neurogenic ulcerに関する研究

―中枢破壌における消化管病変および胃血流量について―

抄録

Neurogenic ulcer is considered to be the lesion in the alimentary tract caused by dis-turbance of the central nervous system, viz. pathological changes such as ulcer, erosion and hemorrhage. Since Rokitansky, many experimental and clinical reports are available, but many problems such as the relationship between brain localization and lesions in the alimentary tract still remain unsolved. As to the cause of gastric ulcer, problems of homeostasis of secretion, motility and circulation of the stomach have been discussed since Shay. Participation of the factor of central nervous system has been accepted without much argument. The author has paid attention to the frequent occurrence of neurogenic ulcer in cases of brain trauma with secondary necrosis localized in the posterior orbital surface of the frontal lobe. In order to study the relationship between the central nervous system and gastric function and the cause of development of peptic ulcer, the following experiments were conducted on 80 adult mongrel dogs to destroy part of the central nervous system and to study the resultant changes of the digestive tract and gastric blood flow in time course.
(1) Gastric changes secondary to the destruction of the posterior part of the frontal lobe and the antero-inferior part of the temporal lobe
In dogs anesthesized by intravenous injection of pentobarbital sodium, one pair of concentric electrodes were inserted into the brain and fixed, with the use of a stereotaxic apparatus and brain atlas by Lim et al. From the lead wire exposed out of the body, stimulation with square wave discharge of 50 cps, 10 msec and 5 V was given with a stimulator after more than 3 weeks following the operation, for 5-24 hours with 30 seconds interval to produce an area of destruction. Gastric lesion was then studied. After 24 hour stimulation, petechial hemorrhage in the stomach was found in 56%, and marked mucosal hyperemia in 33%.
Stimulation lasting less than 10 hours caused petechial hemorrhage in the stomach in 25% of cases. In animals without stimulation despite the indwelling electrodes and in controls without indwelling electrodes, no changes such as petechial hemorrhage were noted.
(2) Chronological changes of the blood flow through the left gastric artery and splenic artery after destruction of posterior hypothalamus and posterior orbital surface.
With the use of operative procedure as described in (1), a pair of stainless steel wires were inserted into the posterior hypothalamus and the posterior orbital surface of the frontal lobe and fixed. The animals were immediately laparotomized, and the left gastric artery and splenic artery were stripped to the branching site and a probe of electromagnetic flow meter was inserted. An electric knife with a constant emitting power was brought into contact with the fixed electrode to destroy the local site of the brain to measure the changes of gastric blood flow. Blood flow through the carotid artery and blood pressure at the femoral artery were also recorded simultaneously. As the result, (a) destruction of the posterior hypothalamus caused an increase of the blood flow through the left gastric artery by 8.36%. Compared to the controls, a marked increase by 300% was seen 30 seconds after destruction. Throughout the whole course of 2 hours following destruction, significant difference was noted. The blood flow through the left gastric artery was increased after destruction of the posterior hypothalamus, indicating a parasympathetic effect. (b) Destruction of the posterior orbital surface of the frontal lobe, blood flow throught the left gastric artery was increased by 8.11%. Compared to the controls, increase by 298% was noted 30 seconds after destruction. Significant difference was noted throughout the whole course, except for 1 hour after destruction. The blood flow through the left gastric artery was increased after destruction of the posterior orbital surface of the frontal