Pressure ventilation increases brain vascular prostacyclin production in newborn pigs

Robert Mirro, Charles Leffler, William M. Armstead, David W. Busija

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Using awake, chronically catheterized newborn pigs, we measured cerebral blood flow (CBF), net cerebral vascular 6-keto-prostaglandin F production, and cerebral metabolic rate of oxygen (CMRO2) during hyper-capnia and during hypercapnia at increased mean airway pressure (Paw), both before and after treatment with in-domethacin. CBF nearly doubled during hypercapnia. The hypercapnia-induced cerebral hyperemia was maintained when Paw was increased from 3 ± 2 to 16 ± 4 cm H2O during hypercapnia. Sagittal sinus pressure increased in proportion to the increase in Paw, and cardiac output was unchanged. Net cerebral production of 6-keto-prostaglandin Fie increased from 9 ± 1 to 15 ± 1 ng/min/100 g tissue during hypercapnia and increased dramatically to 57 ± 1 ng/min/100 g when hypercapnia was coupled with an increase in Paw. CMRO2 was not changed by either hypercapnia or increased Paw. After indomethacin, CBF decreased and cerebral vasodilation to hypercapnia did not occur. After indomethacin, adding increased Paw during hypercapnia dropped CBF below baseline, adversely affecting CMRO2. These results suggest that cerebral hy-percapnic hyperemia requires brain prostanoid production and that when Paw is increased during hypercapnia, the contribution of prostanoids to maintaining CBF is increased. Increasing ventilation pressure during hypercapnia in piglets pretreated with indomethacin compromises CBF sufficiently to reduce CMRO2.

Original languageEnglish (US)
Pages (from-to)609-612
Number of pages4
JournalPediatric Research
Volume28
Issue number6
DOIs
StatePublished - Jan 1 1990

Fingerprint

Hypercapnia
Epoprostenol
Cerebrovascular Circulation
Blood Vessels
Ventilation
Swine
Pressure
Brain
Indomethacin
Prostaglandins
Hyperemia
Vasodilation
Cardiac Output
Oxygen

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health

Cite this

Pressure ventilation increases brain vascular prostacyclin production in newborn pigs. / Mirro, Robert; Leffler, Charles; Armstead, William M.; Busija, David W.

In: Pediatric Research, Vol. 28, No. 6, 01.01.1990, p. 609-612.

Research output: Contribution to journalArticle

Mirro, Robert ; Leffler, Charles ; Armstead, William M. ; Busija, David W. / Pressure ventilation increases brain vascular prostacyclin production in newborn pigs. In: Pediatric Research. 1990 ; Vol. 28, No. 6. pp. 609-612.
@article{4e28d252440846e799334230d848fc6d,
title = "Pressure ventilation increases brain vascular prostacyclin production in newborn pigs",
abstract = "Using awake, chronically catheterized newborn pigs, we measured cerebral blood flow (CBF), net cerebral vascular 6-keto-prostaglandin F1α production, and cerebral metabolic rate of oxygen (CMRO2) during hyper-capnia and during hypercapnia at increased mean airway pressure (Paw), both before and after treatment with in-domethacin. CBF nearly doubled during hypercapnia. The hypercapnia-induced cerebral hyperemia was maintained when Paw was increased from 3 ± 2 to 16 ± 4 cm H2O during hypercapnia. Sagittal sinus pressure increased in proportion to the increase in Paw, and cardiac output was unchanged. Net cerebral production of 6-keto-prostaglandin Fie increased from 9 ± 1 to 15 ± 1 ng/min/100 g tissue during hypercapnia and increased dramatically to 57 ± 1 ng/min/100 g when hypercapnia was coupled with an increase in Paw. CMRO2 was not changed by either hypercapnia or increased Paw. After indomethacin, CBF decreased and cerebral vasodilation to hypercapnia did not occur. After indomethacin, adding increased Paw during hypercapnia dropped CBF below baseline, adversely affecting CMRO2. These results suggest that cerebral hy-percapnic hyperemia requires brain prostanoid production and that when Paw is increased during hypercapnia, the contribution of prostanoids to maintaining CBF is increased. Increasing ventilation pressure during hypercapnia in piglets pretreated with indomethacin compromises CBF sufficiently to reduce CMRO2.",
author = "Robert Mirro and Charles Leffler and Armstead, {William M.} and Busija, {David W.}",
year = "1990",
month = "1",
day = "1",
doi = "10.1203/00006450-199012000-00013",
language = "English (US)",
volume = "28",
pages = "609--612",
journal = "Pediatric Research",
issn = "0031-3998",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

TY - JOUR

T1 - Pressure ventilation increases brain vascular prostacyclin production in newborn pigs

AU - Mirro, Robert

AU - Leffler, Charles

AU - Armstead, William M.

AU - Busija, David W.

PY - 1990/1/1

Y1 - 1990/1/1

N2 - Using awake, chronically catheterized newborn pigs, we measured cerebral blood flow (CBF), net cerebral vascular 6-keto-prostaglandin F1α production, and cerebral metabolic rate of oxygen (CMRO2) during hyper-capnia and during hypercapnia at increased mean airway pressure (Paw), both before and after treatment with in-domethacin. CBF nearly doubled during hypercapnia. The hypercapnia-induced cerebral hyperemia was maintained when Paw was increased from 3 ± 2 to 16 ± 4 cm H2O during hypercapnia. Sagittal sinus pressure increased in proportion to the increase in Paw, and cardiac output was unchanged. Net cerebral production of 6-keto-prostaglandin Fie increased from 9 ± 1 to 15 ± 1 ng/min/100 g tissue during hypercapnia and increased dramatically to 57 ± 1 ng/min/100 g when hypercapnia was coupled with an increase in Paw. CMRO2 was not changed by either hypercapnia or increased Paw. After indomethacin, CBF decreased and cerebral vasodilation to hypercapnia did not occur. After indomethacin, adding increased Paw during hypercapnia dropped CBF below baseline, adversely affecting CMRO2. These results suggest that cerebral hy-percapnic hyperemia requires brain prostanoid production and that when Paw is increased during hypercapnia, the contribution of prostanoids to maintaining CBF is increased. Increasing ventilation pressure during hypercapnia in piglets pretreated with indomethacin compromises CBF sufficiently to reduce CMRO2.

AB - Using awake, chronically catheterized newborn pigs, we measured cerebral blood flow (CBF), net cerebral vascular 6-keto-prostaglandin F1α production, and cerebral metabolic rate of oxygen (CMRO2) during hyper-capnia and during hypercapnia at increased mean airway pressure (Paw), both before and after treatment with in-domethacin. CBF nearly doubled during hypercapnia. The hypercapnia-induced cerebral hyperemia was maintained when Paw was increased from 3 ± 2 to 16 ± 4 cm H2O during hypercapnia. Sagittal sinus pressure increased in proportion to the increase in Paw, and cardiac output was unchanged. Net cerebral production of 6-keto-prostaglandin Fie increased from 9 ± 1 to 15 ± 1 ng/min/100 g tissue during hypercapnia and increased dramatically to 57 ± 1 ng/min/100 g when hypercapnia was coupled with an increase in Paw. CMRO2 was not changed by either hypercapnia or increased Paw. After indomethacin, CBF decreased and cerebral vasodilation to hypercapnia did not occur. After indomethacin, adding increased Paw during hypercapnia dropped CBF below baseline, adversely affecting CMRO2. These results suggest that cerebral hy-percapnic hyperemia requires brain prostanoid production and that when Paw is increased during hypercapnia, the contribution of prostanoids to maintaining CBF is increased. Increasing ventilation pressure during hypercapnia in piglets pretreated with indomethacin compromises CBF sufficiently to reduce CMRO2.

UR - http://www.scopus.com/inward/record.url?scp=0025225678&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025225678&partnerID=8YFLogxK

U2 - 10.1203/00006450-199012000-00013

DO - 10.1203/00006450-199012000-00013

M3 - Article

VL - 28

SP - 609

EP - 612

JO - Pediatric Research

JF - Pediatric Research

SN - 0031-3998

IS - 6

ER -