Effects of nitric oxide on blood-brain barrier disruption caused by intracarotid injection of hyperosmolar mannitol in rats

Oak Chi, Qiang Chang, Guolin Wang, Harvey Weiss

Research output: Contribution to journalArticle

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Abstract

We performed this study to evaluate the effects of changing the level of nitric oxide (NO) on disruption of the blood-brain barrier (BBB) by hyperosmolar mannitol. Under isoflurane anesthesia, control rats (control group, n = 6) were given infusions with 25% mannitol into the internal carotid artery before measuring the transfer coefficient (K(i)) of 14C-α- aminoisobutyric acid (14C-AIB). In the CAS group (n = 6), [3-(cis-2,6- dimethyl piperidino)-sydnonimine] (CAS 754), a NO donor, was injected to decrease the mean arterial pressure (MAP) to 55 mm Hg and in the L-NAME group (n = 6), N(G)-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, was injected before administering mannitol. In additional control animals (control + P group, n = 6) and additional CAS 754-treated animals (CAS + P group, n = 6), phenylephrine was infused to keep MAP at 130 mm Hg during the experimental period. In the control group, with mannitol injection, the K(i) of the ipsilateral cortex (IC) where mannitol was injected increased to 4.3 times that of the contralateral cortex (CC) (17.2 ± 2.9 vs 4.0 ± 2.6 μl · g-1 · min-1). Without blood pressure control, the K(i) of the IC of the CAS group (7.0 ± 4.5) was lower and that of the L-NAME group (26.2 ± 12.7) was higher than that of the control animals. At the same MAP, the K(i) of the IC of the CAS + P group (9.6 ± 3.1) was significantly lower than that of the control + P group (21.3 ± 14.5) or that of the L-NAME group. There was no significant difference in the K(i) of the IC between the control + P and the L-NAME groups. In conclusion, L-NAME worsened BBB disruption induced by hyperosmolar solution, which may be due to the pressure effect of L-NAME. CAS 754 was effective in attenuating disruption of the BBB caused by hyperosmolar mannitol. This effect is apparently not due to decreased MAP.

Original languageEnglish (US)
Pages (from-to)370-375
Number of pages6
JournalAnesthesia and analgesia
Volume84
Issue number2
DOIs
StatePublished - Feb 13 1997

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NG-Nitroarginine Methyl Ester
Mannitol
Blood-Brain Barrier
Nitric Oxide
Injections
Arterial Pressure
Control Groups
Aminoisobutyric Acids
Nitric Oxide Donors
Isoflurane
Internal Carotid Artery
Phenylephrine
Nitric Oxide Synthase
Anesthesia
Blood Pressure
Pressure

All Science Journal Classification (ASJC) codes

  • Anesthesiology and Pain Medicine

Cite this

@article{e56b4872201b4f489a1ec5eea733aff6,
title = "Effects of nitric oxide on blood-brain barrier disruption caused by intracarotid injection of hyperosmolar mannitol in rats",
abstract = "We performed this study to evaluate the effects of changing the level of nitric oxide (NO) on disruption of the blood-brain barrier (BBB) by hyperosmolar mannitol. Under isoflurane anesthesia, control rats (control group, n = 6) were given infusions with 25{\%} mannitol into the internal carotid artery before measuring the transfer coefficient (K(i)) of 14C-α- aminoisobutyric acid (14C-AIB). In the CAS group (n = 6), [3-(cis-2,6- dimethyl piperidino)-sydnonimine] (CAS 754), a NO donor, was injected to decrease the mean arterial pressure (MAP) to 55 mm Hg and in the L-NAME group (n = 6), N(G)-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, was injected before administering mannitol. In additional control animals (control + P group, n = 6) and additional CAS 754-treated animals (CAS + P group, n = 6), phenylephrine was infused to keep MAP at 130 mm Hg during the experimental period. In the control group, with mannitol injection, the K(i) of the ipsilateral cortex (IC) where mannitol was injected increased to 4.3 times that of the contralateral cortex (CC) (17.2 ± 2.9 vs 4.0 ± 2.6 μl · g-1 · min-1). Without blood pressure control, the K(i) of the IC of the CAS group (7.0 ± 4.5) was lower and that of the L-NAME group (26.2 ± 12.7) was higher than that of the control animals. At the same MAP, the K(i) of the IC of the CAS + P group (9.6 ± 3.1) was significantly lower than that of the control + P group (21.3 ± 14.5) or that of the L-NAME group. There was no significant difference in the K(i) of the IC between the control + P and the L-NAME groups. In conclusion, L-NAME worsened BBB disruption induced by hyperosmolar solution, which may be due to the pressure effect of L-NAME. CAS 754 was effective in attenuating disruption of the BBB caused by hyperosmolar mannitol. This effect is apparently not due to decreased MAP.",
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Effects of nitric oxide on blood-brain barrier disruption caused by intracarotid injection of hyperosmolar mannitol in rats. / Chi, Oak; Chang, Qiang; Wang, Guolin; Weiss, Harvey.

In: Anesthesia and analgesia, Vol. 84, No. 2, 13.02.1997, p. 370-375.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Effects of nitric oxide on blood-brain barrier disruption caused by intracarotid injection of hyperosmolar mannitol in rats

AU - Chi, Oak

AU - Chang, Qiang

AU - Wang, Guolin

AU - Weiss, Harvey

PY - 1997/2/13

Y1 - 1997/2/13

N2 - We performed this study to evaluate the effects of changing the level of nitric oxide (NO) on disruption of the blood-brain barrier (BBB) by hyperosmolar mannitol. Under isoflurane anesthesia, control rats (control group, n = 6) were given infusions with 25% mannitol into the internal carotid artery before measuring the transfer coefficient (K(i)) of 14C-α- aminoisobutyric acid (14C-AIB). In the CAS group (n = 6), [3-(cis-2,6- dimethyl piperidino)-sydnonimine] (CAS 754), a NO donor, was injected to decrease the mean arterial pressure (MAP) to 55 mm Hg and in the L-NAME group (n = 6), N(G)-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, was injected before administering mannitol. In additional control animals (control + P group, n = 6) and additional CAS 754-treated animals (CAS + P group, n = 6), phenylephrine was infused to keep MAP at 130 mm Hg during the experimental period. In the control group, with mannitol injection, the K(i) of the ipsilateral cortex (IC) where mannitol was injected increased to 4.3 times that of the contralateral cortex (CC) (17.2 ± 2.9 vs 4.0 ± 2.6 μl · g-1 · min-1). Without blood pressure control, the K(i) of the IC of the CAS group (7.0 ± 4.5) was lower and that of the L-NAME group (26.2 ± 12.7) was higher than that of the control animals. At the same MAP, the K(i) of the IC of the CAS + P group (9.6 ± 3.1) was significantly lower than that of the control + P group (21.3 ± 14.5) or that of the L-NAME group. There was no significant difference in the K(i) of the IC between the control + P and the L-NAME groups. In conclusion, L-NAME worsened BBB disruption induced by hyperosmolar solution, which may be due to the pressure effect of L-NAME. CAS 754 was effective in attenuating disruption of the BBB caused by hyperosmolar mannitol. This effect is apparently not due to decreased MAP.

AB - We performed this study to evaluate the effects of changing the level of nitric oxide (NO) on disruption of the blood-brain barrier (BBB) by hyperosmolar mannitol. Under isoflurane anesthesia, control rats (control group, n = 6) were given infusions with 25% mannitol into the internal carotid artery before measuring the transfer coefficient (K(i)) of 14C-α- aminoisobutyric acid (14C-AIB). In the CAS group (n = 6), [3-(cis-2,6- dimethyl piperidino)-sydnonimine] (CAS 754), a NO donor, was injected to decrease the mean arterial pressure (MAP) to 55 mm Hg and in the L-NAME group (n = 6), N(G)-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, was injected before administering mannitol. In additional control animals (control + P group, n = 6) and additional CAS 754-treated animals (CAS + P group, n = 6), phenylephrine was infused to keep MAP at 130 mm Hg during the experimental period. In the control group, with mannitol injection, the K(i) of the ipsilateral cortex (IC) where mannitol was injected increased to 4.3 times that of the contralateral cortex (CC) (17.2 ± 2.9 vs 4.0 ± 2.6 μl · g-1 · min-1). Without blood pressure control, the K(i) of the IC of the CAS group (7.0 ± 4.5) was lower and that of the L-NAME group (26.2 ± 12.7) was higher than that of the control animals. At the same MAP, the K(i) of the IC of the CAS + P group (9.6 ± 3.1) was significantly lower than that of the control + P group (21.3 ± 14.5) or that of the L-NAME group. There was no significant difference in the K(i) of the IC between the control + P and the L-NAME groups. In conclusion, L-NAME worsened BBB disruption induced by hyperosmolar solution, which may be due to the pressure effect of L-NAME. CAS 754 was effective in attenuating disruption of the BBB caused by hyperosmolar mannitol. This effect is apparently not due to decreased MAP.

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