Lyrenäs E
Scand J Gastroenterol Suppl. 1985;116:1-48. doi: 10.3109/00365528509101536.
Gastrointestinal (GI) motility is centrally controlled through the sympathetic and parasympathetic nerves, sympathetic effects being partly mediated by beta adrenoceptors. Although beta adrenoceptor agonists and antagonists are widely used for different disorders, little is known about the influence of these agents on GI motility. The present study was initiated to investigate whether there is a physiological, beta adrenergic influence on human GI motility and to describe the effects of selective beta adrenoceptor stimulation on motility in the proximal and distal parts of the GI tract. Esophageal peristalsis was measured in healthy subjects using electronic catheters. Distal colonic motility was measured with an open-tipped, water-perfused catheter in the sigmoid colon and from an air-filled balloon in the rectum in healthy subjects and in patients with the irritable bowel syndrome (IBS). In one study, colonic motility was stimulated with continuous infusion of the octapeptide of cholecystokinin (CCK-OP). Esophagus: Peristaltic amplitude was increased in the distal smooth muscle part of the esophageal body after infusion of both the nonselective beta blocker propranolol and the beta-1 selective blocker metoprolol. After infusion of the beta-1 agonist prenalterol and the beta-2 selective agonist terbutaline, a profound decrease in esophageal peristaltic amplitude was seen. Pretreatment with metoprolol selectively blocked the response to a moderate dose of prenalterol but did not block the response to terbutaline. The latter response was blocked by propranolol. Peristaltic velocity in the proximal part of the esophagus was decreased by beta-1 stimulation and in the distal part by beta-2 stimulation. Distal colon: In healthy subjects the sigmoid motility index showed a dose-dependent increase after metoprolol and propranolol, respectively. The increase was more marked after propranolol infusion. Terbutaline decreased the sigmoid motility index both in healthy subjects and in patients with the IBS. Furthermore, the rectal motility index was decreased in the group of healthy subjects. The effects of prenalterol on rectal and sigmoid motility did not differ from those of placebo. The IBS patient group showed larger intraindividual variations in sigmoid motility from day to day and also lower rectal motility indices than the healthy subjects. Infusion of CCK-OP increased the sigmoid motility index compared to non-stimulated conditions. No effects on CCK-OP stimulated motility were seen after either terbutaline, prenalterol or placebo.(ABSTRACT TRUNCATED AT 400 WORDS)
胃肠(GI)动力受交感神经和副交感神经的中枢控制,交感神经效应部分由β肾上腺素能受体介导。尽管β肾上腺素能受体激动剂和拮抗剂广泛用于治疗不同疾病,但这些药物对胃肠动力的影响却知之甚少。本研究旨在调查是否存在生理性的β肾上腺素能对人类胃肠动力的影响,并描述选择性β肾上腺素能受体刺激对胃肠道近端和远端动力的作用。使用电子导管测量健康受试者的食管蠕动。在健康受试者和肠易激综合征(IBS)患者中,使用开放尖端、水灌注导管测量乙状结肠的远端结肠动力,并通过直肠内的充气气球进行测量。在一项研究中,通过持续输注胆囊收缩素八肽(CCK-OP)刺激结肠动力。食管:在输注非选择性β受体阻滞剂普萘洛尔和β-1选择性阻滞剂美托洛尔后,食管体远端平滑肌部分的蠕动幅度增加。在输注β-1激动剂普瑞特罗和β-2选择性激动剂特布他林后,食管蠕动幅度显著降低。用美托洛尔预处理可选择性阻断对中等剂量普瑞特罗的反应,但不阻断对特布他林的反应。后一种反应被普萘洛尔阻断。食管近端的蠕动速度因β-1刺激而降低,远端因β-2刺激而降低。远端结肠:在健康受试者中,乙状结肠动力指数在分别输注美托洛尔和普萘洛尔后呈剂量依赖性增加。普萘洛尔输注后增加更为明显。特布他林降低了健康受试者和IBS患者的乙状结肠动力指数。此外,健康受试者组的直肠动力指数降低了。普瑞特罗对直肠和乙状结肠动力的影响与安慰剂无异。IBS患者组乙状结肠动力的个体内每日变化较大,直肠动力指数也低于健康受试者。与未刺激状态相比,输注CCK-OP可增加乙状结肠动力指数。在输注特布他林、普瑞特罗或安慰剂后,未观察到对CCK-OP刺激的动力有影响。(摘要截断于400字)