Gastric phenotypic expression indicated by paradoxical concanavalin A (Con A) staining for class III mucins and the immunoperoxidase method for pepsinogen (Pg) I and Pg II was found in pyloric gland metaplasia of gallbladder epithelium. Using the same methods, the features of gallbladder cancers and their relationship to pyloric gland metaplasia in the human gallbladder epithelium were studied. Histologically, 57 gallbladder cancers were classified into 5 papillary adenocarcinomas, 29 tubular adenocarcinomas, 8 poorly differentiated adenocarcinomas, 6 signet-ring cell carcinomas, 4 mucinous adenocarcinomas, and 5 squamous cell carcinomas. In papillary and tubular adenocarcinomas, Pg I and/or Pg II staining was detected in 80% and 75.9% of cancers, respectively. Pg II staining was significantly more frequent than Pg I staining. One signetring cell carcinoma also had Pg II activity. Pyloric gland metaplasias all contained class II mucins and were further classified into complete type and incomplete type on the basis of presence or absence Pg I and/or Pg II activities. A few cancer cells with class III mucins were negative for Pg staining; conversely, a few cells with Pg I and/or Pg II had no class III mucins. Phenotypic diversity in both class II mucin reactivity and Pg activities was observed in gallbladder cancer cells with the pyloric gland cell type. By comparison, pyloric gland metaplasia varied only in Pg activities. A few Pg-positive cancers were found in the gallbladder with Pg-negative pyloric gland metaplasia. The present results clearly indicate the appearance of gastric phenotypic expression in both gallbladder epithelium and gallbladder cancers and suggest the independent induction of pyloric gland metaplasia and cancer with gastric phenotypic expression.
EVIDENCE NOW EXISTS that there are at least 2 types of adrenergic innervation of cerebral vessels, one from the cervical sympathetic plexus innervating mainly extracerebral arteries, but also reaching cerebral arterioles of 15 n diameter 1 ' 2 and the other originating in the locus ceruleus and impinging directly on the walls of intramedullary arterioles. 36The influences of these vascular neurogenic systems on cerebral circulatory physiology or metabolism are still not understood.Results of recent physiologic studies of the cerebral sympathetic system have been inconsistent, 7 " 10 probably reflecting the variety of animal models and methodology. There is evidence, however, that the sympathetic innervation of cerebral vessels influences vascular reactivity to changes in Paco 2 and Pao 2 and in some way functions to help maintain autoregulation. 1113 Harper recently proposed that the sympathetic nervous system is the coarse adjuster of cerebral blood flow (CBF), as contrasted to the fine control exerted by tissue metabolism. 14 The concept that mechanisms intrinsic to the brainstem, and probably neurogenic in character, are capable of influencing CBF and cerebral metabolic rate is supported by a variety of studies. Pial and cortical flow, as well as cerebral metabolism, may be increased by electrical stimulation of many areas in the brainstem siveness of cerebral vessels to CO 2 . 21 It has been suggested that these phenomena have a neurogenic origin, mediated by intramedullary neurons whose axons exit the brainstem in the fifth or seventh cranial nerves and eventually innervate cortical arteries. 23- 24 The recent discovery by immunofluorescence studies of an intramedullary adrenergic system speaks for direct neuronal action on parenchymal vessels as one basis for intrinsic control of CBF and metabolism. -*•2S The present experiments were designed to separate and define the roles of the intrinsic and extrinsic cerebral adrenergic neurons in the control of CBF and cerebral energy metabolism. Extrinsic adrenergic neurons are concerned with cerebral vascular autoregulation; the intrinsic (parenchymal) adrenergic system is essential to the metabolic regulation of CBF. MethodsStudies were performed on groups of male Wistar rats weighing between 250 and 350 grams and were designed to examine the effects of unilateral cervical sympathetic denervation on homolateral CBF and vascular resistance and the effects of certain drugs which alter both central and peripheral neuronal monoamine metabolism (reserpine) or block specific actions of monoamines on alpha and beta receptors of cerebral neurons and blood vessels (phenoxybenzamine, propranolol). In order to accomplish this, it was necessary to devise a system of internal controls to minimize the variables. Two major groups of animals were studied: one received no drugs and the other received reserpine, phenoxybenzamine, or propranolol. The animals in group 1 were divided into
An unusual case of pheochromocytoma associated with renal artery stenosis is described. Despite the removal of bilateral adrenal pheochromocytoma, laboratory findings suggested the presence of residual pheochromocytoma and abdominal aortography revealed more pronounced stenosis of the right renal artery. Two months later, the undetected residual pheochromocytoma underwent hemorrhagic necrosis with acute cessation of catecholamine release. Thereafter, the patient's blood pressure decreased to a normal level with marked improvement in hypertensive symptoms. No remaining stenosis was demonstrated on follow up renal angiography. Our case suggests that constant local secretion of catecholamines may be responsible for the development of renal artery stenosis.
A 9 year old Japanese girl was admitted complaining of left hypochondrial pain and a large upper left abdominal tumor. There were no clinical or laboratory signs of hormonal abnormality. Intravenous pyelography showed marked compression and deformity of the kidney by a tumor. This tumor was excised together with the left kidney. The pathological diagnosis was adrenocortical carcinoma. Postoperatively, the child was given neither irradiation nor chemotherapy. Twenty-one months after the surgery, there was a hepatic metastasis, and she died 40 months after surgery from a combination of hepatic metastases and local tumor recurrence.
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