Effects of indomethacin on cardiac output distribution in normal and asphyxiated piglets

Charles Leffler, David W. Busija, Donathan G. Beasley, Anthony M. Fletcher, Robert S. Green

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

We determined the effect of breathing 9% CO2/10% O2/81% N2 (asphyxia) on cardiac output distribution (microspheres) in 4-5 day old unanesthetized, chronically instrumented piglets prior to and following intravenous indomethacin administration. Thirty minutes of asphyxia caused PaCO2 to increase from 35 ± 2 mmHg to 66 ± 2 mmHg, PaO2 to decrease form 73 ± 4 mmHg to 41 ± 1 mmHg, and pH to decrease from 7.52 ± 0.05 to 7.21 ± 0.07. Arterial pressure was increased slightly but cardiac output was not changed significantly. Asphyxia caused blood flow to the brain, diaphragm, liver, heart, and adrenal glands to increase while causing decreases in blood flow to the skin, small intestine, and colon. Blood flows to the stomach and kidneys tended to decrease, but the changes were not significant. Treatment with indomethacin during asphyxia did not alter arterial pressure or cardiac output but decreased cerebral blood flow to the preasphyxiated level and decreased adrenal blood flow about 20%. Indomethacin did not alter blood flow to any other systemic organ. At this time the piglet was allowed to breathe air for 2.5 hr undisturbed. Two and a half hours after indomethacin administration, blood flows to all organs returned to the preasphyxia control levels with the exception of cerebral blood flow which was reduced (93 ± 13 to 65 ± 5 ml/100 g·min. Three hours after indomethacin administration, the cerebral hyperemia caused by asphyxia was less (134 ± 17b ml/100 g·min) than prior to indomethacin (221 ± 15 ml/100 g·min. Indomethacin did not alter the asphyxia-induced changes to any other systemic organ. We conclude that in newborn pigs, systemic treatment with indomethacin decreases cerebral blood flow and cerebral hyperemia in response to asphyxia, without affecting blood flow to any other systemic organ.

Original languageEnglish (US)
Pages (from-to)183-190
Number of pages8
JournalProstaglandins
Volume31
Issue number2
DOIs
StatePublished - Jan 1 1986
Externally publishedYes

Fingerprint

Normal Distribution
Asphyxia
Indomethacin
Cardiac Output
Blood
Cerebrovascular Circulation
Hyperemia
Arterial Pressure
Adrenal Glands
Diaphragm
Microspheres
Intravenous Administration
Small Intestine
Level control
Stomach
Diaphragms
Respiration
Colon
Swine
Liver

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Endocrinology

Cite this

Effects of indomethacin on cardiac output distribution in normal and asphyxiated piglets. / Leffler, Charles; Busija, David W.; Beasley, Donathan G.; Fletcher, Anthony M.; Green, Robert S.

In: Prostaglandins, Vol. 31, No. 2, 01.01.1986, p. 183-190.

Research output: Contribution to journalArticle

Leffler, Charles ; Busija, David W. ; Beasley, Donathan G. ; Fletcher, Anthony M. ; Green, Robert S. / Effects of indomethacin on cardiac output distribution in normal and asphyxiated piglets. In: Prostaglandins. 1986 ; Vol. 31, No. 2. pp. 183-190.
@article{c10d814804b04aa99ff2b1133cef38d7,
title = "Effects of indomethacin on cardiac output distribution in normal and asphyxiated piglets",
abstract = "We determined the effect of breathing 9{\%} CO2/10{\%} O2/81{\%} N2 (asphyxia) on cardiac output distribution (microspheres) in 4-5 day old unanesthetized, chronically instrumented piglets prior to and following intravenous indomethacin administration. Thirty minutes of asphyxia caused PaCO2 to increase from 35 ± 2 mmHg to 66 ± 2 mmHg, PaO2 to decrease form 73 ± 4 mmHg to 41 ± 1 mmHg, and pH to decrease from 7.52 ± 0.05 to 7.21 ± 0.07. Arterial pressure was increased slightly but cardiac output was not changed significantly. Asphyxia caused blood flow to the brain, diaphragm, liver, heart, and adrenal glands to increase while causing decreases in blood flow to the skin, small intestine, and colon. Blood flows to the stomach and kidneys tended to decrease, but the changes were not significant. Treatment with indomethacin during asphyxia did not alter arterial pressure or cardiac output but decreased cerebral blood flow to the preasphyxiated level and decreased adrenal blood flow about 20{\%}. Indomethacin did not alter blood flow to any other systemic organ. At this time the piglet was allowed to breathe air for 2.5 hr undisturbed. Two and a half hours after indomethacin administration, blood flows to all organs returned to the preasphyxia control levels with the exception of cerebral blood flow which was reduced (93 ± 13 to 65 ± 5 ml/100 g·min. Three hours after indomethacin administration, the cerebral hyperemia caused by asphyxia was less (134 ± 17b ml/100 g·min) than prior to indomethacin (221 ± 15 ml/100 g·min. Indomethacin did not alter the asphyxia-induced changes to any other systemic organ. We conclude that in newborn pigs, systemic treatment with indomethacin decreases cerebral blood flow and cerebral hyperemia in response to asphyxia, without affecting blood flow to any other systemic organ.",
author = "Charles Leffler and Busija, {David W.} and Beasley, {Donathan G.} and Fletcher, {Anthony M.} and Green, {Robert S.}",
year = "1986",
month = "1",
day = "1",
doi = "10.1016/0090-6980(86)90045-6",
language = "English (US)",
volume = "31",
pages = "183--190",
journal = "Prostaglandins",
issn = "0090-6980",
publisher = "Elsevier BV",
number = "2",

}

TY - JOUR

T1 - Effects of indomethacin on cardiac output distribution in normal and asphyxiated piglets

AU - Leffler, Charles

AU - Busija, David W.

AU - Beasley, Donathan G.

AU - Fletcher, Anthony M.

AU - Green, Robert S.

PY - 1986/1/1

Y1 - 1986/1/1

N2 - We determined the effect of breathing 9% CO2/10% O2/81% N2 (asphyxia) on cardiac output distribution (microspheres) in 4-5 day old unanesthetized, chronically instrumented piglets prior to and following intravenous indomethacin administration. Thirty minutes of asphyxia caused PaCO2 to increase from 35 ± 2 mmHg to 66 ± 2 mmHg, PaO2 to decrease form 73 ± 4 mmHg to 41 ± 1 mmHg, and pH to decrease from 7.52 ± 0.05 to 7.21 ± 0.07. Arterial pressure was increased slightly but cardiac output was not changed significantly. Asphyxia caused blood flow to the brain, diaphragm, liver, heart, and adrenal glands to increase while causing decreases in blood flow to the skin, small intestine, and colon. Blood flows to the stomach and kidneys tended to decrease, but the changes were not significant. Treatment with indomethacin during asphyxia did not alter arterial pressure or cardiac output but decreased cerebral blood flow to the preasphyxiated level and decreased adrenal blood flow about 20%. Indomethacin did not alter blood flow to any other systemic organ. At this time the piglet was allowed to breathe air for 2.5 hr undisturbed. Two and a half hours after indomethacin administration, blood flows to all organs returned to the preasphyxia control levels with the exception of cerebral blood flow which was reduced (93 ± 13 to 65 ± 5 ml/100 g·min. Three hours after indomethacin administration, the cerebral hyperemia caused by asphyxia was less (134 ± 17b ml/100 g·min) than prior to indomethacin (221 ± 15 ml/100 g·min. Indomethacin did not alter the asphyxia-induced changes to any other systemic organ. We conclude that in newborn pigs, systemic treatment with indomethacin decreases cerebral blood flow and cerebral hyperemia in response to asphyxia, without affecting blood flow to any other systemic organ.

AB - We determined the effect of breathing 9% CO2/10% O2/81% N2 (asphyxia) on cardiac output distribution (microspheres) in 4-5 day old unanesthetized, chronically instrumented piglets prior to and following intravenous indomethacin administration. Thirty minutes of asphyxia caused PaCO2 to increase from 35 ± 2 mmHg to 66 ± 2 mmHg, PaO2 to decrease form 73 ± 4 mmHg to 41 ± 1 mmHg, and pH to decrease from 7.52 ± 0.05 to 7.21 ± 0.07. Arterial pressure was increased slightly but cardiac output was not changed significantly. Asphyxia caused blood flow to the brain, diaphragm, liver, heart, and adrenal glands to increase while causing decreases in blood flow to the skin, small intestine, and colon. Blood flows to the stomach and kidneys tended to decrease, but the changes were not significant. Treatment with indomethacin during asphyxia did not alter arterial pressure or cardiac output but decreased cerebral blood flow to the preasphyxiated level and decreased adrenal blood flow about 20%. Indomethacin did not alter blood flow to any other systemic organ. At this time the piglet was allowed to breathe air for 2.5 hr undisturbed. Two and a half hours after indomethacin administration, blood flows to all organs returned to the preasphyxia control levels with the exception of cerebral blood flow which was reduced (93 ± 13 to 65 ± 5 ml/100 g·min. Three hours after indomethacin administration, the cerebral hyperemia caused by asphyxia was less (134 ± 17b ml/100 g·min) than prior to indomethacin (221 ± 15 ml/100 g·min. Indomethacin did not alter the asphyxia-induced changes to any other systemic organ. We conclude that in newborn pigs, systemic treatment with indomethacin decreases cerebral blood flow and cerebral hyperemia in response to asphyxia, without affecting blood flow to any other systemic organ.

UR - http://www.scopus.com/inward/record.url?scp=0022640402&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022640402&partnerID=8YFLogxK

U2 - 10.1016/0090-6980(86)90045-6

DO - 10.1016/0090-6980(86)90045-6

M3 - Article

VL - 31

SP - 183

EP - 190

JO - Prostaglandins

JF - Prostaglandins

SN - 0090-6980

IS - 2

ER -