The study investigated the role of α2-adrenergic receptors of the caudal raphe region in the sympathetic and cardiovascular responses to the acute intermittent hypercapnia (AIHc). Urethane-anesthetized, vagotomized, mechanically ventilated Sprague-Dawley rats (n=38) were exposed to the AIHc protocol (5×3 min, 15 % CO2+50 % O2) in hyperoxic background (50 % O2). α2-adrenergic receptor antagonist-yohimbine was applied intravenously (1 mg/kg, n=9) or microinjected into the caudal raphe region (2 mM, n=12) prior to exposure to AIHc. Control groups of animals received saline intravenously (n=7) or into the caudal raphe region (n=10) prior to exposure to AIHc. Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP) and heart rate (HR) were monitored before exposure to the AIHc protocol (T0), during five hypercapnic episodes (THc1-5) and at 15 min following the end of the last hypercapnic episode (T15). Following intravenous administration of yohimbine, RSNA was significantly greater during THc1-5 and at T15 than in the control group (P<0.05). When yohimbine was microinjected into the caudal raphe region, AIHc elicited greater increases in RSNA during THc1-5 when compared to the controls (THc1: 138.0±4.0 % vs. 123.7±4.8 %, P=0.032; THc2: 137.1±5.0 % vs. 124.1±4.5 %, P=0.071; THc3: 143.1±6.4 % vs. 122.0±4.8 %, P=0.020; THc4: 146.1±6.2 % vs. 120.7±5.7 %, P=0.007 and THc5: 143.2±7.7 % vs. 119.2±7.2 %, P=0.038). During THc1-5, significant decreases in HR from T0 were observed in all groups, while changes in MAP were observed in the group that received yohimbine intravenously. These findings suggest that blockade of the α2-adrenegic receptors in the caudal raphe region might have an important role in sympathetic responses to AIHc.
The involvement of rapheal and medial parts of the medullary reticular formation in both generation of airway reflexes and changes in breathing were studied in 18 chloralose or pentobarbitone anaesthetized, non-paralyzed cats. Chemical lesions to the medullary midline region (0—4 mm rostral to the obex) produced by localized injections of the neurotoxin kainic acid regularly abolished the cough reflexes evoked from the tracheobronchial and laryngopharyngeal regions and in most cases also the expiration reflex induced from the glottal area. The aspiration reflex elicited from the nasopharynx was spared, but was less intense. However, the signs of cough and expiration reflexes were preserved in the neurogram of the recurrent laryngeal nerve. The experiments have shown the importance of raphe nuclei and other medullary midline structures for the occurrence of cough and expiration reflexes. One possible explanation for the elimination of these expulsive processes is the removal of an important source of facilitatory input to the spinal respiratory motoneurons or to the brainstem circuitries that mediate cough and expiration reflexes . The role of the medullary midline in modulation of eupnoeic breathing and blood pressure is also discussed.