Role of ischemic modified albumin in the early diagnosis of increased intracranial pressure and brain death.

AIM: Increased intracranial pressure following trauma and subsequent possible development of brain death are important factors for morbidity and mortality due to ischemic changes. We aimed to establish the role of ischemic modified albumin (IMA) in the early diagnosis of the process, starting with increased intracranial pressure and ending with brain death. MATERIALS AND METHODS: Eighteen Wistar-Albino rats were divided into three groups; control (CG, n = 6), increased intracranial pressure (ICPG, n = 6), and brain death (BDG, n = 6). Intracranial pressure elevation and brain death were constituted with the inflation of a balloon of a Fogarty catheter in the epidural space. In all three groups, blood samples were drawn before the procedure, and at minutes 150 and 240 for IMA and malondialdehyde (MDA) analysis. RESULTS: Serum IMA levels at 150 and 240 minutes were higher in ICPG than in CG (p < 0.05). IMA levels were similar in ICPG and BDG. Serum MDA levels at 150 and 240 minutes increased in ICPG and BDG groups compared to CG (p < 0.05). MDA levels were similar in ICP and BD groups. CONCLUSION: IMA should be considered as a biochemical parameter in the process starting from increased intracranial pressure elevation and ending at brain death (Tab. 3, Fig. 5, Ref. 31).

Role of nicotinic acetylcholine receptor subtypes on nicotine's enhancing effect on electrical field stimulation elicited contractile responses in rabbit urine bladder.

OBJECTIVE: This study aims to investigate the contribution of presynaptic nicotinic acetylcholine receptors (nAChRs) sub-types to nicotine-induced enhancement in electrical field stimulation (EFS) EFS-mediated contractile responses in rabbit urine bladder smooth muscle preparations. MATERIALS AND METHODS: Rabbit urine bladder smooth muscle strips were placed in organ baths containing 20 ml of an aerated Krebs-Henseleit solution, and contractions were recorded using isometric force displacement transducers. Following the acquisition of control EFS (60 V, 8 Hz, 1 ms) responses, nicotine was added to the bath at a 3×10-5 M concentration, and EFS responses were obtained. The effect of nAChR antagonists on nicotine-induced augmentation in EFS-mediated responses was investigated in the presence of hexamethonium, dihydro-ß-erythroidine, mecamylamine, and α-bungarotoxin. RESULTS: Tetrodotoxin (TTX; 10-6 M) completely blocked EFS-induced contractile responses in smooth muscle strips. Similarly, Atropine (10-6 M), when administered with α,ß-methylene adenosine triphosphate (α,ß-methylene-ATP) (10-5 M), completely blocked EFS responses. Nicotine significantly enhanced EFS-mediated contractile responses (23.67% ± 1.75). Nicotine-induced increases in EFS responses were largely inhibited by hexamethonium, mecamylamine, and dihydro-ß-erythroidine, whereas α-bungarotoxin only partly inhibited these enhancements. CONCLUSIONS: These findings demonstrate that EFS-induced neurogenic contractions in rabbit urine bladder smooth muscle strips are mediated by purinergic and cholinergic transmissions, and the α4ß2, α3ß4, and α7 sub-types of nAChRs contribute to the enhancement effect of nicotine on EFS-induced contractile responses.