Hoeldtke R D, Davis K M, Joseph J, Gonzales R, Panidis I P, Friedman A C
General Clinical Research Center, Temple University Hospital, Philadelphia.
Circulation. 1991 Jul;84(1):168-76. doi: 10.1161/01.cir.84.1.168.
The somatostatin analogue, ectrootide, is being used to treat postprandial hypotension in patients with autonomic neuropathy. Although the therapeutic effect of the drug is presumably secondary to a splanchnic vasoconstrictor action, its effect on splanchnic hemodynamics has never been characterized in patients with autonomic neuropathy. Moreover, it is unknown whether octreotide acts on other vascular beds in this group of patients or whether it affects cardiac output. We, therefore, measured splanchnic, forearm, and systemic vascular resistance and cardiac output before and after administering octreotide (0.4 microgram/kg s.c.) to patients with idiopathic autonomic neuropathy and diabetic autonomic neuropathy.
Splanchnic blood flow was determined from the clearance of indocyanine green in seven patients. We observed that octreotide decreased splanchnic blood flow (from 850 +/- 77 to 664 +/- 48 ml/min, p less than 0.005), increased mean blood pressure (from 97 +/- 6 to 115 +/- 3 mm Hg, p less than 0.005), and increased splanchnic vascular resistance (from 0.118 +/- 0.012 to 0.18 +/- 0.018 mm Hg/ml/min, p less than 0.005). Forearm blood flow was measured by plethysmography in 13 patients. Octreotide increased forearm vascular resistance in patients with idiopathic autonomic neuropathy (n = 8) from 19.1 +/- 1.0 to 27.2 +/- 3.8 mm Hg/ml/min/100 ml forearm volume (p less than 0.01) and from 25.2 +/- 3.9 to 41.0 +/- 6.8 mm Hg/ml/min/100 ml (p less than 0.01) in patients with diabetic autonomic neuropathy (n = 5). Cardiac output was measured by two-dimensional echocardiography. Octreotide administration increased cardiac output in five of six patients with idiopathic autonomic neuropathy (from 4.4 +/- 0.4 to 5.0 +/- 0.5 l/min, p less than 0.02) and five of five patients with diabetic autonomic neuropathy (from 3.8 +/- 0.4 to 5.1 +/- 0.4 l/min, p less than 0.02). Systemic vascular resistance increased in patients with idiopathic autonomic neuropathy from 21.2 +/- 2 to 24.9 +/- 2.6 (p less than 0.05) but did not change in patients with diabetic autonomic neuropathy.
The pressor effect of octreotide in patients with autonomic neuropathy is associated with increased splanchnic and forearm vascular resistance and with increased cardiac output.
生长抑素类似物依克多肽正用于治疗自主神经病变患者的餐后低血压。尽管该药的治疗效果可能继发于内脏血管收缩作用,但其对自主神经病变患者内脏血流动力学的影响尚未得到明确描述。此外,在这类患者中,奥曲肽是否作用于其他血管床或是否影响心输出量尚不清楚。因此,我们在特发性自主神经病变和糖尿病性自主神经病变患者中,于皮下注射奥曲肽(0.4微克/千克)前后测量了内脏、前臂和全身血管阻力以及心输出量。
通过测量7例患者吲哚菁绿清除率来测定内脏血流量。我们观察到,奥曲肽可降低内脏血流量(从850±77降至664±48毫升/分钟,p<0.005),升高平均血压(从97±6升至115±3毫米汞柱,p<0.005),并增加内脏血管阻力(从0.118±0.012升至0.18±0.018毫米汞柱/毫升/分钟,p<0.005)。通过体积描记法测量了13例患者的前臂血流量。奥曲肽使特发性自主神经病变患者(n = 8)的前臂血管阻力从19.1±1.0升至27.2±3.8毫米汞柱/毫升/分钟/1OO毫升前臂容积(p<0.01),使糖尿病性自主神经病变患者(n = 5)的前臂血管阻力从25.2±3.9升至41.0±6.8毫米汞柱/毫升/分钟/1OO毫升(p<0.01)。通过二维超声心动图测量心输出量。在6例特发性自主神经病变患者中有5例(从4.4±0.4升至5.0±0.5升/分钟,p<0.02),在5例糖尿病性自主神经病变患者中有5例(从3.8±0.4升至5.1±0.4升/分钟,p<0.02),奥曲肽给药后心输出量增加。特发性自主神经病变患者的全身血管阻力从21.2±2升至24.9±2.6(p<0.05),而糖尿病性自主神经病变患者的全身血管阻力未发生变化。
奥曲肽对自主神经病变患者的升压作用与内脏和前臂血管阻力增加以及心输出量增加有关。