner similarly to cerebral ischemia. OX, which generated more brain surface superoxide than reperfusion after ischemia, dilated pial arterioles. This dilation was reversed within 10 min of the end of exposure. OX produced ultrastructural changes in pial vessel endothelium and appeared to cause intravascular aggregation of granulocytes. After OX, prostanoid-dependent pial arteriolar dilations in response to hypercapnia and hypotension were attenuated, whereas constrictor responses to norepinephrine and acetylcholine and dilator responses to prostaglandin E2 and isoproterenol were not affected. After OX, hypercapnia increased cortical periarachnoid cerebrospinal fluid prostanoids modestly, whereas acetylcholine produced the normal strong stimulation of prostanoid synthesis. Arachidonate (10-4 M and 7 x 10-4 M) also caused reversible pial arteriolar dilation but did not alter subsequent pial arteriolar responses. Therefore, although arachidonate did not mimic the effects of ischemia-reperfusion on pial arteriolar reactivity, OX produced alterations that are qualitatively similar, although quantitatively less, than those produced by ischemia.

AB - We have observed that pial arteriolar dilation in response to hypercapnia and hypotension is abolished after cerebral ischemia in newborn pigs. We determined whether direct generation of activated oxygen on the brain surface (OX: xanthine oxidase, hypoxanthine, FeCl3, and FeSO4) or topical arachidonate altered pial arteriolar responsiveness in a manner similarly to cerebral ischemia. OX, which generated more brain surface superoxide than reperfusion after ischemia, dilated pial arterioles. This dilation was reversed within 10 min of the end of exposure. OX produced ultrastructural changes in pial vessel endothelium and appeared to cause intravascular aggregation of granulocytes. After OX, prostanoid-dependent pial arteriolar dilations in response to hypercapnia and hypotension were attenuated, whereas constrictor responses to norepinephrine and acetylcholine and dilator responses to prostaglandin E2 and isoproterenol were not affected. After OX, hypercapnia increased cortical periarachnoid cerebrospinal fluid prostanoids modestly, whereas acetylcholine produced the normal strong stimulation of prostanoid synthesis. Arachidonate (10-4 M and 7 x 10-4 M) also caused reversible pial arteriolar dilation but did not alter subsequent pial arteriolar responses. Therefore, although arachidonate did not mimic the effects of ischemia-reperfusion on pial arteriolar reactivity, OX produced alterations that are qualitatively similar, although quantitatively less, than those produced by ischemia.

UR - http://www.scopus.com/inward/record.url?scp=0025096182&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025096182&partnerID=8YFLogxK

M3 - Article

VL - 259

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6135

IS - 4 28-4

ER -