The respiratory effects of Ketamine bronchodilation are noticeable, mainly involving bronchodilation, which is mainly observed in asthmatic patients. Supposedly, Ketamine bronchodilation relaxes the bronchiolar musculature and prevents the bronchoconstriction induced by histamine, which would be an obvious advantage for asthmatic patients.
The bronchodilatory activity is as effective as halothane or enflurane in preventing experimentally-induced Ketamine bronchodilation .
Ketamine has been used in sub anesthetic doses to treat bronchospasm in the operating room and ICU in mechanically ventilated patients. Successful treatment of status asthmaticus with ketamine has been reported. Continuous infusion of ketamine relieved refractory bronchospasm in mechanically ventilated children with improved gas exchange and dynamic compliance of the chest.
In the presence of active bronchospasm, Ketamine bronchodilation may be recommended as the IV induction drug of choice. The mechanism by which ketamine produces airway relaxation is unclear, although several mechanisms have been suggested, including increased circulating catecholamine concentrations, inhibition of catecholamine uptake, antagonizing the effect of histamine, voltage-sensitive calcium channel, and inhibition of postsynaptic nicotinic or muscarinic receptors.
Beta adrenergic blockade with propranolol abolished the protective effect of ketamine so that there was no significant difference in the maximal increase in pulmonary airway resistance in dogs anesthetized with ketamine. However, later Gateau et al demonstrated that propranolol and indomethacin did not inhibit the effect of ketamine, excluding the involvement of beta activation and of prostaglandins.
They found Ketamine bronchodilation caused bronchial relaxation irrespective of the constricting agent, and exerted a partial and non-competitive antagonism to histamine and acetylcholine. Brown and Wagner proved the bronchodilatation property is due to attenuation of the vagal nerve stimulation-induced bronchoconstriction in dose dependent fashion.
Recent studies shows the possible role of NMDA receptor in pedunculopontine tegmental nucleus controlling respiratory rhythm and upper airway muscle tone. Ketamine bronchodilation has been shown to block the effect of glutamate induced respiratory dysrhythmia and genioglossal tonic activity by acting on NMDA receptor in pedunculopontine tegmental nucleus