Aim. To test in experiment a pathogenetically adequate model of brain death due to increased intracranial pressure with gradual induction, allowing the evaluation of the changes occurring in the organs of a potential donor. Materials and methods. 6–8 months old outbred male rats of the experimental group ( n = 18) and the control group ( n = 8) were anesthetized, the left common carotid artery was catheterized to record systolic, diastolic blood pressure (BP) and heart rate (HR), the mean BP (MBP) was calculated. After transfer to artifi cial ventilation, brain death was simulated in the experimental group using the developed method. Results. All animals in the experimental group suffered brain death 30 minutes from the start of the experiment;10 rats (56%) died within 3 hours due to progression of circulatory failure. Initially, in anesthetized animals, MBP was 101 (90; 105) mm Hg, HR 310 (297; 315) beats/min. After 5 minutes from the start of brain death induction, MBP increased to 147 (140; 150) mm Hg ( p = 0.01), HR to 396 (384; 406) beats/min ( p = 0.03). Further, within 20 minutes there was a decrease in MBP to 94 (90; 100) mm Hg and HR to 290 beats/min. During the observation period from 26 to 90 minutes, there was a stabilization of MBP at the level of 87–92 mm Hg, there was a tendency to bradycardia with HR from 263 to 274 beats/min ( p = 0.01). Then after 120–150 minutes from the beginning of brain death induction, MBP continued to decrease to 75–80 mmHg ( p = 0,03), HR to 256–264 beats/min ( p = 0,01). At the end of the experiment, despite volemic support, MBP decreased to 64 (61; 67) mm Hg ( p = 0.02), bradycardia worsened with HR to 250 (248; 260) beats/min ( p = 0.01), indicating the hemodynamic decompensation. Conclusion. The results of experimental testing of an animal brain death model on outbred rats showed that this model is pathogenetically adequate and useful to assess the condition of potential donor organs within 3 hours after the induction of brain death.
Objective: to experimentally reveal possible systemic hemodynamic changes after maximally allowable liver resection, by determining the time of their formation in the early postoperative period. Materials and methods. The experiments on 22 outbred male albino rats recorded an electrocardiogram, left carotid blood pressure by a direct method, an integral rheogram and its first derivative by the tetrapolar rheographic procedure developed by Sh. I. Ismailov et al. and modified by V. V. Karpitsky et al. 1, 3, 6, and 12 hours and 1, 3, and 7 days after maximally allowable liver resection. Stroke volume, mean blood pressure, cardiac output, and specific peripheral vascular resistance (SPVR) were calculated. Blood loss was estimated by the gravimetric method. The significance of differences was defined by Friedman ANOVA. Results . At postoperative hour 1, the low cardiac output syndrome the basis for which is a considerable reduction in stroke volume developed and persisted during the first 24 hours; an additional contribution was made by moderate bradycardia observed within the first 24 hours. On day 3 postsurgery, the hemodynamic parameters were similar to those at baseline. By 7 day of an observation, cardiac depression changed into moderate myocardial hyperdynamia in the presence of moderate tachycardia and a moderate decrease in SPVR. Conclusion . The critical time found by the authors for the minimum cardiac output was an hour after surgery. The distinctive features of low cardiac output syndrome after maximally allowable liver resection are its reversible pattern and reflectory bradycardia on postoperative day 1. By day 7, cardiac depression changed into moderate myocardial hyperdynamia due to a tendency towards tachycardia.
Aim. Assessment of stomach and duodenal injury early after extended hemihepatectomy. Material and Methods. The experiment was performed on 100 white mongrel male rats. 80 of them underwent advanced hemihepatectomy, 20 animals consisted of control group. After 12 hours, 1, 3 and 7 days after surgery stomach and duodenum were histologically analyzed to detect chemiluminescent homogenates. Results. After 12 hours light sum and “fast” flash in the stomach were increased by 2.5 and 1.5 times, respectively, “slow” flash was decreased by 2 times. Growth of all parameters was observed in duodenum. There were significant decrease of “fast” flash and increase of light sum and “slow” flash in homogenates during 3 postoperative days. By the 7th day light sum was increased in stomach and duodenum, besides the duodenum increased “slow” flash. Structural changes were visualized after 12 hours in the form of erosions and ulcers of the stomach and duodenum. In 7 days reparative changes were predominant. Conclusion. In 12 hours after hemihepatectomy rapid activation of free-radical oxidation was observed in stomach and duodenum. Herewith inhibition of antioxidant enzymes have been already showed in stomach. Structural changes in the stomach (ulcers) have already been irreversible by this time. So, this period is critical for acute stomach and duodenal injury.
