Analysis of biochemical laboratory values to determine etiology and prognosis in patients with subarachnoid hemorrhage: a clinical study.

OBJECTIVES: The aim of this study was to establish prognostic and predictive markers in patients with subarachnoid hemorrhage (SAH) using simple laboratory methods. METHODS: A retrospective examination was made of patients with SAH diagnosed secondary to isolated head trauma, isolated anterior communicating artery aneurysm rupture, and angiography-negative SAH. Age, gender, Glasgow Coma Scale (GCS) scores, and Fisher's grade scores, Glasgow Outcome Scale (GOS) scores, leukocyte count, neutrophil count, lymphocyte count, platelet count, neutrophil-lymphocyte ratio (NLR) and platelet-lymphocyte ratio results (PLR) were evaluated. RESULTS: NLR and PLR values, which were similar in patients with spontaneous SAH, were significantly high in patients with traumatic SAH. NLR and PLR values could be 80% sensitive and 75% specific for distinguishing traumatic SAH from spontaneous SAH. Eosinophil count was lower in patients with angiography-negative SAH and patients with aneurysmal SAH than in patients with traumatic SAH. Initially measured GCS score, Fisher's grade score, eosinophil, neutrophil and lymphocyte counts could be prognostic in all patients with SAH. Moreover, it was concluded that the initially measured number of eosinophils might be directly related to patient prognosis. The eosinophil count was generally found to be high in traumatic SAH patients and it was observed that this parameter could be predictive for these patients. Lymphocyte count and NLR values could be prognostic markers in patients with angiography-negative SAH. CONCLUSION: NLR, PLR and eosinophil count values could be predictive for etiological factors (traumatic SAH or spontaneous SAH) of patients who were admitted unconscious to the emergency room with SAH detected on radiological imaging.

Cerebral ischaemia/reperfusion injury could be managed by using tramadol.

OBJECTIVES: No valid treatment modality that will repair stroke damage and provide neurological recovery has yet been identified in literature. Studies demonstrated that adequate quality of life could be provided if post-stroke pain could be treated sufficiently and timely. Besides its pain relief effects, tramadol has oedema-reducing and anti-inflammatory properties. With these in mind, this study investigated the influence of tramadol in acute and/or chronic ischaemia/reperfusion (I/R) injury. METHODS: Putting aside the Control group, 23 Wistar albino rats were distributed to four groups to investigate the acute (Sham-A, TR-A) and chronic (Sham-C, TR-C) periods of I/R injury, and temporary aneurysm clips were applied to their internal carotid arteries for 30 min. Four hours after clippage, tramadol was administered to animals of TR-A and TR-C groups intraperitoneally. After sacrificing all animals, pyknotic and necrotic neuronal cells in hippocampal cornu ammonis (CA)1, CA2, CA3 and parietal cortical regions were counted, and perivascular oedema, intercellular organization disorder (IOD) and inflammatory cell infiltration were scaled histopathologically. Additionally, tissue interleukin (IL)-1ß, IL-10, malondialdehyde, nitric oxide, tumour necrosis factor-α, caspase-3, beclin-1, Atg12, LC3II/LC3I levels were measured biochemically. RESULTS: Tramadol could minimize perivascular oedema, IOD, parietal and hippocampal neuronal necrosis, inflammatory cell infiltration in both periods of I/R injury histopathologically. Apart from inhibiting apoptosis and enhancing autophagy, tramadol had no influence on any other biochemical result. DISCUSSION: Tramadol can ameliorate the histopathological structure of ischaemic tissue in both periods of I/R injury in rat. We suggest further research investigating various dosages with different administration methods of tramadol in stroke should be conducted by adopting different explorative techniques.

Effects of Sulphasalazine in Cerebral Ischemia Reperfusion Injury in Rat.

BACKGROUND: Management of cerebral ischemia/reperfusion (I/R) injury is still difficult process today. AIMS OF THE STUDY: Aim of present study was to investigate therapeutic properties of sulfasalazine in cerebral transient I/R injury in rat. METHODS: Except Control group (n = 5), 20 Wistar albino rats were allocated for acute and chronic stage investigation of I/R injury, and temporary aneurysm clips were attempted to both internal carotid arteries for thirty min. Four hours later, 40 mg/kg once a day sulfasalazine was administered to animals of SL-A and SL-C groups, orally. Animals were decapitated, following which pyknotic and necrotic neuronal cells, perivascular edema, irregularities of intercellular organization (IIO) of hippocampal regions, and cortical necrotic neurons of parietal lobe were counted or scaled histopathologically. Tissue malonyldialdehyde (MDA), myeloperoxidation (MPO), total nitrite/nitrate (NO), interleukin 1-beta (IL-1ß), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) level values were evaluated biochemically. RESULTS: Sulfasalazine could reduce perivascular edema, IIO, cortical and hippocampal neuronal cell death in both stages. It could decrease MDA in acute stage, but not reduce IL-1ß, IL-6, MPO, NO, and TNFα levels. It could increase IL-1ß levels in chronic stage but not affect to IL-6, MPO, MDA, NO, TNF-α levels. CONCLUSION: Sulfasalazine could improve histopathological architecture of hypoxic tissue in both stages of I/R injury in rat. It could inhibit lipid peroxidation cascades just in acute stage. These results suggested that therapeutic mechanisms of sulfasalazine in cerebral I/R injury should be investigated by using more specific laboratory methods in future studies.