The correlation of between the endoscopic findings of esophageal varices and endoscopic ultrasound findings of the collaterals outside the esophageal wall in patients with portal hypertension remains unclear. We investigated the relationship between esophageal varices and the collaterals by endoscopy and endoscopic ultrasound. Moreover, we investigated the correlation between the collaterals around the esophagus and recurrence of esophageal varices in patients with portal hypertension who had undergone endoscopic injection sclerotherapy. The collaterals were divided into two groups : 1 ; those with peri-esophageal collateral veins (peri-ECVs) adjacent to the muscularis externa of the esophagus, and 2 ; those with para-esophageal collateral veins (para-ECVs) distal to the esophageal wall without contact with the muscularis externa. Peri-and para-ECVs were scored as mild or severe according to the stage of development. According to endoscopy, the varix form was significantly larger in severe peri-ECVs group than in mild peri-ECVs group. In contrast, the varix form did not differ significantly between the mild and severe para-ECVs group. The prevalence of perforating veins increased according to the varix form. With regard to variceal recurrence, in patients with variceal recur-rences, EUS findings included a significantly higher incidence of severe-type peri-ECVs, a significantly larger number of perforating veins, and a significantly larger diameter of perforating veins compared with patients without recurrence. Moreover, when EUS found the abnormalities when no endoscopic recurrence was found, the results were the almost same as the findings when EUS was performed at the same time when endoscopic recurrence was found. In conclusion, the presence of severe peri-ECVs and large perforating veins in the esophageal wall strongly correlates with occurrence and recurrence of esophageal varices in patients with portal hypertension. An understanding of these EUS abnormalities on the basis of hemodynamics around the esophagus is thought to be important for management of esophageal varices in patients with portal hypertension.
It has been proposed that T helper (Th) 2 cells play a key role in the pathogenesis of atopic dermatitis (AD) because of clinical and experimental findings including hyper IgE, eosinophilia and Th2 type cytokine overexpression, etc. In contrast, several observations such as Th1 type cytokine detection in chronic lesions and histological features resembling allergic contact dermatitis suggest that Th1 rather than Th2 cells are important for the pathogenesis of skin lesions. In order to clarify this paradox, we investigated the function of T cell clones established from AD patients. Most T cell clones induced by house dust mite antigen and interleukin (IL)-2 from peripheral blood mononuclear cells of two AD patients exhibited CD4+/CD8−, CD45RO+/CD45RA−, and produced high levels of IL-4 and low levels of interferon-γ (IFN-γ) after phytohemagglutinin (PHA) (1 μg/ml) stimulation, suggesting a Th2 subtype. When stimulated with a high dose of concanavalin A (conA) (10 μg/ml), however, these clones produced high amounts of IFN-γ. IL-4 production reached a peak 24 hours after conA (10 μg/ml) stimulation, whereas IFN-γ production was increased up to 48 hours after stimulation. The findings of T cell receptor (TCR) stimulation with immobilized anti-CD3 monoclonal antibody (mAb) showed that the suitable strength of TCR stimulation for IFN-γ production was higher than for IL-4. Also, in the TCR stimulated condition, the peak of IFN-γ production was later than that of IL-4. These results indicate that T cell clones which exhibited a Th2 profile under weak stimulation can produce IFN-γ in the late phase of stimulation when strong stimuli are used. The results are consistent with the previous observation that IFN-γ production prominently appears in the chronic and late phase lesions of AD.
An isolated rabbit aortic preparation, on which administered drugs act selectively from intimal or adventitial surface, was made. Epinephrine (0.1 nM∼10 μM) produced concentration-dependent increase of intraluminal pressure, which is due to increase of contraction of the vascular smooth muscle. Sensitivity of contractile response to epinephrine administered from intimal surface was significantly higher than that administered from adventitial surface. The contractile response to epinephrine administered from intimal surface was reduced by removal of the endothelium. Cocaine (100 μM) potentiated the contractile response to epinephrine administered from adventitial surface. Cocaine also potentiated the contractile response to high concentration of epinephrine administered from intimal surface, while the drug reduced the contractile response to low concentration of epinephrine. Methylene blue (100 μM) administered from adventitial surface produced a marked contraction, while methylene blue administered from intimal surface produced a marked relaxation. The relaxing response to methylene blue administered from intimal surface was reduced by the removal of endothelium. Prazosin (1 μM) suppressed the contractile response to methylene blue administered from adventitial surface, indicating that methylene blue released norepinephrine from adrenergic nerve terminals. The contractile response to epinephrine adminis-tered from intimal surface was reduced by methylene blue administered from intimal surface. The present study clearly demonstrated variation in mechanical response of isolated rabbit aortic preparation with intimal or adventitial surface of drug entry.
It has generally been thought that the neurogenic control of cerebral circulation is decided mainly by the autonomic nervous system. Recent studies, however, indicate that sensory nerves rich in calcitonin gene-related peptide (CGRP) are also distributed on cerebral arteries. CGRP is one of neuropeptides that has strong vasodilative effect. This indicates that sensory nerves may antidromically dilate cerebral arteries mediated by CGRP. The aim of this study is to investigate the relationship between the CGRP containing nerves and cerebral circulation. Firstly, we developed a selective denervation model of CGRP containing nerves. The denervation was performed with intrathecal administration of capsaicin in rats. Secondly, we measured the change of regional cerebral blood flow (rCBF) during the occlusion of bilateral common carotid artery or systemic hypotension. CGRP immunoreactivity around cerebral arteries disappeared after capsaicin treatment. The rCBF during the occlusion of bilateral common carotid artery decreased more in the capsaicin group than in the control group. There was no significant difference in the changes of rCBF during systemic hypotension. These results showed that CGRP containing nerves would participate in the vascular response of cerebral arteries. It is likely that sensory nerves with CGRP should have antidromic effect on cerebral circulation.