Reduction of the infarct size by simultaneous administration of L-histidine and diphenhydramine in ischaemic rat brains
| Autor: | Keyue Liu, Eiko Matsuoka, Naoto Adachi, Yumi Irisawa, Masahiro Nishibori, Atsuko Motoki, Kanji Ninomiya |
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| Rok vydání: | 2010 |
| Předmět: |
Brain Infarction
Male medicine.drug_class Brain damage Emergency Nursing Pharmacology Brain Ischemia chemistry.chemical_compound medicine Animals Histidine Rats Wistar Stroke business.industry Diphenhydramine Receptor antagonist medicine.disease Rats medicine.anatomical_structure Cerebral blood flow chemistry Cerebral cortex Anesthesia Emergency Medicine Histamine H1 Antagonists Drug Therapy Combination medicine.symptom Cardiology and Cardiovascular Medicine business Reperfusion injury Histamine medicine.drug |
| Zdroj: | Resuscitation. 82(2) |
| ISSN: | 1873-1570 |
| Popis: | Aims While diphenhydramine is a histamine H 1 receptor antagonist, the agent has been shown to inhibit histamine- N -methyltransferase, a histamine inactivating enzyme in the brain. Since an increase in the brain concentration of histamine ameliorates reperfusion injury after cerebral ischaemia, effects of postischaemic administration of diphenhydramine were evaluated in rats treated with l-histidine, a precursor of histamine. Methods The right middle cerebral artery was occluded for 2h, and the infarct size was determined 24h after reperfusion of cerebral blood flow. Brain oedema was evaluated by comparing the area of the right hemisphere to that of the left hemisphere. Results Focal cerebral ischaemia provoked marked damage in saline-treated control rats, and infarct volumes in the striatum and cerebral cortex were 56 (49–63) mm 3 and 110 (72–148) mm 3 , respectively (means and 95% confidence intervals, n =6). Administration of l-histidine (1000mg/kg, intraperitoneal) immediately after reperfusion did not affect the infarct size. Simultaneous administration of diphenhydramine (20mg/kg, intraperitoneal) with l-histidine reduced the infarct size to 25% and 21% of that in the control group, respectively. The combination therapy completely reduced ischaemia-induced brain oedema. Conclusion Because histamine H 1 action does not influence ischaemic brain damage, elevation of the central histamine concentration by blockade of histamine- N -methyltransferase may be a likely mechanism responsible for the alleviation. |
| Databáze: | OpenAIRE |
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