ABSTRACT
The pathophysiology underlying the high incidence of post-stroke infectious complications has not been fully understood. We measured the respiratory burst of neutrophils as an index of their bactericidal function in patients with haemorrhagic stroke, and we also measured the plasma concentrations of noradrenalin, cortisol and neutrophil function-related amino acids. Blood samples were obtained from patients who underwent emergency craniotomies for haemorrhagic stroke (n=11) or CT-guided stereotaxic aspiration of intracerebral haematomas (n=6). Neutrophils were isolated, and their chemiluminescence response to N-formyl-methionyl-leucyl-phenylalanine was measured. Healthy volunteers served as controls (n=15). In patients with stroke, the chemiluminescence response of the isolated neutrophils was significantly lower than in the controls, and it was significantly inversely correlated with the plasma noradrenalin concentration. By Day 30, this value approached control levels. Other parameters measured were not significantly correlated with the chemiluminescence response. Stroke-induced suppression of the neutrophil respiratory burst may be responsible for frequent post-stroke infectious complications.
Subject(s)
Cerebral Hemorrhage/physiopathology , Immunity, Innate/physiology , Neutrophils/physiology , Respiratory Burst/physiology , Stroke/physiopathology , Subarachnoid Hemorrhage/physiopathology , Adult , Aged , Amino Acids/analysis , Amino Acids/blood , Bacterial Infections/immunology , Bacterial Infections/metabolism , Bacterial Infections/physiopathology , Biomarkers/analysis , Biomarkers/blood , Cerebral Hemorrhage/immunology , Cerebral Hemorrhage/metabolism , Female , Humans , Hydrocortisone/analysis , Hydrocortisone/blood , Immune Tolerance/immunology , Immunocompromised Host/immunology , Luminescence , Male , Middle Aged , Norepinephrine/analysis , Norepinephrine/blood , Oxidative Stress/physiology , Phagocytes/immunology , Phagocytes/metabolism , Reactive Oxygen Species/metabolism , Stroke/immunology , Stroke/metabolism , Subarachnoid Hemorrhage/immunology , Subarachnoid Hemorrhage/metabolismABSTRACT
BACKGROUND: Venous hypertension is regarded as an important factor in the pathogenesis of dural arteriovenous fistula (DAVF). We investigate histologic reaction of dural sinus under the condition of venous hypertension using a rat venous hypertension model to present hemodynamic and immunohistochemical effect in the development of DAVF. METHODS: Twenty-four Sprague-Dawley male rats were divided into venous hypertension and control groups. Venous hypertension was induced with a left common carotid artery-external jugular vein anastomosis and an occlusion of a right posterior facial vein. Measurements of systemic mean arterial pressure, draining vein pressure (DVP), and cerebral perfusion pressure (CPP) were conducted on the next day, at 7 days, and at 28 days after surgery, and the rats were killed for histologic examinations. RESULTS: Postoperative DVP increased significantly in venous hypertension group compared to control group (35 +/- 5 vs 13 +/- 2 mm Hg, P < .05). Increased DVP remained above 30 mm Hg throughout the observation period. Postoperative CPP decreased significantly in venous hypertension group compared to control group (49 +/- 8 vs 86 +/- 9 mm Hg, P < .05). In venous hypertension group, there was a significant difference between days 1 and 28 (49 +/- 8 vs 64 +/- 8 mm Hg, P < .05). Histologic examination revealed thickening of connective tissues, proliferation of fibroblasts, and strong expression of vascular endothelial growth factor (VEGF) in endothelium under venous hypertension condition. Immunostained VEGF cells decreased significantly from day 7 to day 28 (100 +/- 16 vs 72 +/- 19 cells, P < .05). A positive correlation was observed between DVP and VEGF expression (Pearson correlation coefficient; r = 0.671, P = .0017). There was a negative correlation between CPP and immunostained VEGF cells (r = -0.702, P = .0089). CONCLUSIONS: These results suggest that venous hypertension is associated with increased expression of VEGF, and a decreased CPP may have a potential effect in VEGF expression under venous hypertension condition. These factors are speculated to play an important role in progression of DAVF.
Subject(s)
Central Nervous System Vascular Malformations/etiology , Cranial Sinuses/metabolism , Cranial Sinuses/pathology , Vascular Endothelial Growth Factor A/metabolism , Venous Pressure/physiology , Animals , Cerebrovascular Circulation/physiology , Cranial Sinuses/physiopathology , Disease Models, Animal , Male , Rats , Rats, Sprague-Dawley , Time FactorsABSTRACT
A 33-year-old man presented with consciousness disturbance (Glasgow Coma Scale score 7) and right hemiplegia after suffering headache persisting for 10 days. Head computed tomography revealed an irregular intracerebral hematoma in the left temporoparietal region, associated with a tubular high density area compatible with a thrombosed transcerebral vein in the left temporal lobe. The patient was free of coagulopathy. Craniectomy was performed to remove the intracerebral hematoma and venous thrombosis was confirmed. Postoperative cerebral angiography demonstrated extensive venous malformation in the left parietal and occipital lobes. Multiple transcerebral draining veins converged in the vein of Galen associated with a varix. Segmental narrowing of the straight sinus was suggestive of congestion in the venous anomaly. The patient showed progressive recovery following surgery, and was discharged with moderate aphasia, mild right hemiparesis, and right homonymous hemianopsia 1 month later. Venous malformations are usually silent, but occasionally become symptomatic due to thrombosis of the draining vein. The presence of stenosis in the draining route may lead to venous congestion, thrombus formation, and catastrophic hemorrhagic venous infarct.
