Pial arteriolar constriction following cortical spreading depression is mediated by prostanoids

Masaaki Shibata, Charles Leffler, David W. Busija

Research output: Contribution to journalArticle

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Abstract

The mechanism of pial arteriolar constriction during post-cortical spreading depression (CSD) was examined in anesthetized adult rabbits. Using a closed cranial window and intravital microscopy, the diameter of a pial arteriole was determined. A single CSD was induced by KCl micro-injection and its propagation was monitored by recording slow potential changes accompanying CSD. Prostanoid levels in cortical cerebrospinal fluid (CSF) were determined by radioimmunoassay. Pial arteriolar diameter increased significantly from 76 ± 6 to a maximum of 119 ± 5 μm (57%, n = 8) for 1.6 ± 0.1 min when CSD (velocity, 2.8 ± 0.1 mm/min) reached the cortex just beneath the vessel irrespective of its location. Shortly after CSD expiration from the cortex, pial arteriolar diameter decreased from the pre-CSD level to a minimum of 67 ± 5 μm (12%, n = 8) for 19.5 ± 2.1 min. CSD was elicited again in the same animal while the cortical surface under the window was continuously superfused with artificial CSF at a flow rate of 3.2-4.5 ml/min. Pial arteriolar dilation (from 75 ± 6 to 115 ± 3 μm, 53 ± 9%, for 1.6 ± 0.1 min, n = 8) was observed again during CSD (velocity, 2.7 ± 0.2 mm/min), however, no constriction of the vessel was seen after CSD expiration. Indomethacin pretreatment (n = 11) to inhibit prostanoid production enhanced the magnitude of CSD-induced vasodilation from the pretreatment levels of 59 ± 9% (from 82 ± 5 to 130 ± 8 μm for 1.7 min) to the post-treatment levels of 82 ± 13% (from 78 ± 5 to 142 ± 12 μm for 1.8 min). In contrast, the post-CDS vasoconstriction observed before indomethacin (11 ± 2% for 16.6 ± 2 min) was completely ablated after indomethacin. CSF prostanoids (pg/ml, n = 11) increased during the CSD-induced vasodilation from 1429 ± 100 to 2889 ± 283 (102%) for prostaglandin E2 (PGE2), from 1453 ± 106 to 1945 ± 138 (34%) for 6-keto-PGF, and from 3506 ± 390 to 6777 ± 745 (93%) for PGF. Thromboxane B2 (TXB2) did not increase significantly. CSF prostanoids increased further during the post-CSD vasoconstriction; PGE2, 213% (n = 8); 6-keto-PGF, 99% (n = 7); PGF, 236% (n = 8) and TXB2, 56% (n = 6). Indomethacin decreased the resting levels of all the prostanoids and blocked their increases during the CSD-induced vasodilation and during the post-CSD period. These results suggest that while prostanoids attenuate pial arteriolar dilation during CSD, they mediate the post-CSD constriction of the vessel.

Original languageEnglish (US)
Pages (from-to)190-197
Number of pages8
JournalBrain Research
Volume572
Issue number1-2
DOIs
StatePublished - Feb 14 1992

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Cortical Spreading Depression
Constriction
Prostaglandins
Indomethacin
Cerebrospinal Fluid
Vasodilation
Thromboxane B2
Dinoprost
Vasoconstriction
Dinoprostone
Dilatation

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

Cite this

Pial arteriolar constriction following cortical spreading depression is mediated by prostanoids. / Shibata, Masaaki; Leffler, Charles; Busija, David W.

In: Brain Research, Vol. 572, No. 1-2, 14.02.1992, p. 190-197.

Research output: Contribution to journalArticle

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title = "Pial arteriolar constriction following cortical spreading depression is mediated by prostanoids",
abstract = "The mechanism of pial arteriolar constriction during post-cortical spreading depression (CSD) was examined in anesthetized adult rabbits. Using a closed cranial window and intravital microscopy, the diameter of a pial arteriole was determined. A single CSD was induced by KCl micro-injection and its propagation was monitored by recording slow potential changes accompanying CSD. Prostanoid levels in cortical cerebrospinal fluid (CSF) were determined by radioimmunoassay. Pial arteriolar diameter increased significantly from 76 ± 6 to a maximum of 119 ± 5 μm (57{\%}, n = 8) for 1.6 ± 0.1 min when CSD (velocity, 2.8 ± 0.1 mm/min) reached the cortex just beneath the vessel irrespective of its location. Shortly after CSD expiration from the cortex, pial arteriolar diameter decreased from the pre-CSD level to a minimum of 67 ± 5 μm (12{\%}, n = 8) for 19.5 ± 2.1 min. CSD was elicited again in the same animal while the cortical surface under the window was continuously superfused with artificial CSF at a flow rate of 3.2-4.5 ml/min. Pial arteriolar dilation (from 75 ± 6 to 115 ± 3 μm, 53 ± 9{\%}, for 1.6 ± 0.1 min, n = 8) was observed again during CSD (velocity, 2.7 ± 0.2 mm/min), however, no constriction of the vessel was seen after CSD expiration. Indomethacin pretreatment (n = 11) to inhibit prostanoid production enhanced the magnitude of CSD-induced vasodilation from the pretreatment levels of 59 ± 9{\%} (from 82 ± 5 to 130 ± 8 μm for 1.7 min) to the post-treatment levels of 82 ± 13{\%} (from 78 ± 5 to 142 ± 12 μm for 1.8 min). In contrast, the post-CDS vasoconstriction observed before indomethacin (11 ± 2{\%} for 16.6 ± 2 min) was completely ablated after indomethacin. CSF prostanoids (pg/ml, n = 11) increased during the CSD-induced vasodilation from 1429 ± 100 to 2889 ± 283 (102{\%}) for prostaglandin E2 (PGE2), from 1453 ± 106 to 1945 ± 138 (34{\%}) for 6-keto-PGF1α, and from 3506 ± 390 to 6777 ± 745 (93{\%}) for PGF2α. Thromboxane B2 (TXB2) did not increase significantly. CSF prostanoids increased further during the post-CSD vasoconstriction; PGE2, 213{\%} (n = 8); 6-keto-PGF1α, 99{\%} (n = 7); PGF2α, 236{\%} (n = 8) and TXB2, 56{\%} (n = 6). Indomethacin decreased the resting levels of all the prostanoids and blocked their increases during the CSD-induced vasodilation and during the post-CSD period. These results suggest that while prostanoids attenuate pial arteriolar dilation during CSD, they mediate the post-CSD constriction of the vessel.",
author = "Masaaki Shibata and Charles Leffler and Busija, {David W.}",
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N2 - The mechanism of pial arteriolar constriction during post-cortical spreading depression (CSD) was examined in anesthetized adult rabbits. Using a closed cranial window and intravital microscopy, the diameter of a pial arteriole was determined. A single CSD was induced by KCl micro-injection and its propagation was monitored by recording slow potential changes accompanying CSD. Prostanoid levels in cortical cerebrospinal fluid (CSF) were determined by radioimmunoassay. Pial arteriolar diameter increased significantly from 76 ± 6 to a maximum of 119 ± 5 μm (57%, n = 8) for 1.6 ± 0.1 min when CSD (velocity, 2.8 ± 0.1 mm/min) reached the cortex just beneath the vessel irrespective of its location. Shortly after CSD expiration from the cortex, pial arteriolar diameter decreased from the pre-CSD level to a minimum of 67 ± 5 μm (12%, n = 8) for 19.5 ± 2.1 min. CSD was elicited again in the same animal while the cortical surface under the window was continuously superfused with artificial CSF at a flow rate of 3.2-4.5 ml/min. Pial arteriolar dilation (from 75 ± 6 to 115 ± 3 μm, 53 ± 9%, for 1.6 ± 0.1 min, n = 8) was observed again during CSD (velocity, 2.7 ± 0.2 mm/min), however, no constriction of the vessel was seen after CSD expiration. Indomethacin pretreatment (n = 11) to inhibit prostanoid production enhanced the magnitude of CSD-induced vasodilation from the pretreatment levels of 59 ± 9% (from 82 ± 5 to 130 ± 8 μm for 1.7 min) to the post-treatment levels of 82 ± 13% (from 78 ± 5 to 142 ± 12 μm for 1.8 min). In contrast, the post-CDS vasoconstriction observed before indomethacin (11 ± 2% for 16.6 ± 2 min) was completely ablated after indomethacin. CSF prostanoids (pg/ml, n = 11) increased during the CSD-induced vasodilation from 1429 ± 100 to 2889 ± 283 (102%) for prostaglandin E2 (PGE2), from 1453 ± 106 to 1945 ± 138 (34%) for 6-keto-PGF1α, and from 3506 ± 390 to 6777 ± 745 (93%) for PGF2α. Thromboxane B2 (TXB2) did not increase significantly. CSF prostanoids increased further during the post-CSD vasoconstriction; PGE2, 213% (n = 8); 6-keto-PGF1α, 99% (n = 7); PGF2α, 236% (n = 8) and TXB2, 56% (n = 6). Indomethacin decreased the resting levels of all the prostanoids and blocked their increases during the CSD-induced vasodilation and during the post-CSD period. These results suggest that while prostanoids attenuate pial arteriolar dilation during CSD, they mediate the post-CSD constriction of the vessel.

AB - The mechanism of pial arteriolar constriction during post-cortical spreading depression (CSD) was examined in anesthetized adult rabbits. Using a closed cranial window and intravital microscopy, the diameter of a pial arteriole was determined. A single CSD was induced by KCl micro-injection and its propagation was monitored by recording slow potential changes accompanying CSD. Prostanoid levels in cortical cerebrospinal fluid (CSF) were determined by radioimmunoassay. Pial arteriolar diameter increased significantly from 76 ± 6 to a maximum of 119 ± 5 μm (57%, n = 8) for 1.6 ± 0.1 min when CSD (velocity, 2.8 ± 0.1 mm/min) reached the cortex just beneath the vessel irrespective of its location. Shortly after CSD expiration from the cortex, pial arteriolar diameter decreased from the pre-CSD level to a minimum of 67 ± 5 μm (12%, n = 8) for 19.5 ± 2.1 min. CSD was elicited again in the same animal while the cortical surface under the window was continuously superfused with artificial CSF at a flow rate of 3.2-4.5 ml/min. Pial arteriolar dilation (from 75 ± 6 to 115 ± 3 μm, 53 ± 9%, for 1.6 ± 0.1 min, n = 8) was observed again during CSD (velocity, 2.7 ± 0.2 mm/min), however, no constriction of the vessel was seen after CSD expiration. Indomethacin pretreatment (n = 11) to inhibit prostanoid production enhanced the magnitude of CSD-induced vasodilation from the pretreatment levels of 59 ± 9% (from 82 ± 5 to 130 ± 8 μm for 1.7 min) to the post-treatment levels of 82 ± 13% (from 78 ± 5 to 142 ± 12 μm for 1.8 min). In contrast, the post-CDS vasoconstriction observed before indomethacin (11 ± 2% for 16.6 ± 2 min) was completely ablated after indomethacin. CSF prostanoids (pg/ml, n = 11) increased during the CSD-induced vasodilation from 1429 ± 100 to 2889 ± 283 (102%) for prostaglandin E2 (PGE2), from 1453 ± 106 to 1945 ± 138 (34%) for 6-keto-PGF1α, and from 3506 ± 390 to 6777 ± 745 (93%) for PGF2α. Thromboxane B2 (TXB2) did not increase significantly. CSF prostanoids increased further during the post-CSD vasoconstriction; PGE2, 213% (n = 8); 6-keto-PGF1α, 99% (n = 7); PGF2α, 236% (n = 8) and TXB2, 56% (n = 6). Indomethacin decreased the resting levels of all the prostanoids and blocked their increases during the CSD-induced vasodilation and during the post-CSD period. These results suggest that while prostanoids attenuate pial arteriolar dilation during CSD, they mediate the post-CSD constriction of the vessel.

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