Hematoma-induced enhanced cerebral vasoconstrictions to leukotriene C4 and endothelin-1 in piglets

Role of prostanoids

M. A. Yakubu, M. Shibata, Charles Leffler

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Cerebral hematoma enhances vasoconstriction induced by topical application of the vasoconstrictor agents endothelin-1 (ET-1) and leukotriene C4 (LTC4). We investigated the influence of dilator prostanoids on vasoconstrictions induced by ET-1 and LTC4 in piglets. Newborn pigs anesthetized with α-chloralose were fitted with closed cranial windows 4 d after cortical subarachnoid injections of artificial cerebrospinal fluid (aCSF) (control) or blood (hematoma). The responsiveness of pial arterioles to topical application of the vasoconstrictors ET-1 and LTC4 was examined in the control and hematoma groups before and after treatment with indomethacin (5 mg/kg, i.v.). Vasoconstriction to topical application of LTC4 and ET-1 was enhanced by hematoma compared with the control (28 ± 2% versus 21 ± 2% for 10−8 M LTC4 and by 25 ± 2% versus 15 ± 1% for 1(T8 M ET-1, respectively). The lower dose of ET-1 (10−12 M) dilated pial arterioles in the control group by 6 ± 2%, hematoma blocked this dilation and it was converted to constriction (10 ± 1%). Indomethacin treatment enhanced vasoconstriction to LTC4 in the control group to a similar constriction to that observed in the hematoma group. Indomethacin treatment also enhanced vasoconstriction to ET-1 in the control group (25 ± 1% for 10−8 M) to similar constrictions to those observed in the hematoma I group (25 ± 2% for 10−8 M). Dilation to the lower dose of ET-1 was blocked and converted to constriction (17 ± 2% for 10−12 M) by indomethacin treatment. These results show that indomethacin and cerebral hematoma similarly enhance vasoconstriction to topical application of LTC4 and ET-1. Loss of dilator prostanoid influence caused by hematoma may result in prolonged and uninhibited constriction of pial arterioles by constrictor vasoactive agents, leading to the sustained and prolonged arteriolar wall narrowing observed after cerebral hemorrhage.

Original languageEnglish (US)
Pages (from-to)119-123
Number of pages5
JournalPediatric Research
Volume38
Issue number1
DOIs
StatePublished - Jan 1 1995

Fingerprint

Leukotriene C4
Endothelin-1
Vasoconstriction
Hematoma
Prostaglandins
Constriction
Indomethacin
Arterioles
Control Groups
Vasoconstrictor Agents
Dilatation
Chloralose
Cerebral Hemorrhage
Therapeutics
Cerebrospinal Fluid
Swine
Injections

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health

Cite this

Hematoma-induced enhanced cerebral vasoconstrictions to leukotriene C4 and endothelin-1 in piglets : Role of prostanoids. / Yakubu, M. A.; Shibata, M.; Leffler, Charles.

In: Pediatric Research, Vol. 38, No. 1, 01.01.1995, p. 119-123.

Research output: Contribution to journalArticle

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abstract = "Cerebral hematoma enhances vasoconstriction induced by topical application of the vasoconstrictor agents endothelin-1 (ET-1) and leukotriene C4 (LTC4). We investigated the influence of dilator prostanoids on vasoconstrictions induced by ET-1 and LTC4 in piglets. Newborn pigs anesthetized with α-chloralose were fitted with closed cranial windows 4 d after cortical subarachnoid injections of artificial cerebrospinal fluid (aCSF) (control) or blood (hematoma). The responsiveness of pial arterioles to topical application of the vasoconstrictors ET-1 and LTC4 was examined in the control and hematoma groups before and after treatment with indomethacin (5 mg/kg, i.v.). Vasoconstriction to topical application of LTC4 and ET-1 was enhanced by hematoma compared with the control (28 ± 2{\%} versus 21 ± 2{\%} for 10−8 M LTC4 and by 25 ± 2{\%} versus 15 ± 1{\%} for 1(T8 M ET-1, respectively). The lower dose of ET-1 (10−12 M) dilated pial arterioles in the control group by 6 ± 2{\%}, hematoma blocked this dilation and it was converted to constriction (10 ± 1{\%}). Indomethacin treatment enhanced vasoconstriction to LTC4 in the control group to a similar constriction to that observed in the hematoma group. Indomethacin treatment also enhanced vasoconstriction to ET-1 in the control group (25 ± 1{\%} for 10−8 M) to similar constrictions to those observed in the hematoma I group (25 ± 2{\%} for 10−8 M). Dilation to the lower dose of ET-1 was blocked and converted to constriction (17 ± 2{\%} for 10−12 M) by indomethacin treatment. These results show that indomethacin and cerebral hematoma similarly enhance vasoconstriction to topical application of LTC4 and ET-1. Loss of dilator prostanoid influence caused by hematoma may result in prolonged and uninhibited constriction of pial arterioles by constrictor vasoactive agents, leading to the sustained and prolonged arteriolar wall narrowing observed after cerebral hemorrhage.",
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