Objective Previous studies in normotensive anesthetized rats (Lapi Arch.Ital.Biol 151:11-23,2013) showed that peripheral stimulation of the trigeminal nerve induced by submaximal mouth opening (mandibular extension, ME) caused prolonged (at least 80min) bradycardia, hypotension and cerebral hemodynamic changes (pial arterioles showed a characteristic response pattern consisting in a significant constriction during ME followed by a dilatation for the entire remaining observation time). Design and method In this study we assessed the in vivo effects of ME on HR, MABP and pial microcirculation in hypertensive rats. Experiments were performed in male Wistar rats weighing 250-300g (n = 8). Hypertension was induced by intraperitoneal daily injection of dexamethasone (0.03mg/kg/day) for 10 days. ME was obtained by inserting an ad hoc developed retractor between the dental arches. HR and MABP were recorded by ECG and a catheter placed in the left femoral artery and measured by a computer-assisted system. Pial arterioles were observed through a closed cranial window implanted above the left parietal cortex and visualized by an in vivo fluorescence microscopy technique to assess vessel diameter changes before (baseline), during 10min ME and thereafter until 160min. Arteriolar diameters were measured with a computer-assisted method (MIP Image program, frame by frame). Results In sham-treated (no ME) hypertensive rats (n=3) HR, MABP and pial microcirculation did not change during whole observation period. Hypertensive rats subjected to ME (n=5) showed a significant decrease of HR and MABP. HR declined by 42bpm, (p<0.01) starting from 60 min after ME up to 160min, while MABP by 18mmHg (p<0.05) starting from 20min after ME up to 100min, compared with baseline. Pial arterioles exhibited a biphasic response: the arteriolar diameter decreased by 2.94?m (p<0.05) during ME, afterwards it significantly increased by 3.46?m (p<0.01) starting from 20min after ME; this vasodilatation lasted for the whole observation period. Conclusions Our results suggest that ME is able to exert profound and prolonged regulatory effects on systemic arterial blood pressure and pial arteriolar tone in hypertensive rats.
The Hypotensive and bradycardic effects of mouth opening: evidence in an animal model.
Del Seppia C;
2014
Abstract
Objective Previous studies in normotensive anesthetized rats (Lapi Arch.Ital.Biol 151:11-23,2013) showed that peripheral stimulation of the trigeminal nerve induced by submaximal mouth opening (mandibular extension, ME) caused prolonged (at least 80min) bradycardia, hypotension and cerebral hemodynamic changes (pial arterioles showed a characteristic response pattern consisting in a significant constriction during ME followed by a dilatation for the entire remaining observation time). Design and method In this study we assessed the in vivo effects of ME on HR, MABP and pial microcirculation in hypertensive rats. Experiments were performed in male Wistar rats weighing 250-300g (n = 8). Hypertension was induced by intraperitoneal daily injection of dexamethasone (0.03mg/kg/day) for 10 days. ME was obtained by inserting an ad hoc developed retractor between the dental arches. HR and MABP were recorded by ECG and a catheter placed in the left femoral artery and measured by a computer-assisted system. Pial arterioles were observed through a closed cranial window implanted above the left parietal cortex and visualized by an in vivo fluorescence microscopy technique to assess vessel diameter changes before (baseline), during 10min ME and thereafter until 160min. Arteriolar diameters were measured with a computer-assisted method (MIP Image program, frame by frame). Results In sham-treated (no ME) hypertensive rats (n=3) HR, MABP and pial microcirculation did not change during whole observation period. Hypertensive rats subjected to ME (n=5) showed a significant decrease of HR and MABP. HR declined by 42bpm, (p<0.01) starting from 60 min after ME up to 160min, while MABP by 18mmHg (p<0.05) starting from 20min after ME up to 100min, compared with baseline. Pial arterioles exhibited a biphasic response: the arteriolar diameter decreased by 2.94?m (p<0.05) during ME, afterwards it significantly increased by 3.46?m (p<0.01) starting from 20min after ME; this vasodilatation lasted for the whole observation period. Conclusions Our results suggest that ME is able to exert profound and prolonged regulatory effects on systemic arterial blood pressure and pial arteriolar tone in hypertensive rats.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
