Involvement of brain thromboxane A(2) in hypotension induced by haemorrhage in rats
| Autor: | M. Sertac Yilmaz, Fahrunisa Cengiz, Sinan Cavun, Murat Yalcin, Vahide Savci |
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| Přispěvatelé: | Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Bölümü., Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji ve Klinik Farmakoloji Anabilim Dalı., Yalçın, Murat, Cavun, Sinan, Yılmaz, M. Sertaç, Cengiz, Fahrünisa, Savcı, Vahide, AAH-1571-2021, AAG-6956-2021, AAC-9702-2019 |
| Jazyk: | angličtina |
| Rok vydání: | 2005 |
| Předmět: |
Cerebral blood-flow
Vasopressin Physiology Vasopressin secretion Microdialysis Rats Sprague-Dawley Thromboxane A2 chemistry.chemical_compound Chlorpheniramine maleate Medicine Carotid artery flow Adrenalin blood level Rat strain Blood volume Cerebral blood flow Hypothalamus Anesthesia Catecholamine Blood pressure U-46619 Thromboxane synthase inhibitor Hypotension Sympatho-adrenomedullary outflow Thromboxane-A synthase medicine.drug medicine.medical_specialty Epinephrine Vasopressin blood level Vasopressins Intraventricular Sodium chloride Heart rate Activation Hemorrhage Acid cascade Disease models Injections Vasoconstrictor agents Physiology (medical) Internal medicine Pressure Animal model Animal experiment 15 hydroxy 11alpha 9alpha epoxymethanoprosta 5 13 dienoic acid Disease severity Benzofurans Pharmacology Histamine H4 receptors Thromboxane A(2) business.industry Pharmacology & pharmacy Bleeding Body weight Endocrinology chemistry Haemorrhage 15-Hydroxy-11 alpha 9 alpha-(epoxymethano)prosta-5 13-dienoic Acid Prostaglandins Thioperamide Furegrelate Adrenalin business |
| Popis: | Bu çalışma, 8-12 Kasım 2003 tarihleri arasında 33. Nörobilim Cemiyeti Toplantısında bildiri olarak sunulmuştur. 1. In the present study, we aimed to determine the involvement of brain thromboxane A(2) (TXA(2)) in blood pressure decreases evoked by acute and/or graded haemorrhage in rats. 2. Sprague-Dawley rats were used throughout the study. Acute haemorrhage was achieved by withdrawing a total volume of 2.1 and 2.5 mL blood/100 g bodyweight over a period of 10 min. A microdialysis study was performed in a hypothalamic area to measure extracellular TXA(2) levels. Graded haemorrhage was conducted successively by withdrawing carotid arterial blood (0.55 mL/100 g bodyweight) over a 10 s period four times (S1-S4) at 5 min intervals. Furegrelate (125, 250 and 500 mu g), a TXA(2) synthase inhibitor, was injected intracerebroventricularly (i.c.v.) 60 min before acute or graded haemorrhage was initiated. U-46619 (0.5, 1 and 2 mu g, i.c.v.), a synthetic TXA(2) analogue, was administered 5 min before acute haemorrhage (2.1 mL/100 g bodyweight). 3. Acute haemorrhage produced a severe and long-lasting decrease in blood pressure and had a tendency to increase heart rate. Both haemorrhage protocols (2.1 or 2.5 mL/100 g) generated similar approximate twofold increases in extracellular hypothalamic TXA(2) levels. Intracerebroventricular furegrelate (250 mu g) pretreatment completely blocked the TXA(2) increases induced by acute haemorrhage. Furegrelate administration (100, 250 and 500 mu g, i.c.v.) attenuated the fall in arterial pressure evoked by acute haemorrhage and caused significant increases in heart rate at all doses injected. 4. Graded haemorrhage progressively lowered arterial pressure and increased plasma vasopressin and adrenaline levels in the last period. Furegrelate-injected rats were greatly resistant to the hypotensive effect of haemorrhage for all degrees of blood removed. Plasma adrenaline and vasopressin levels were significantly elevated in furegrelate-pretreated rats compared with the saline-treated group during S2-S3 and S4, respectively. U-46619 administration caused small but statistically significant decreases in arterial pressure induced by haemorrhage. 4. The results show that acute hypotensive haemorrhage increases extracellular hypothalamic TXA(2) levels. The increase in brain endogenous TXA(2) levels involves a decrease in blood pressure evoked by haemorrhage because the blockade of TXA(2) synthesis by furegrelate pretreatment attenuated the haemorrhagic hypotension. Increases in plasma adrenaline and vasopressin levels may mediate this effect. |
| Databáze: | OpenAIRE |
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