中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2011年
6期
727-730
,共4页
洛沙坦/药理学%高血压/代谢/病理学%肾/代谢%钙/代谢%肾动脉/药物作用
洛沙坦/藥理學%高血壓/代謝/病理學%腎/代謝%鈣/代謝%腎動脈/藥物作用
락사탄/약이학%고혈압/대사/병이학%신/대사%개/대사%신동맥/약물작용
Losartan/PD%Hypertension/ME/PA%Kidney/ME%Calcium/ME%Renal artery/DE
目的 探讨钙超负荷与高血压肾小动脉重建的关系及氯沙坦(Losartan)的治疗作用.方法 正常血压Wistar-Kyoto(WKY)大鼠和同种的16周龄自发高血压大鼠(spontaneously hypertensive rat,SHR)大鼠随机分为WKY对照组、SHR对照组、高剂量losartan组(SHR+HL)、低剂量losartan组(SHR+LL).每组6只动物.给予正常饮食,饲养至24周.losartan溶于10 ml生理盐水中灌胃,余组等量生理盐水灌胃.测量尾动脉血压、肾组织钙离子浓度、肾小动脉内羟脯氨酸含量并观察肾脏病理测量肾入球小动脉中膜厚度、血管内径及中膜厚度与内径比值(MT/LR).结果 SHR组肾组织钙离子浓度[(18.42±2.34)μmol/g]、肾小动脉内羟脯氨酸含量[(8.26±2.02)mg/g]均大于WKY组[(11.83±1.98)μmol/g,(5.16±0.98)mg/g](t=3.116,3.258,P<0.05),但两治疗组均有所降低,小于SHR组(t=2.946,P<0.05).SHR组肾内小动脉的壁厚[(5.25±1.13)μm]、壁厚内径比[(9.57±1.78)%]均大于WKY组相应比值[(4.03±0.16)μm,(7.12±1.35)%](t=2.836,3.425,P<0.05),但两治疗组壁厚内径比[(7.64±1.29)%,(7.85±1.32)%]小于SHR组(t=3.512,3.648,P<0.05).结论 losartan可以通过抑制细胞内钙超负荷、降低纤维化程度来改善肾小动脉的血管阻力,对高血压大鼠的肾小动脉重建有逆转作用.
目的 探討鈣超負荷與高血壓腎小動脈重建的關繫及氯沙坦(Losartan)的治療作用.方法 正常血壓Wistar-Kyoto(WKY)大鼠和同種的16週齡自髮高血壓大鼠(spontaneously hypertensive rat,SHR)大鼠隨機分為WKY對照組、SHR對照組、高劑量losartan組(SHR+HL)、低劑量losartan組(SHR+LL).每組6隻動物.給予正常飲食,飼養至24週.losartan溶于10 ml生理鹽水中灌胃,餘組等量生理鹽水灌胃.測量尾動脈血壓、腎組織鈣離子濃度、腎小動脈內羥脯氨痠含量併觀察腎髒病理測量腎入毬小動脈中膜厚度、血管內徑及中膜厚度與內徑比值(MT/LR).結果 SHR組腎組織鈣離子濃度[(18.42±2.34)μmol/g]、腎小動脈內羥脯氨痠含量[(8.26±2.02)mg/g]均大于WKY組[(11.83±1.98)μmol/g,(5.16±0.98)mg/g](t=3.116,3.258,P<0.05),但兩治療組均有所降低,小于SHR組(t=2.946,P<0.05).SHR組腎內小動脈的壁厚[(5.25±1.13)μm]、壁厚內徑比[(9.57±1.78)%]均大于WKY組相應比值[(4.03±0.16)μm,(7.12±1.35)%](t=2.836,3.425,P<0.05),但兩治療組壁厚內徑比[(7.64±1.29)%,(7.85±1.32)%]小于SHR組(t=3.512,3.648,P<0.05).結論 losartan可以通過抑製細胞內鈣超負荷、降低纖維化程度來改善腎小動脈的血管阻力,對高血壓大鼠的腎小動脈重建有逆轉作用.
목적 탐토개초부하여고혈압신소동맥중건적관계급록사탄(Losartan)적치료작용.방법 정상혈압Wistar-Kyoto(WKY)대서화동충적16주령자발고혈압대서(spontaneously hypertensive rat,SHR)대서수궤분위WKY대조조、SHR대조조、고제량losartan조(SHR+HL)、저제량losartan조(SHR+LL).매조6지동물.급여정상음식,사양지24주.losartan용우10 ml생리염수중관위,여조등량생리염수관위.측량미동맥혈압、신조직개리자농도、신소동맥내간포안산함량병관찰신장병리측량신입구소동맥중막후도、혈관내경급중막후도여내경비치(MT/LR).결과 SHR조신조직개리자농도[(18.42±2.34)μmol/g]、신소동맥내간포안산함량[(8.26±2.02)mg/g]균대우WKY조[(11.83±1.98)μmol/g,(5.16±0.98)mg/g](t=3.116,3.258,P<0.05),단량치료조균유소강저,소우SHR조(t=2.946,P<0.05).SHR조신내소동맥적벽후[(5.25±1.13)μm]、벽후내경비[(9.57±1.78)%]균대우WKY조상응비치[(4.03±0.16)μm,(7.12±1.35)%](t=2.836,3.425,P<0.05),단량치료조벽후내경비[(7.64±1.29)%,(7.85±1.32)%]소우SHR조(t=3.512,3.648,P<0.05).결론 losartan가이통과억제세포내개초부하、강저섬유화정도래개선신소동맥적혈관조력,대고혈압대서적신소동맥중건유역전작용.
Objective To investigate the effects of losartan on aortic elasticity and remodeling in spontaneously hypertensive rats (spontaneously hypertensive rats SHR). Methods WKY (Wistar - Kyoto ) rats with normal blood pressure and 16 weeks spontaneously hypertensive rats were randomly divided into WKY control group, SHR control group, high dose losartan group (SHR + HL), low doses losartan group (SHR + LL). Each group has six animals which were given normal diet for 24 weeks. Losartan which was dissolved in 10 ml physiological saline was filling in stomach, other groups were filling with physiological saline. Tail arterial blood pressure, kidney tissues calcium concentration, renal small artery hydroxyproline content was measured and small arteries wall thickness of Glomerularwas detected, and the ratio of thickness and inner diameter (MT/LR) in kidney pathological were observed. Results The calcium concentration of SHR group in kidney tissues was [(18.42±2.34)μmol/g], kidney small artery hydroxyproline content was [(8.26±2.02)mg/g], which were greater than WKY group [(11.83±1.98)μmol/g,(5.16±0.98)mg/g] (t=3.116,3.258,P<0.05), but the two treatment groups were less than SHR group (t=2.946,P<0.05), the difference was significant. Small arteries wall thickness of Glomerular was [(5.25±1.13)μm], the ratio of thickness and inner diameter (MT/LR) was [(9.57±1.78)%], which were greater than WKY group[(4.03±0.16)μm ,(7.12±1.35)%](t=2.836,3.425,P<0.05), but the wall thickness of two treatment groups were [(7.64±1.29)%,(7.85±1.32)%], the two treatment groups were less than SHR group (t=3.512,3.648,P<0.05). Conclusions Losartanmay inhibit intracellular calcium overload, reduce fibrosis degree and improve renal arteriole resistance and reverse the renal arteriole reconstruction of SHR rats.