ABSTRACT
To study the stimulation of the genioglossus with percutaneous biphasic current pulses as a new therapeutical method to treat the obstructive sleep apnea syndrome (OSAS), polysomnography (PSG) was used to synchronously monitor the patient. When OSAS was occurring, the stimulation with the optimal parameter was given in time to make the tongue move forward, the glossopharyngeal airway dilated, the resistance of the upper respiratory tract reduced, the hypoxia at night to be improved and the sleeping structure to be ameliorated because of the function of the dilated muscle of the upper airway. The results of the clinical therapeutic effect indicated that 17 of 22 patients with OSAS had cured effects, 2 of whom improved and 3 of whom were without effect. The effective rate was 77.27%. It is preliminarily proved that this is a new method in the treatment of patients suffered from OSAS.
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Electric Stimulation Therapy , Methods , Sleep Apnea, Obstructive , Therapeutics , Treatment OutcomeABSTRACT
AIM: To investigate the roles of nitric oxide/L-arginine(NO/L-Arg) pathway and urotensin-Ⅱ(UⅡ) in the development of pulmonary hypertension induced by chronic hypoxia-hypercapnia in rats.METHODS: Forty male Sprague-Dawley rats were randomly divided into four groups(n=10): normal control group(A),hypoxia-hypercapnia+saline group(B),hypoxia-hypercapnia+L-Arg liposome group(C) and hypoxia-hypercapnia+N-nitro-L-arginine methyl ester(L-NAME) group(D).Contents of UⅡ,UⅡ mRNA and receptor of UⅡ(UT) mRNA in pulmonary arterioles were measured with immunohistochemistry analysis and in situ hybridization,respectively.Change of small pulmonary vascular microstructure was also investigated.RESULTS:(1) The mean pulmonary artery pressure(mPAP) and the weight ratio of right ventricle to left ventricle plus septum [RV/(LV+S)] in B and D groups were all higher than those in A group(respectively,P
ABSTRACT
AIM:To investigate rat Urotensin-II(ra t U-II)-induced vasoconstriction of rat main pulmonary arteries and the role of mitogen-activated protein kinase(MAPK). METHODS: The main pulmon ary artery was dissected from the male Sprague -Dawley rats and artery ring width was 3-4 mm. Concentration-response curves wer e gene rated to rat U-II(0 03 nmol/L-30 nmol/L).Inhibitor of MAPK,PD 98059(0 1 ?mol/ L -10 ?mol/L) were added into the medium after rat U-II(30 nmol/L)induced vasoc onstriction had reached plateau to construct the relaxant concentration-respons e curves and their EC 50 and E max . RESULTS: Rat U-II was a potent vasoconstrictor of isolated rat main pulmonary arteries [EC 50 =7 95?0 4 0, E max =(14 28?6 34)% of the response to 60 mmol/L KCl]; PD 98059 caused c oncentration-dependent relaxations of rat U-II precontracted arteries [EC 50 =5 91?0 45, E max =(81 39?13 65)%]. CONCLUSION: Rat U- II was a potent vasoconstrictor of rat main pulmonary arteries and this response was med iated through MAPK.
ABSTRACT
AIM:To investigate the effect of puerarin on pulmonary vessel collagen metabolism in pulmonary hypertension rats induced by chronic hypoxia and hypercapnia. METHODS: Collagen Ⅰ,Ⅲ and their mRNA were observed in pulmonary arterioles by the technique of immunohistochemistry and in situ hybridization. RESULTS: ① Light microscopy showed media thickness of pulmonary arterioles was much higher in HH(hypoxic-hypercapnia) group than that of NC(normal control) group, and, vessel cavity turned more straiter in HH group than that of NC group.However, the damage of pulmonary arterioles in HP(hypoxic-pueratin) group was much slighter than that of HH group. ② The levels of plasma ET-1 and lung homogenates Hyr were much higher in HH group than those of NC group( P 0.05). CONCLUSION: Puerarin inhibited the deposition of collagen and improved pulmonary vessel remodeling.
ABSTRACT
AIM: To investigate the effect of chronic hypoxia-hypercapnia and L-arginine (L-Arg) liposome on L-Arg transport in rats pulmonary artery. METHODS: Forty Sprague-Dawley rats were randomly divided into four groups, normal control group (NC), chronic hypoxia-hypercapnia group (HH), chronic hypoxia- hypercapnia group+L-Arg (HL) and chronic hypoxia-hypercapnia group+L-Arg liposome (HP). Changes in pulmonary artery L-Arg transport and pulmonary arterial microscopy were observed. RESULTS: (1) The mean pulmonary artery pressure (mPAP) and weight ratio of right ventricle to left ventricle and septum (RV/LV+S) in HH group were higher than those in NC group, and in HP group was lower than that in HH group and HL group, but there was no significant difference between HL group and HH group; (2) At 0.005 mmol/L, 0.01mmol/L, 0.02mmol/L, 0.05 mmol/L, 0.1 mmol/L and 0.2mmol/L concentration of L-Arg, the velocity of L-Arg transport in HH group was lower than that in NC group, and in HL group higher than in HH group, and in HP group was much higher than that in HH group and in HL group. (3) Light microscopy showed that vessel well area/total area (WA/TA) and media thickness of pulmonary arterioles (PAMT) were much higher in rats of HH group than those in NC group, WA/TA and PAMT in HP group were obviously improved. CONCLUSION: The above results indicated that there existed a functional disturbance in L-Arg transport of pulmonary artery in rats chronically exposed to hypoxia-hypercapnia, and it was obviously enhanced when liposome was used as L-Arg carrier. Thus, it appears that liposome-L-Arg may have clinical perspective in the treatment of chronic hypoxic pulmonary hypertension.
ABSTRACT
AIM: To investigate the expression of matrix metalloproteinases(MMPs) in pulmonary arterioles of rats with chronic hypoxia and hypercapnia-induced pulmonary hypertension. METHODS: MMP-2, MMP-9 and MMP-2 mRNA, MMP-9 mRNA were observed in pulmonary arterioles by the techniques of immunohistochemistry and in situ hybridization. RESULTS: ①The mean pulmonary artery pressure (mPAP) and weight ratio of right ventricle to left ventricle and septum (RV/LV+S) of hypoxia-hypercapnia groups were higher than those of normal control group ( P