RESUMEN
BACKGROUND: Remote cerebellar hemorrhage (RCH) is an extremely rare and potentially fatal complication after supratentorial craniotomy. However, the exact pathophysiological mechanism of RCH remains unclear, so clinicians often lack clinical experience in prevention, early diagnosis, and standardized treatment. OBSERVATIONS: The authors retrospectively analyzed data of patients who underwent surgery for supratentorial lesions at their center between 2012 and 2021. They identified 4 patients who developed RCH among 4,075 patients who underwent supratentorial craniotomy. All 4 patients were male, with an average age of 57.5 years. One RCH occurred after tumor resection, and the other 3 occurred after aneurysm clipping. One patient was asymptomatic and received conservative treatment with a favorable outcome. The remaining 3 patients underwent lateral ventricular drainage and/or suboccipital decompression; 2 died, and 1 recovered well. LESSONS: The authors believe that RCH should be considered as a multifactorial cause, and massive cerebrospinal fluid loss plays a key role in the development and progression of RCH. Asymptomatic RCH can be treated conservatively. However, in the case of conscious disturbance, hydrocephalus, and brain stem compression, surgery should be performed immediately. Early detection and individualized treatment would be helpful to avoid potentially fatal outcomes caused by RCH.
RESUMEN
BACKGROUND: Recent evidence has demonstrated that rosiglitazone can attenuate cerebral vasospasm following subarachnoid hemorrhage (SAH). Some studies have shown that rosiglitazone can suppress inflammation and immune responses after SAH. However, the precise molecular mechanisms by which cerebral vasospasm is attenuated is not clear. METHODS: In this study, SAH was created using a "double hemorrhage" injection rat model. Rats were randomly divided into three groups and treated with saline (control group), untreated (SAH group), or treated with rosiglitazone. Using immunocytochemistry, hematoxylin and eosin (HE) staining, and measurement of the basilar artery, we investigated the formation of pathologic changes in the basilar artery, measured the expression of caveolin-1 and proliferating cell nuclear antigen (PCNA), and investigated the role of rosiglitazone in vascular smooth muscle cell (VSMC) proliferation in the basilar artery after SAH. RESULTS: In this study, we observed significant pathologic changes in the basilar artery after experimental SAH. The level of vasospasm gradually increased with time during the 1st week, peaked on day 7, and almost recovered on day 14. After rosiglitazone treatment, the level of vasospasm was significantly attenuated in comparison with the SAH group. Immunocytochemistry staining showed that caveolin-1 expression was significantly increased in the rosiglitazone group, compared with the SAH group. Inversely, the expression of PCNA showed a notable decrease after rosiglitazone treatment. CONCLUSIONS: The results indicate that rosiglitazone can attenuate cerebral vasospasm following SAH. Up-regulation of caveolin-1 by rosiglitazone may be a new molecular mechanism for this response, which is to inhibit proliferation of VSMCs after SAH, and this study may provide a novel insight to prevent delayed cerebral vasospasm (DCVS).
Asunto(s)
Arteria Basilar/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Músculo Liso Vascular/efectos de los fármacos , Miocitos del Músculo Liso/efectos de los fármacos , Hemorragia Subaracnoidea/complicaciones , Tiazolidinedionas/farmacología , Vasoconstricción/efectos de los fármacos , Vasodilatadores/farmacología , Vasoespasmo Intracraneal/etiología , Animales , Arteria Basilar/patología , Caveolina 1/efectos de los fármacos , Caveolina 1/metabolismo , Modelos Animales de Enfermedad , Inmunohistoquímica , Masculino , Músculo Liso Vascular/metabolismo , Músculo Liso Vascular/patología , Miocitos del Músculo Liso/metabolismo , Antígeno Nuclear de Célula en Proliferación/efectos de los fármacos , Antígeno Nuclear de Célula en Proliferación/metabolismo , Ratas , Ratas Sprague-Dawley , Rosiglitazona , Hemorragia Subaracnoidea/patología , Hemorragia Subaracnoidea/fisiopatología , Regulación hacia Arriba , Vasoespasmo Intracraneal/fisiopatología , Vasoespasmo Intracraneal/prevención & controlRESUMEN
The present study sought to understand the mechanisms of attenuation of severe acute pancreatitis (SAP) by resveratrol (RES). SAP was experimentally induced in rats by injection of 4% sodium taurocholate in the retrograde pancreatic duct. Three study groups were evaluated: Group I (sham-operated animals), Group II (SAP animals), and Group III (SAP animals treated with RES at 20 mg/kg/body weight, 5 min after induction of SAP). The study outcomes were histopathologic changes and alterations in biochemical markers: plasma renin activity and levels of angiotensin II, endothelin, and nitric oxide in plasma. Biochemical markers were evaluated at 3, 6, and 12 h after induction of SAP. SAP was associated with significant (p < 0.05) histopathologic changes (saponification spots in the intraperitoneal cavity, severe pancreatic edema, blood congestion, varying degrees of necrosis, etc.), as well as with elevation of biochemical markers in blood plasma. RES treatment significantly (p < 0.05) attenuated changes of both histopathologic and biochemical markers induced by SAP. In conclusion, this study provides evidence that RES treatment is a promising therapeutic approach to suppress microcirculatory disturbance in SAP.