Inhibitory effect on gastric motility of chloroquine and mepacrine.

Measured on isolated rat-stomach fundus strips, the isolated cervical sympathetic trunk, and on the superior cervical ganglion, chloroquine and mepacrine have parasympatholytic, spasmolytic, ganglionic blocking and local anaesthetic effects. On rising the doses these manifest themselves in a given sequence. On the basis of this fact it is concluded that the inhibition of gastric motility by chloroquine and mepacrine in the rat, is based on the parasympatholytic property of the drugs in question.     

下丘脑室旁核胃动素对胃运动影响的探讨

目的 :研究下丘脑室旁核 (paraventricularnucleus,PVN)胃动素对胃运动调节的参与作用及机制。 方法 :应用免疫组织化学的方法检测室旁核内胃动素神经元的表达情况及室旁核与延髓迷走复合体 (dorsalvagalcomplex ,DVC)间的神经联系 ,应用室旁核内微量注入胃动素的方法观察清醒大鼠胃运动的变化。结果 :①下丘脑室旁核有胃动素免疫阳性细胞 ,在饥饿组和十二指肠灌酸组 ,阳性细胞数有明显增加 (P <0 .0 1)。②迷走背核注入辣根过氧化物酶 (horseradishperoxidase ,HRP) ,在室旁核发现HRP标记细胞 ,证实室旁核与DVC间的纤维联系。③清醒大鼠室旁核内微量注射胃动素可使胃运动的幅度和频率明显增加 (P <0 .0 5 ) ,切断双侧膈下迷走神经后 ,胃动素对胃运动的作用消失。结论 :下丘脑室旁核内胃动素可增强胃运动 ,其作用可能是通过下丘脑 延髓迷走复合体 迷走神经实现的     

The effect of extragastric vagotomy on gastric emptying and motility of the small intestine

Selective parasympathetic denervation of small and some large intestine has been performed in dogs. Chronic experiment on these dogs has revealed that this operation: has no effect on frequency and amplitude of intestine contractions during the first phase of the digestive process but it is accompanied by significant relaxation of the motor intestine activity in the second phase, causes a retardation of the rate of evacuation from stomach by 56.0% in dogs subjected to extragastric vagotomy as well as pH of chyme in the duodenum by 1-1.5 units above the norm.     

Excitatory regulation of angiotensin II on gastric motility and its mechanism in guinea pig

In the present study, we investigated the effect of Ang II on gastric smooth muscle motility and its mechanism using intracellular recording and whole-cell patch clamp techniques. Ang II dose-dependently increased the tonic contraction and the frequency of spontaneous contraction in the gastric antral circular smooth muscles of guinea pig. ZD7155, an Ang II type 1 receptor (AT(1)R) blocker, completely blocked the effect of Ang II on the spontaneous contraction of gastric smooth muscle. In contrast, TTX, a sodium channel blocker, failed to block the effect. Furthermore, nicardipine, a voltage-gated Ca(2+)-channel antagonist, did not block the effect of Ang II on the tonic contraction of gastric smooth muscle, but external free-calcium almost completely blocked this effect. Both ryanodine, an inhibitor of calcium-induced Ca(2+) release (CICR) from ryanodine-sensitive calcium stores, and thapsigargin, which depletes calcium in calcium stores, almost completely blocked the effect of Ang II on tonic contraction. However, 2-APB, an inositol trisphosphate (IP(3)) receptor blocker, significantly, but not completely, blocked the Ang II effect on tonic contraction. We also determined that Ang II depolarized membrane potential and increased slow wave frequency in a dose-dependent manner. It also inhibited delayed rectifying potassium currents in a dose-dependent manner, but did not affect L-type calcium currents or calcium-activated potassium currents. These results suggest that Ang II plays an excitatory regulation in gastric motility via AT(1)R-IP(3) and the CICR signaling pathway. The Ang II-induced inhibition of delayed rectifying potassium currents that depolarize membrane potential is also involved in the potentiation of tonic contraction and the frequency of spontaneous contraction in the gastric smooth muscle of guinea pig.     

The stomach as a bioreactor: dietary lipid peroxidation in the gastric fluid and the effects of plant-derived antioxidants.

Atherosclerosis may result partly from processes that occur following food consumption and that involve oxidized lipids in chylomicrons. We investigated reactions that could occur in the acidic pH of the stomach and accelerate the generation of lipid hydroperoxides and co-oxidation of dietary constituents. The ability of dietary polyphenols to invert catalysis from pro-oxidation to antioxidation was examined. The acidic pH of gastric fluid amplified lipid peroxidation catalyzed by metmyoglobin or iron ions. Metmyoglobin catalyzed peroxidation of edible oil, resulting in 8-fold increase of hydroperoxide concentration. The incubation of heated muscle tissue in simulated gastric fluid for 2 h enhanced hydroperoxides accumulation by 6-fold to 1200 microM. In the presence of catechin or red wine polyphenols, metmyoglobin catalyzed the breakdown of hydroperoxides to zero, totally preventing lipid peroxidation and beta-carotene cooxidation. We suggest that human gastric fluid may be an excellent medium for enhancing the oxidation of lipids and other dietary constituents. The results indicate the potentially harmful effects of oxidized fats intake in the presence of endogenous catalysts found in foods, and the major benefit of including in the meal plant dietary antioxidants.     

Different effects of D-glucose anomers on enhanced motility of the stomach

The injection of alpha, beta, or equilibrated (alpha: 36%, beta: 64%) D-glucose solution into the cranial side of carotid artery decreased gastric pressure caused by insulin in rats with bilateral adrenalectomy. This effect was not reproduced after vagotomy at the cervical level. The effect of beta-D-glucose was more rapid and potent than that of alpha-D-glucose. The injection of isotonic NaCl solution, however, produced no change in pressure.     

Toxoplasma as a novel system for motility

Motility is a characteristic of most living organisms and often requires specialized structures like cilia or flagella. An alternative is amoeboid movement, where the polymerization/depolymerization of actin leads to the formation of pseudopodia, filopodia and/or lamellipodia that enable the cell to crawl along a surface. Despite their lack of locomotive organelles and in absence of cell deformation, members of the apicomplexan parasites employ a unique form of locomotion called gliding motility to promote their migration across biological barriers and to power host-cell invasion and egress. Detailed studies in Toxoplasma gondii and Plasmodium species have revealed that this unique mode of movement is dependent on a myosin of class XIV and necessitates actin dynamics and the concerted discharge and processing of adhesive proteins. Gliding is essential for the survival and infectivity of these obligate intracellular parasites, which cause severe disease in humans and animals.