Small Dose Naloxone Effects on Respiratory Frequency and Blood Pressure with Ketamine in Rats
Intravenous injection of 8 mg/kg ketamine was given to two groups of rats, and the respiratory and blood pressure curves were recorded before and after. After intravenous ketamine administration, 0.01 g/kg naloxone or saline was immediately injected intravenously into each group, with a volume of 1 ml/kg. The changes in respiratory rate and blood pressure in the two groups were compared.
1.4 Statistical Processing
All data are expressed as mean ± s, analyzed using SPSS11.5 statistical software for statistical processing. Paired t-tests were used for within-group comparisons, and analysis of variance (ANOVA) was used for between-group comparisons. Inspection standard: α = 0.05.
2 Results
Naloxone had no significant effect on blood pressure induced by ketamine in rabbits (P > 0.05), but it could antagonize the slowing of respiratory frequency induced by ketamine (P < 0.01). See Table 1.
Table 1 Small Dose Naloxone Effects on Respiratory Frequency and Blood Pressure with Ketamine (x-s, n=6)
Before and after treatment: P<0.01; Compared with physiological saline group: P<0.01.
3 Discussion
The experimental results show that small doses of naloxone (0.01 g/kg) can antagonize the inhibitory effect of ketamine on respiration in rabbits without obvious effects on blood pressure. Ketamine anesthesia increases lung compliance, reduces airway resistance, relieves bronchial spasm, and slows down the respiratory rate. Injection at too fast a speed, excessive dosage, or overdose of narcotic analgesics as an auxiliary may cause respiratory inhibition. Opioid receptor agonists act through binding to opioid receptors in different parts of the body, simulating the role of endogenous opioid peptides. In the central and peripheral nervous systems, endogenous opioid peptides coexist with other neuropeptides or neurotransmitters and may act as neurotransmitters, neurohormones, or neuromodulators. Together with opioid receptors, they constitute a powerful endogenous pain modulation system and play important roles in regulating cardiovascular activity, gastrointestinal function, immune responses, and endocrine function.
The mechanism of small-dose naloxone's antagonism to ketamine-induced respiratory slowing may be as follows: small doses of naloxone bind to opioid receptors distributed in the brain and other parts, effectively blocking various effects mediated by endorphins and having antagonistic effects on each type of opioid receptor. Studies have shown that naloxone can antagonize the effects of endorphins, reconstruct the circulating mechanisms of prostaglandins and catecholamines, reverse neurological dysfunction induced by cerebral ischemia, increase blood flow in the ischemic region, expand the area of cerebral perfusion, redistribute anoxic cerebral blood flow, ensure the blood supply to the brainstem and other important parts, reduce brain edema, and alleviate symptoms such as coma and paralysis. Additionally, small doses of naloxone can excite the central nervous system, dilate bronchial vessels, increase pulmonary ventilation, improve pulmonary microcirculation, increase breathing frequency, improve ventilation, reduce carbon dioxide pressure, and alleviate hypoxemic respiratory failure.
The experimental results indicate that small doses of naloxone may be used as an antagonist when ketamine induces respiratory depression. However, due to species differences, animal experimental results do not necessarily apply to humans and serve only as a reference value.