Impact if Desflurane Preconditioning on the Content of the Phospho-GSK-3b in the Rat's Neurons in the Model of I/R
Last updated on July 2021Recruitment
- Recruitment Status
- Withdrawn
Summary
- Conditions
- Heart Arrest
- Type
- Interventional
- Phase
- Phase 4
- Design
- Allocation: Non-RandomizedIntervention Model: Parallel AssignmentMasking: None (Open Label)Primary Purpose: Basic Science
Participation Requirements
- Age
- Younger than 125 years
- Gender
- Only males
Description
Endpoint implementation of reactions initiated by ischemia is the mitochondrial transition pore permeability. Mitochondria pores opening results in a release of factors triggering apoptosis. primarily the cytochrome ? Inhibition of the pores opening protects ischemic damage of the cells. The key enz...
Endpoint implementation of reactions initiated by ischemia is the mitochondrial transition pore permeability. Mitochondria pores opening results in a release of factors triggering apoptosis. primarily the cytochrome ? Inhibition of the pores opening protects ischemic damage of the cells. The key enzyme regulating the mitochondrial permeability transition pore is glycogen synthase-kinase 3b (GSK-3b): the phosphorylation of the enzyme inactivates the enzyme and prevents pore opening. We have shown in previous study that preconditioning with sevoflurane increases the content of the phosphorylated form of 6SK-3b and protects the mitochondria of neurons in rats brain during ischemia/reperfusion. Aim of studi is to determine content of the phosphorylated GS K-3b in neurons of rat brain in the model of total ischemia/reperfusion influenced by: 1 MAC desflurane vs control group; 1 MAC desflurane vs 1 MAC sevoflurane and 1 MAC desflurane vs training ischemia.
Tracking Information
- NCT #
- NCT04287842
- Collaborators
- Not Provided
- Investigators
- Principal Investigator: Valery Likhvantsev, MD,PhD V. Negovskij Reanimatology Research Institute RAMS
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