PURPOSE: The balance between the sympathetic and parasympathetic nervous systems alters heart rate variability (HRV). A decrease in HRV is associated with myocardial infarction (MI) and congestive heart failure (CHF), which are both co-morbidities that accompany lung disease. Since the role of suppression of vagal control on HR variation remains controversial, we used the M2-/- muscarinic receptor mutant mouse as a surrogate for vagal deficit and examined the effect on circadian variation and HRV.
METHODS: Telemetered (DSI International) signals for heart rate (HR), body temperature (Tb), and activity (ACT) were measured in control wild type (WT) and M2-/- mutant mice (KO). Mice were housed at 22ºC in a 12:12 light dark cycle and data were collected and analyzed for 13 days.
RESULTS: The average (582 + 4) and bottom 10th centile (462for HR was not different between M2-/- mice (582±4, 462±5 bpm) and WT controls (573±6, 440±10 bpm), however the KO displayed a significant increase in the top 10th centile for HR (740±5 vs 712±6; p<0.05). The KO group also displayed a lower average ( 36.6ºC±0.05 vs 36.8±0.05) and bottom 10th centile (35.4±0.06 vs 35.9±0.05) Tb. Time domain analysis of the heart rate revealed a lower standard deviation of the interbeat interval (SDNN - total autonomic variability) for the KO group.
CONCLUSION: The murine model of loss of M2 receptor function caused small but significant changes in HR and body temp that suggest alterations in autonomic function.
CLINICAL IMPLICATIONS: The murine M2-/- model may be useful in exploring autonomic function during lung disease.
DISCLOSURE: Ruoxi Hu, No Financial Disclosure Information; No Product/Research Disclosure Information