دانلود رایگان مقاله تفاوت بیهوشی در احیا قلبی ریوی مدل موش

Abstract

Objective: Our asphyxia cardiac arrest (ACA) rat model is well established. The original model was designed in the 1990th using halothane and nitrous oxide for pre-insult anesthesia. Because of its hepato-toxicity and its potential to induce severe liver failures, halothane is no longer used in clinical anesthesia for several years. In order to minimize the health risk for our laboratory staff as well as to keep the experimental settings of our model on a clinically oriented basis we decided to replace halothane by sevoflurane. In this study we intended to determine if the change of the narcotic gas regiment causes changes in the neurological damage and how far our model had to be adjusted. Methods: Adult rats were subjected to 5 min of ACA followed by resuscitation. There were four treatment groups: ACA - halothane, ACA - sevoflurane and with halothane or sevoflurane sham operated animals. Vital and blood parameters were monitored during the 45 min post-resuscitation intensive care phase. After a survival time of 7 days histological evaluation of the hippocampus was performed. Results: We observed that resuscitated rats anesthetized prior by sevoflurane (i) have had a lower heart rate and a higher MAP compared to halothane anesthetized animals; (ii) The neurological damaged were significantly reduced in the hippocampal CA1 region in sevoflurane treated rats. Conclusion: Using sevoflurane instead of halothane for anesthesia requires some physiological and experimental changes. However the model keeps its validity. Sevoflurane caused less pronounced neurodegeneration in the CA1 region of the hippocampus. This had to be considered in further resuscitation-studies containing sevoflurane as anesthetic.

5.3. Statistical analysis

All vital parameters are presented as the mean ± SD. After verifying that the results were normally distributed using a Smirnov test, a student t-test was performed to compare group effects. A p value≤0.05 was considered statistically significant. The stainings were computer-assisted semi-quantitative analyzed using ImageJ software (http:/rsbweb.nih.gov/ij/). Therefore, 3 alternating slices per animal and staining (MAP2, GFAP, IBA1) were scanned in with a Plan-Neofluar objective (×5.0/0.16) getting an image (1388×1040 pixels) representing the complete hippocampal CA1 region, being the most sensitive to/damaged by ischemia brain area, with its adjacent parts. The microscopic settings and the exposure time of the fluorescence channels were set on the basis of control slices and kept equal for the corresponding preparation. The immunostaining intensities were measured in a standard evaluation window (1380×540 pixels) which was placed manually and included the complete CA1 region with all strata. Data are given as mean ± SD. The 3 slices per animal were analyzed individually. The mean was calculated and used as one value for the statistical analyses. Per staining, corresponding sham and ACA animals were compared directly using a paired T. Esser et al. Brain Research 1652 (2016) 144–150 149 Student's t-test (GraphPad Software, La Jolla, USA). A p value ≤0.05 was considered statistically significant.