Fiorucci S, Scionti L, Bosso R, Desando A, Bottini P, Marino C, Morelli A
Istituto di Gastroenterologia ed Endoscopia Digestiva, Università di Perugia, Italy.
Dig Dis Sci. 1992 Nov;37(11):1671-7. doi: 10.1007/BF01299857.
A reduction of gallbladder emptying in response to neural or hormonal stimulation has been reported in patients with diabetes mellitus. Decreased gallbladder emptying may be a key factor in the pathogenesis of gallbladder stones. Few drugs, if any, are able to stimulate gallbladder emptying. However, in a previous study we demonstrated that erythromycin, a macrolide antibiotic, stimulates gallbladder emptying and motilin release in healthy human subjects by an atropine-sensitive pathway. Therefore, the present study was designed to evaluate the effect of erythromycin on gallbladder emptying and motilin release in diabetic patients with or without cardiac autonomic neuropathy (AN). Thirteen diabetic patients, six with AN, and 10 healthy subjects were enrolled in the study protocol. Gallbladder emptying was determined by sonography after ingestion of a standard meal and during infusion of erythromycin alone or together with 6 micrograms/kg/hr atropine. We found that 100 mg/hr erythromycin caused a significant reduction in gallbladder volume in both healthy subjects and diabetic patients. The ejection fraction (mean +/- SE) of 45.3 +/- 8.2% and 37.3 +/- 5.0% was similar. The presence of AN had no influence on gallbladder emptying induced by erythromycin. Basal motilin plasma levels were 111.5 +/- 14.5 pmol/liter in diabetic patients and 63.3 +/- 6.0 pmol/liter in healthy subjects (P < 0.01). However, patients with AN had higher (130.0 +/- 11.9 pmol/liter) motilin plasma levels than patients without (74.0 +/- 9.4 pmol/liter, P < 0.01). Erythromycin administration caused an approximately twofold increase in plasma motilin concentrations in healthy subject and patients without AN, but did not stimulate motilin release in neuropathic patients.(ABSTRACT TRUNCATED AT 250 WORDS)
据报道,糖尿病患者对神经或激素刺激的胆囊排空功能降低。胆囊排空减少可能是胆结石发病机制的关键因素。几乎没有药物能够刺激胆囊排空。然而,在之前的一项研究中,我们证明了大环内酯类抗生素红霉素可通过对阿托品敏感的途径刺激健康人体的胆囊排空和胃动素释放。因此,本研究旨在评估红霉素对患有或未患有心脏自主神经病变(AN)的糖尿病患者胆囊排空和胃动素释放的影响。13名糖尿病患者(6名患有AN)和10名健康受试者纳入了研究方案。在摄入标准餐后以及单独输注红霉素或与6微克/千克/小时阿托品一起输注期间,通过超声检查确定胆囊排空情况。我们发现,每小时100毫克的红霉素可使健康受试者和糖尿病患者的胆囊体积显著减小。射血分数(平均值±标准误)分别为45.3±8.2%和37.3±5.0%,二者相似。AN的存在对红霉素诱导的胆囊排空没有影响。糖尿病患者的基础胃动素血浆水平为111.5±14.5皮摩尔/升,健康受试者为63.3±6.0皮摩尔/升(P<0.01)。然而,患有AN的患者胃动素血浆水平(130.0±11.9皮摩尔/升)高于未患AN的患者(74.0±9.4皮摩尔/升,P<0.01)。给予红霉素后,健康受试者和未患AN的患者血浆胃动素浓度增加了约两倍,但并未刺激神经病变患者的胃动素释放。(摘要截断于250字)