Influence of an abrupt increase in blood pressure on the blood-brain barrier permeability during acute hypertension and epileptic seizures.
The interrelationship between the breakdown of the blood-brain barrier according to the Evans-blue passage and an abrupt increase in blood pressure (DeltaP) was studied in rats subjected to adrenaline-induced acute hypertension and also pentylenetetrazol-induced seizures. Arterial blood pressure was increased by adrenaline, then immediately i.v. nifedipine was injected and subsequently decreased to the control value in the acute hypertensive group. Arterial blood pressure was increased by pentylenetetrazol, then immediately GABA (gamma-aminobutiric acid) was injected and the blood pressure was decreased to the control value in the seizure group. The animals were divided into five groups. Group I: control; Group II: acute hypertension; Group III: acute hypertension + nifedipine; Group IV: seizure; Group V: seizure + GABA. The Evans-blue dye content was found to be 0.25 +/- 0.01 mg% in the whole brain in the control animals, and 0.803 +/- 0.1 mg% in the acute hypertensive group. This difference between these groups was found to be significant: P< 0.01. In the nifedipine group (Group III) the Evans-blue content was 0.30 +/- 0.1 mg% in the whole brain; and there was no significant difference between control values and nifedipine-treated animals (P> 0.5). The Evans-blue content was 1.6 +/- 0.2 mg% in the whole brain during seizure, and decreased to 0.36 +/- 0.1 mg% after GABA injection was administered. There was also no significant difference between the control value and the GABA-treated animals (P> 0.5). These results have shown that an abrupt increase in blood pressure (DeltaP) did not change the blood-brain barrier permeability in both acute hypertension and seizures.[1]References
- Influence of an abrupt increase in blood pressure on the blood-brain barrier permeability during acute hypertension and epileptic seizures. Oztaş, B., Türkel, N. Pharmacol. Res. (2001) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
