摘要
目的探讨犬急性心功能不全状态下肾动脉血流和肾微血管床血流灌注的改变及血管紧张素转换酶抑制剂对其影响。方法12只杂种犬,结扎冠状动脉前降支并快速右室起搏,制作急性心功能不全模型,同时开腹暴露左侧肾脏及肾动脉,应用多普勒血流探测仪监测升主动脉根部血流量(心输出量,CO)和肾动脉血流量(RBF)。在基础及CO下降25%(LCO25%)和50%(LCO50%)时,观察CO和RBF改变。同时进行肾脏对比超声检查,测定肾微血管血流速度(β)、微血管容积(A)和微血管血流量(A×β)。在LCO50%后给予卡托普利1mg/kg及2mg/kg静脉注射,并在注射前后重复完成CO、RBF和肾对比超声检测。结果基础状态下,CO、RBF、肾皮质β、A和A×β值分别为(1·46±0·16)ml/min、(107·5±35·7)ml/min、1·39±0·14、120·3±14·8和167·4±25·0。当LCO25%和LCO50%时,RAF、肾皮质β、A和A×β值分别减至(72·50±32·4)ml/min、0·87±0·082、117·6±13·1、102·6±15·5和(44·1±17·2)ml/min、0·61±0·039、106·9±12·0、64·7±8·83。表明在LCO25%时,随CO和RBF的下降,肾皮质微血管床血流灌注即减少(A×β减少,P<0·05),其中以β减少为主,A无明显变化。当LCO50%时,肾动脉和肾微血管床血流灌注进一步下降,此时肾皮质血管床容积亦减少(与LCO25%比较,P<0·05)。在LCO50%时,应用卡托普利1mg/kg和2mg/kg后,平均动脉压由(85·4±7·8)mmHg(1mmHg=0·133kPa)降低至(78·7±7·3)mmHg和(69·1±6·3)mmHg(P<0·05);CO由0·73±0·084增至0·83±0·065和0·9±0·054(P<0·05);RBF由(44·1±17·2)ml/min增至(60·3±17·8)ml/min和(79·4±17·8)ml/min(P<0·05)。两种剂量的卡托普利使CO增加的比值分别为0·15±0·084和0·31±0·0111,而RBF增加的比值分别为0·290±0·089和0·522±0·040,均显著大于CO的增加比值。与此同时,卡托普利1mg/kg和2mg/kg使肾皮质β由0·61±0·039增至0·75±0·020和0·86±0·027;A由106·9±11·9增至115·4±11·1和116·6±8·9;A×β由64·7±8·83增至87·0±8·6和100·6±8·9。结论在急性心功能不全伴肾功能衰竭的情况下,应用加强肾微循环血流灌注的治疗措施可能有益于肾功能及心功能的恢复。
Objective To investigate the changes and the effects of captopril on the renal blood flow and microvascular perfusion in dogs with acute cardiac insufficiency. Methods Acute cardial insufficiency was induced by combining occlusion of the left anterior descending artery with right ventricular pacing in 12 mongrel dogs. The ascending aorta and left kidney were dissected and ultrasonic flow probes were placed on ascending aorta and renal artery to monitor cardiac output （CO） and renal blood flow （RBF）. Contrast-enhanced ultrasound of the kidney was performed as CO was reduced to 25% （LCO25%） and 50% （LCO50%） from the basic measurement and microvascular flow velocity （β） , microvascular volume （A） and microvascular blood flow（ renal cortex） were observed. Mter CO reduced to 50%, captopril 1 mg/kg and 2 mg/kg were injected successively and contrast-enhanced ultrasound of the kidney were performed again before and after injection. Results At baseline, CO, RBF, C×β（ β of renal cortex）, A and A×β were （ 1. 46 ± 0. 16） ml/min,（ 107.5 ± 35.7）ml/min, 1.39 ± 0. 14, 120.3 ± 14.8 and 167.4 ± 25.0, respectively. After the LCO25% was reached, RAF, CXβ, A and A×β decreased to （72. 50 ± 32.4）ml/min, 0. 87 ± 0. 082, 117. 6 ± 13.1, and 102. 6 ± 15.5, respectively. The corresponding values after the LCO50% was reached were （44. 1 ± 17. 2）ml/min, 0. 61 ± 0. 039, 106. 9 ± 12. 0, and 64.7 ± 8.83, respectively. It is suggested that the volume of the renal microvasculature remained stable until the LCO50% was reached. When captopril 1 mg/kg and 2mg/kg were injected successively at LCO50%, MAP decreased from （85.4 ± 7.8） mm Hg to （78. 7 ± 7. 3）mm Hg and to （69. 1 ± 6. 3 ） mm Hg （ P 〈 0. 05 ）, respectively, while CO increased from 0. 73 ± 0. 084 to 0. 83 ± 0. 065 and to 0. 9 ± 0. 054 （P 〈 0. 05）, respectively. RBF increased from （44. 1 ± 17. 2） ml/min to 60. 3 ± 17.8 and to 79.4 ± 17. 8 （ P 〈 0. 05 ）, respectively. After captopril 1 mg/kg and 2 mg/kg were injected, the increased flow ratios with CO were 0. 15 ± 0. 084 and 0. 31 ± 0. 011, respectively, and with RBF were 0. 29 ± 089 and 0. 522 ± 0. 040, respectively. The increased renal blood flow ratio was higher than that of CO after captopril was used. The corresponding increases were from 0. 61 ± 0. 039 to 0. 75 ± 0. 020 and to 0. 86 ± 0. 027 for CX β, from 106. 9 ± 11.9 to 115.4 ± 11.1 and to 116. 6 ± 8. 9 for A, from 64. 7 ± 8.83 to 87.0 ± 8. 6 and to 100. 6 ± 8.9 for A × β, respectively. Conclusion The renal microvasculature plays a role by keeping its volume stable in the protection against renal ischemia when acute cardiac output decreases slightly. The role of captopril to improve renal microvascular perfusion is independent of increased total cardiac output or increased systemic blood pressure.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
2005年第7期643-647,共5页
Chinese Journal of Cardiology
