Premedication and anesthesia are common procedures prior to surgery. One of the main tasks of sedation is to reduce the level of stress that inevitably arises before the operation. For sedation is usually used tranquilizers and narcotic analgesics, as well as drugs that stabilize the exchange. Substances used for anesthesia inhibit the activity of the nervous system, interrupt the flow of painful afferentation and make possible the successful course of surgery.
We investigated the effect of premedication and anesthesia on SCP in 20 patients of both sexes (8 people suffering from lumbosacral radiculitis, aged from 44 to 50 years, 12 patients with brain tumors of different localization from 25 to 62 years old). Patients suffering lumbar sacral radiculitis, surgical treatment was performed – decompression of the roots of the spinal cord squeezed by disc hernias. In patients with tumors, surgical removal of the tumor was performed. SCP was recorded 15 minutes before the premedication, 30 minutes after the premedication and 10 minutes after the start of the anesthesia.
Seduxen and promedol were used for premedication, hexenal for anesthesia with transfer of patients to artificial respiration.
Seduxen is a tranquilizer that enhances inhibition in the brain systems, where the mediator is gamma-aminobutyric acid (GABA). Benzodiazepine tranquilizers have been shown to reduce cerebral glucose metabolism by approximately 20% (NL Foster et al., 1987). Promedol has analgesic and hypnotic effects. By chemical structure, it can be considered as an analogue of a part of the morphine molecule. In general, substances used in sedation, reduce the level of preoperative stress by inhibition of the central nervous system. In conditions of preoperative stress, the normalization of EEG parameters and evoked potentials during sedation is shown (LR Zenkov, PV Melnichuk, 1985).
Hexenal is a drug for general anesthesia from the group of barbiturates that have a stimulating effect on the system of the inhibitory mediator GABA. Using PET, barbiturates have been found to reduce cerebral glucose metabolism by about 50% in both the cortex and the subcortex (JB Blacklock; et al., 1987). The effect of barbiturates on energy metabolism due to inhibition of the respiratory chain of mitochondria. Therefore, one could expect a noticeable decrease in SCP in our studies.
Before sedation, patients were in a state of preoperative stress, which was the main reason for the increase in AMR in patients with lumbosacral and radiculitis ( “Preoperative stress”). In tumors, changes in cerebral energy metabolism were of complex origin (see section 7.6 “Cerebral energy metabolism in patients with brain tumors”). When sedation revealed a significant decrease in SCP, reflecting a decrease in energy metabolism. With anesthesia, there was a further reduction in SCP. The differences between the mean AMR after sedation and anesthesia were statistically significant and indicated a more pronounced inhibition of brain energy metabolism under the influence of anesthesia. The reduction in SCP was especially significant in the group of patients with lumbosacralm radiculitis .
According to glucose consumption, energy metabolism decreases under the influence of anesthesia by half, the SCP has dropped, on average, by about the same – from 13.4 mV to 5.0 mV. Thus, two different methods for assessing cerebral energy metabolism (PET and SCP) in case of anesthesia give similar results.
Conclusion
This section discusses cerebral energy metabolism in brain diseases of different etiology, developmental mechanisms and severity. However, in all cases, energy changes play a prominent role in the development of the disease. There are several leading links in the chain of energy disorders that are characteristic of many diseases of the central nervous system:
1. Energetic disorders associated with the primary defect of the mitochondrial respiratory chain enzymes.
Such diseases include parkinsonism, in which a defect of NADH-ubiquinone oxidase, and Alzheimer’s disease, in which cytochrome oxidase is probably affected.
As a result of these defects, the normal transfer of electrons along the respiratory chain of mitochondria is disturbed, and the formation of free radicals of acidic acids, directly damaging neuron structures and triggering apoptosis , is enhanced . Due to disruptions in mitochondria, the relative contribution of aerobic processes to the cell energy balance decreases, and anaerobic oxidation, on the contrary, increases, which is accompanied by lactic acidosis. Glycolysis is less energetically beneficial as compared to aerobic oxidation, therefore the energy deficit increases.
2. Energy disorders caused by insufficiency of cerebral circulation .
Hypoxia, which is a natural consequence of low blood supply, leads to a decrease in the aerobic metabolism of glucose. Anaerobic glucose metabolism increases compensatory, as a result of which lactate accumulates and intrheuronal pH decreases. Acidosis causes secondary disruption of the mitochondrial respiratory chain. In this case, just as with the primary defects of the respiratory chain, oxygen free radicals are formed, oxidative stress increases, damaging nerve and glial cells.
Insufficiency of cerebral circulation occurs not only in vascular pathology, but as an additional pathogenic factor in many other diseases, in particular in Alzheimer’s disease, parkinsonism, cerebral tumors, drug addiction. These disorders are especially characteristic of senile pathology.
3. Energy disorders associated with stress-like metabolic changes .
Stress is included in the pathogenesis of many diseases of the central nervous system, in particular neurosis. With an increase in the level of glucocorticoid stress hormones, the energy processes are rearranged, and ketone bodies and some amino acids are used as the energy substrate in the brain, along with glucose. The catabolism of ketone bodies naturally leads to acidosis.
As follows from these data, in case of insufficiency of cerebral circulation, with primary mitochondrial defects and stress-like changes in energy metabolism, in general, the cerebral pH decreases, therefore, in all these cases, the brain UPA is increased.