ABSTRACT
Objective To evaluate the role of A1 adenosine receptor ( A1 AR) within the nucleus tractus solitarii ( NTS ) in dexmedetomidine-induced increase in baroreflex sensitivity ( BRS ) in rats. Methods Thirty-two clean-grade healthy male Sprague-Dawley rats, weighing 240-280 g, were divided in-to 4 groups ( n=8 each) using a random number table method: control group ( group C) , solvent control group ( group S) , dexmedetomidine group ( group D) , and dexmedetomidine plus 8-cyclopentyl-1,3-diprop-ylxanthine (DPCPX, a highly selective A1AR blocker) group (group DD). After the rats were anesthe-tized, 1 μl drug liquid was injected into the right NTS with a brain stereotaxic apparatus. Oneμl normal sa-line was injected into the right NTS in C and D groups, 1 μl dimethyl sulfoxide in group S, and 1 μl DPCPX in group DD. After catheters were implanted into the femoral vein, dexmedetomidine was intrave-nously infused as a bolus of 100μg/kg over 15 min followed by an infusion of 50μg·kg-1 ·h-1 for 105 min in D and DD groups. The equal volume of normal saline was given instead of dexmedetomidine in C and S groups. BRS was measured using phenylephrine immediately before intravenous infusion (T0) and at 60 and 120 min after beginning of infusion ( T1,2 ) . Results Compared with C and S groups, the BRS was signifi-cantly increased at T1,2 in D and DD groups ( P＜0. 05) . Compared with group D, the BRS was significantly decreased at T1,2 in group DD ( P＜0. 05) . Conclusion A1 AR within the NTS is involved in dexmedetomi-dine-induced increase in BRS in rats.
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Objective: To investigate the changes of the amino acid receptors in solitary tract nucleus(NTS)of rats after spinal cord injury (SCI). Methods: The rat model of T4 spinal cord transection was used in this study. The study was divided into SCI group(n=5)and Control group(n=5). Changes in mean arterial pressure (MAP) and heart rate (HR) were observed at 1,2,3,4, and 6 weeks after SCI; and the protein expression of the glutamate N-methyl-D-aspartate receptor 1 (NMDA-R1) and gamma-aminobutyric acid receptor A α1 (GABAA-α1) in the NTS were detected by Western blotting analysis at different time points. Results: The MAP level was significantly decreased at 1-3 weeks after SCI (P<0.05), and it gradually recovered 4 weeks after SCI; the HR was significantly increased 1-4 weeks after SCI (P<0.05) and recovered at the 6th week. The results of Western blotting analysis showed that the protein expression of GABAA-α1 was significantly increased 2 weeks after SCI and significantly reduced at 4 and 6 weeks after SCI (P<0.05). Moreover, the ratio of NMDA-R1 to GABAA-α1 expression in NTS was significantly elevated after SCI(P<0.05). Conclusion: The adaptable changes of important receptors in the NTS following SCI may improve SCI-induced cardiovascular dysfunction.
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Objective To determine the role of the nucleus tractus solitarii (NTS) superoxide in mediating the chronic heart failure (CHF)-induced reduction in baroreflex control of sympathetic activity. Methods CHF model was produced by coronary ligation in SD rats, and rats receiving sham operation (Sham) served as controls. Changes in renal sympathetic nerve activity (RSNA) and baroreflex sensitivity control of sympathetic activity were observed after microinjections of SOD mimic Tempol into the NTS in Shamand CHF rats. Results In anesthetized rats, the baseline level of sympathetic nerve activity was significantly higher in CHF group than in Sham group (P<0. 05), whereas the baroreflex sensitivity control of sympathetic activity was lower in CHF group than in Sham group. Bilateral microinjection of Tempol (10 nmol in 50 nL) into the NTS had no effect on baseline RSNA and baroreflex sensitivity in the Sham group. In contrast, injection of Tempol notably reduced the baseline RSNA and increased baroreflex sensitivity in CHF group. Conclusion Superoxide in the NTS contributes to sympathetic overactivity and baroreflex impairment in rats with CHF, suggesting that increased oxidative stress in the NTS is responsible for cardiovascular dysfunctions in CHF.
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Objective To investigate the effect of jejunal casein perfusion on pancreatic exocrine secretion in experimental acute necrotic pancreatitis (ANP) rats and analyze the neuromechanism that may be involved. Methods 30 SD rats were randomly divided into three groups (control group, ANP group and ANP jejunal nutrition group). Experimental ANP was induced by intra pancreatic duct injection of sodium taurocholate (STC). Animals in ANP jejunal nutrition group were given jejunal casein perfusion 24h after model induction, while control group and ANP group received jejunal saline perfusion. Pancreatic juice was collected every 15 min for six times and the volume of pancreatic juice and protein in pancreatic juice were detected. After jejunal nutrition c-Fos expression in nucleus tractus solitarii (NTS) was determined by immunohistochemistry method in three groups. Results There was no significant difference between the volume of pancreatic juice at different time points in ANP group and ANP jejunal nutrition group, however, these parameters were significantly lower than that of control group (P < 0. 05). There was no significant difference among the 3 groups in the protein level in the pancreatic juice during jejunal nutrition infusion, however, during the periods of 0 ～ 15 min, 15 ～30 min, 30 ～45 min and 75 ～90 min, the protein levels in the pancreatic juice in ANP and ANP jejunal nutrition group were lower than that of control group (P < 0.05). After jejunal perfusion, c-Fos expression was found in ANP jejunal nutrition group but not found in ANP and control groups. Conclusions Jejunal casein perfusion enhanced NTS c-Fos expression, but did not increase the volume of pancreatic juice and protein.
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Objective To investigate the inhibitory effects of RNA silencing via adenovirusmediated angiotensin Ⅱ receptor subtypes shRNA(Ad-ATlaR-shRNA and Ad-ATlbR-shRNA)in mice brainstem nucleus tractus solitarius(NTS)in vivo. Methods C57BL mice were used as animal model.The microinjection into the nucleus of NTS was adopted.Two groups of male C57BL mice(n =7,n=8)were selected.After 10 days of microinjection,mice were killed and their brain tissue were fixed and sectioned.The levels of ATlaR mRNA and ATlbR mRNA at both sides of NTS were examined by in situ hybridization. Results The expression of ATlaR mRNA was significantly inhibited from 1.81/μCi/mg to 0.71μCi/mg[(61.6±6.8)%,P<0.01]by Ad-ATlaR-shRNA.Meanwhile,ATlbR mRNA expression was consistent at both sides,with no significant difference(P>0.05)after Ad-ATlaR-shRNA microinjection.ATlbR mRNA expression at the side with AdATlbR-shRNA injection was significantly inhibited from 10.28/μCi/mg to 4.97μCi/mg[(51.6±5.2)%,P<0.01]by Ad-ATlbR-shRNA.Meanwhile,ATlaR mRNA probe were consistent at both sides,with no significant difference(P>0.05). Conclusions The results show that both AdATlaR-shRNA and Ad-ATlbR-shRNA inhibit the corresponding receptor mRNA expression,and there is no cross-action for each other.