Heart Arrest
Conditions
Keywords
desflurane, preconditioning
Brief summary
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 С Inhibition of the pores opening protects ischemic damage of the cells. The key enzyme regulating the mitochondrial permeability transition pore is GSK-3b: the phosphorylation of the enzyme inactivates the enzyme and prevents pore opening. Aim of studi is to determine content of the phosphorylatcd GS K-3b in neurons of rat brain in the model of total tschemia/reperfusion.
Detailed 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 С 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.
Interventions
DRUGDesflurane
Desflurane anesthesia is introduced. This provides complete suppression of animal responses to pain, fixation, tracheal intubation and cardiac arrest.
DRUGSevoflurane
Desflurane anesthesia is introduced. This provides complete suppression of animal responses to pain, fixation, tracheal intubation and cardiac arrest. After fixation of the animal in the supine position trachea is intubated and mechanic ventlation with air using an animal respirator is performed. Cardiac arrest is induced by intrathoracic clamping of the supracardiac bundle of vessels by means of a special hook. Period of cardiac arrest and absence of ventilation lasts 10 min. The animal is then resuscitated by means of chest compressions and mechanichal ventilation with air. Cardiac activity and systemic blood circulation recovers within 1 min; spontaneous respiration will be resumed after a period of 4-6 min.
PROCEDURECardiac arrest
Cardiac arrest is induced by intrathoracic clamping of the supracardiac bundle of vessels by means of a special hook. Period of cardiac arrest and absence of ventilation lasts 10 min. The animal is then resuscitated by means of chest compressions and mechanichal ventilation with air. Cardiac activity and systemic blood circulation recovers within 1 min; spontaneous respiration will be resumed after a period of 4-6 min.
Sponsors
Negovsky Reanimatology Research Institute
Study design
Allocation
NON_RANDOMIZED
Intervention model
PARALLEL
Primary purpose
BASIC_SCIENCE
Masking
NONE
Eligibility
Sex/Gender
MALE
Healthy volunteers
No
Inclusion criteria
* breeding albino male rats weigh from 180 to 240 g
Exclusion criteria
* N/A
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| total GSK-3b and phosphorilated (pGSK-3b) | after 15 minutes of exposition |
Outcome results
None listed