RESUMO
BACKGROUND: Intra-arterial injection of medications may cause acute and severe ischemia and result in morbidity and mortality. There is no information in the literature evaluating the arterial endothelial effects of sugammadex and dexmedetomidine. The hypothesis of our study is that sugammadex and dexmedetomidine will cause histological changes in arterial endothelial structure when administered intra-arterially. METHODS: Rabbits were randomly divided into 4 groups. Group Control (n=7); no intervention performed. Group Catheter (n=7); a cannula inserted in the central artery of the ear, no medication was administered. Group Sugammadex (n=7); rabbits were given 4mg/kg sugammadex into the central artery of the ear, and Group Dexmedetomidine (n=7); rabbits were given 1µg/kg dexmedetomidine into the central artery of the ear. After 72h, the ears were amputated and histologically investigated. RESULTS: There was no significant difference found between the control and catheter groups in histological scores. The endothelial damage, elastic membrane and elastic fiber damage, smooth muscle hypertrophy and connective tissue increase scores in the dexmedetomidine and sugammadex groups were significantly higher than both the control and the catheter groups (p<0.05). There was no significant difference found between the dexmedetomidine and sugammadex groups in histological scores. CONCLUSION: Administration of sugammadex and dexmedetomidine to rabbits by intra-arterial routes caused histological arterial damage. To understand the histological changes caused by sugammadex and dexmedetomidine more clearly, more experimental research is needed.
Assuntos
Dexmedetomidina/farmacologia , Endotélio Vascular/efeitos dos fármacos , Hipnóticos e Sedativos/farmacologia , gama-Ciclodextrinas/farmacologia , Animais , Artérias/anatomia & histologia , Artérias/efeitos dos fármacos , Dexmedetomidina/administração & dosagem , Orelha Externa/irrigação sanguínea , Endotélio Vascular/anatomia & histologia , Hipnóticos e Sedativos/administração & dosagem , Injeções Intra-Arteriais , Masculino , Músculo Liso Vascular/anatomia & histologia , Músculo Liso Vascular/efeitos dos fármacos , Coelhos , Sugammadex , gama-Ciclodextrinas/administração & dosagemRESUMO
BACKGROUND: Intra-arterial injection of medications may cause acute and severe ischemia and result in morbidity and mortality. There is no information in the literature evaluating the arterial endothelial effects of sugammadex and dexmedetomidine. The hypothesis of our study is that sugammadex and dexmedetomidine will cause histological changes in arterial endothelial structure when administered intra-arterially. METHODS: Rabbits were randomly divided into 4 groups. Group Control (n=7); no intervention performed. Group Catheter (n=7); a cannula inserted in the central artery of the ear, no medication was administered. Group Sugammadex (n=7); rabbits were given 4mg/kg sugammadex into the central artery of the ear, and Group Dexmedetomidine (n=7); rabbits were given 1µg/kg dexmedetomidine into the central artery of the ear. After 72h, the ears were amputated and histologically investigated. RESULTS: There was no significant difference found between the control and catheter groups in histological scores. The endothelial damage, elastic membrane and elastic fiber damage, smooth muscle hypertrophy and connective tissue increase scores in the dexmedetomidine and sugammadex groups were significantly higher than both the control and the catheter groups (p<0.05). There was no significant difference found between the dexmedetomidine and sugammadex groups in histological scores. CONCLUSION: Administration of sugammadex and dexmedetomidine to rabbits by intra-arterial routes caused histological arterial damage. To understand the histological changes caused by sugammadex and dexmedetomidine more clearly, more experimental research is needed.
RESUMO
BACKGROUND AND OBJECTIVES: The aim of this study was to evaluate the effects of remote ischemic preconditioning by brief ischemia of unilateral hind limb when combined with dexmedetomidine on renal ischemia-reperfusion injury by histopathology and active caspase-3 immunoreactivity in rats. METHODS: 28 Wistar albino male rats were divided into 4 groups. Group I (Sham, n=7): Laparotomy and renal pedicle dissection were performed at 65th minute of anesthesia and the rats were observed under anesthesia for 130min. Group II (ischemia-reperfusion, n=7): At 65th minute of anesthesia bilateral renal pedicles were clamped. After 60min ischemia 24h of reperfusion was performed. Group III (ischemia-reperfusion+dexmedetomidine, n=7): At the fifth minute of reperfusion (100µg/kg intra-peritoneal) dexmedetomidine was administered with ischemia-reperfusion group. Reperfusion lasted 24h. Group IV (ischemia-reperfusion+remote ischemic preconditioning+dexmedetomidine, n=7): After laparotomy, three cycles of ischemic preconditioning (10min ischemia and 10min reperfusion) were applied to the left hind limb and after 5min with group III. RESULTS: Histopathological injury scores and active caspase-3 immunoreactivity were significantly lower in the Sham group compared to the other groups. Histopathological injury scores in groups III and IV were significantly lower than group II (p=0.03 and p=0.05). Active caspase-3 immunoreactivity was significantly lower in the group IV than group II (p=0.01) and there was no significant difference between group II and group III (p=0.06). CONCLUSIONS: Pharmacologic conditioning with dexmedetomidine and remote ischemic preconditioning when combined with dexmedetomidine significantly decreases renal ischemia-reperfusion injury histomorphologically. Combined use of two methods prevents apoptosis via active caspase-3.
RESUMO
Background and objectives: The aim of this study was to evaluate the effects of remote ischemic preconditioning by brief ischemia of unilateral hind limb when combined with dexmedetomidine on renal ischemia-reperfusion injury by histopathology and active caspase-3 immunoreactivity in rats. Methods: 28 Wistar albino male rats were divided into 4 groups. Group I (Sham, n = 7): Laparotomy and renal pedicle dissection were performed at 65th minute of anesthesia and the rats were observed under anesthesia for 130min. Group II (ischemia-reperfusion, n = 7): At 65th minute of anesthesia bilateral renal pedicles were clamped. After 60 min ischemia 24 h of reperfusion was performed. Group III (ischemia-reperfusion + dexmedetomidine, n = 7): At the fifth minute of reperfusion (100 μg/kg intra-peritoneal) dexmedetomidine was administered with ischemia-reperfusion group. Reperfusion lasted 24 h. Group IV (ischemia-reperfusion + remote ischemic preconditioning + dexmedetomidine, n = 7): After laparotomy, three cycles of ischemic preconditioning (10 min ischemia and 10 min reperfusion) were applied to the left hind limb and after 5 min with group III. Results: Histopathological injury scores and active caspase-3 immunoreactivity were significantly lower in the Sham group compared to the other groups. Histopathological injury scores in groups III and IV were significantly lower than group II (p = 0.03 and p = 0.05). Active caspase-3 immunoreactivity was significantly lower in the group IV than group II (p = 0.01) and there was no significant difference between group II and group III (p = 0.06). Conclusions: Pharmacologic conditioning with dexmedetomidine and remote ischemic preconditioning when combined with dexmedetomidine significantly decreases renal ischemia- reperfusion injury histomorphologically. Combined use of two methods prevents apoptosis via active caspase-3. .
Justificativa e objetivos: Avaliar os efeitos do pré-condicionamento isquêmico remoto, mediante breve isquemia de membro posterior unilateral, em combinação com dexmedetomidina em lesão de isquemia-reperfusão renal por meio de histopatologia e imunorreatividade da caspase-3 ativa em ratos. Métodos: Foram divididos em quatro grupos 28 ratos machos albinos Wistar. Grupo I (Sham cirurgia controle], n = 7): laparotomia e dissecção do pedículo renal foram feitas em 65 minutos de anestesia e os ratos foram observados sob anestesia por 130 minutos. Grupo II (isquemia-reperfusão, n = 7): no 65° minuto de anestesia, os pedículos renais bilaterais foram pinçados; após 60 minutos de isquemia, foi feita reperfusão de 24 horas. Grupo III (isquemia-reperfusão + dexmedetomidina, n = 7): no quinto minuto de reperfusão, dexmedetomidina (100 mg/kg intraperitoneal) foi administrada ao grupo com isquemia-reperfusão. A reperfusão durou 24 horas. Grupo IV (isquemia-reperfusão + pré-condicionamento isquêmico remoto + dexmedetomidina, n = 7): após a laparotomia, três ciclos de pré-condicionamento isquêmico (10minutos de isquemia e 10minutos de reperfusão) foram aplicados no membro posterior esquerdo e depois de cincominutos ao grupo III. Resultados: Os escores de lesão histopatológica e imunorreatividade da caspase-3 ativa foram significativamente menores no grupo Sham em comparação com os outros. Os escores de lesão histopatológica dos grupos III e IV foram significativamente menores do que os do II (p = 0,03 e p = 0,05). A imunorreatividade da caspase-3 foi significativamente menor no grupo IV do que no II (p = 0,01) e não houve diferença significante entre os grupos II e III (p = 0,06). Conclusões: O condicionamento farmacológico com dexmedetomidina e o pré...
Introducción y objetivos: El objetivo de este estudio fue evaluar los efectos del precondicionamiento isquémico remoto mediante breve isquemia del miembro posterior unilateral en combinación con la dexmedetomidina en la lesión de isquemia-reperfusión renal por medio de histopatología e inmunoreactividad de la caspasa-3 activa en ratones. Métodos: 28 ratones machos albinos Wistar fueron divididos en 4 grupos. Grupo I (Sham cirugía control], n =7): se realizó laparotomia y disección del pediculo renal en 65 min de anestesia y los ratones fueron observados bajo anestesia durante 130min. Grupo II (isquemia-reperfusión, n = 7): en el sexagésimo quinto minuto de anestesia, los pídiculos renales bilaterales fueron pinzados; después de 60min de isquemia, se realizaron 24h de reperfusión. Grupo III (isquemia-reperfusión + dexmedetomidina, n = 7): al quinto minuto de reperfusión, la dexmedetomidina (100 μg/kg intraperitoneal) fue administrada en el grupo con isquemia-reperfusión; la reperfusión duró 24 h. Grupo IV (isquemia-reperfusión + precondicionamiento isquémico remoto + dexmedetomidina, n=7): después de la laparotomía, se aplicaron 3 ciclos de precondicionamiento isquémico (10 min de isquemia y 10 min de reperfusión) en el miembro posterior izquierdo y después de 5 min en el grupo in. Resultados: Las puntuaciones de lesión histopatológica e inmunoreactividad de la caspasa-3 activa fueron significativamente menores en el grupo Sham en comparación con los otros grupos. Las puntuaciones de lesión histopatológica de los grupos III y IV fueron significativamente menores que las del grupo II (p = 0,03 y p = 0,05). La inmunorreactividad de la caspasa-3 fue significativamente menor en el grupo IV que en el grupo II (p = 0,01) y no hubo diferencia significativa entre los grupos II ...