Bergdahl A, Valdemarsson S, Pantev E, Ottosson A, Feng Q P, Sun X Y, Hedner T, Edvinsson L
Department of Cell Biology, University Hospital, Lund, Sweden.
Acta Physiol Scand. 1995 Aug;154(4):429-37. doi: 10.1111/j.1748-1716.1995.tb09928.x.
In order to evaluate adaptational changes in vascular function in congestive heart failure (CHF), we studied the contractile responses of isolated arterial and venous blood vessels from rats suffering from CHF induced by coronary artery ligature, resulting in a myocardial infarction. The contractile responses of the basilar, femoral and renal arteries and of the iliac vein were examined in relation to adrenergic and neuropeptide Y (NPY) receptor function by the action of the alpha 1 agonist phenylephrine, the alpha 2 agonist clonidine and NPY. The contractile force was measured (in mN) and in % of K(+)-induced contraction as well as pD2 to each agonist. When stimulated by a 60 mM K(+)-buffer solution, the femoral and renal arteries from CHF rats responded with a stronger contraction (Emax; 9.4 +/- 0.6 and 9.8 +/- 0.6 mN) than the corresponding Sham vessels (Emax; 6.2 +/- 0.7 and 5.6 +/- 0.4 mN respectively, P < 0.001). On the contrary, the iliac vein of CHF responded less to K+ than the Sham iliac vein (Emax 2.5 +/- 0.2 and 3.7 +/- 0.5 mN, P < 0.01). The CHF iliac vein responded with a weaker contraction when stimulated with phenylephrine (Emax 1.9 +/- 0.4 mN) and showed a lower sensitivity (pD2 5.6 +/- 0.1) than the corresponding sham vessel (Emax 5.7 +/- 2.3 mN and pD2 6.3 +/- 0.5, P < 0.05). The CHF renal artery was less sensitive to clonidine (pD2 6.4 +/- 0.6) than the Sham renal artery (pD2 7.2 +/- 0.1, P < 0.05). The results indicate differences between CHF and Sham vessel segments according to both contractile capacity induced by K(+)-depolarization and to agonist induced contractile capacity and sensitivity. The differences are not of general nature but vary according to the vascular bed examined.
为了评估充血性心力衰竭（CHF）时血管功能的适应性变化，我们研究了冠状动脉结扎诱导心肌梗死所致CHF大鼠的离体动脉和静脉血管的收缩反应。通过α1激动剂去氧肾上腺素、α2激动剂可乐定和神经肽Y（NPY）的作用，检测基底动脉、股动脉、肾动脉和髂静脉的收缩反应与肾上腺素能和NPY受体功能的关系。测量收缩力（以mN为单位），并以K⁺诱导收缩的百分比以及每种激动剂的pD2表示。当用60 mM K⁺缓冲溶液刺激时，CHF大鼠的股动脉和肾动脉的收缩反应（Emax；9.4±0.6和9.8±0.6 mN）比相应的假手术组血管更强（Emax；分别为6.2±0.7和5.6±0.4 mN，P<0.001）。相反，CHF大鼠的髂静脉对K⁺的反应比假手术组的髂静脉弱（Emax 2.5±0.2和3.7±0.5 mN，P<0.01）。用去氧肾上腺素刺激时，CHF大鼠的髂静脉收缩反应较弱（Emax 1.9±0.4 mN），且敏感性较低（pD2 5.6±0.1），而相应的假手术组血管则为（Emax 5.7±2.3 mN和pD2 6.3±0.5，P<0.05）。CHF大鼠的肾动脉对可乐定的敏感性（pD2 6.4±0.6）低于假手术组的肾动脉（pD2 7.2±0.1，P<0.05）。结果表明，根据K⁺去极化诱导的收缩能力以及激动剂诱导的收缩能力和敏感性，CHF组和假手术组血管节段之间存在差异。这些差异并非普遍存在，而是因所检查的血管床而异。
