No abstract available.
Aorta* ; Endothelium-Dependent Relaxing Factors*

No abstract available.
Blood Pressure* ; Obesity*

BACKGROUND AND OBJECTIVES: Nitric oxide (NO) reduces the intracellular Ca2+ concentration ([Ca2+]i) in smooth muscle cells, whereas the effect of NO on [Ca2+]i in endothelial cells is still controversial. Therefore, the effect of NO on the [Ca2+]i, and its mechanism in mouse aortic endothelial cells (MAEC) and human umbilical vein endothelial cells (HUVEC) were examined. MATERIALS AND METHODS: In primary cultured MAEC and HUVEC, cells were loaded with fura 2-AM and [Ca2+]i and measured using a microfluorometer. RESULTS: The NO donor, sodium nitroprusside (SNP), reduced the [Ca2+]i in 72% of the cells tested (n=100). In the remaining cells, the effect of SNP was biphasic, or the [Ca2+]i was increased. In addition, the membrane-permeable cGMP, 8-bromo cGMP, decreased the [Ca2+]i. The effects of SNP and 8-bromo cGMP were inhibited by the soluble guanylate cyclase inhibitor, 1H-[1,2,4] oxadiazole[4,3-a]quinoxalin-1-one (ODQ), and the cGMP-dependent protein kinase inhibitor, KT5823, respectively. In contrast, in the presence of 8-bromo cGMP or ODQ, SNP increased the [Ca2+]i. CONCLUSION: These results suggest that NO inhibits the [Ca2+]i through a cGMP-dependent mechanism and increases the [Ca2+]i through a cGMP-independent mechanism.
Animals ; Cyclic GMP ; Endothelial Cells* ; Endothelium ; Guanylate Cyclase ; Human Umbilical Vein Endothelial Cells ; Humans ; Mice ; Myocytes, Smooth Muscle ; Nitric Oxide ; Nitroprusside ; Protein Kinases ; Tissue Donors

No abstract available.
Neuroma*

Acinic cell carcinoma is a slow-growing solid neoplasm of salivary gland. Although their cytological and histological finding is bland-looking, their biological behavior is unpredictable. We experienced two cases of acinic cell carcinoma of the salivary gland diagnosed by fine needle aspiration biopsy and confirmed by tissue examination. They showed different clinical courses. We compared their cytologic and histologic findings. The first case was a right preauricular mass in a 58 year-old female of 3 years duration. The cytologic smear revealed sheets or small clusters of monotonous cells mimicking normal serous acinar cells with little cellular pleomorphism. She underwent superficial parotid lobectomy. The tumor was a well demarcated 1.5cm sized nodular mass without infiltration into surrounding parenchyme. The second case was a left submandibular mass in a 23 year-old male of 4 years duration. The smear showed more severe pleomorphism of the tumor cells than those of previous case. Excisional biopsy was done. The excised tumor was 5.5*3.5*3cm sized multilobulated solid mass with invasion into surrounding parenchyme. The tumor recurred after 20months, thus total excision of the mass and modified radical neck dissection was carried out. From the above findings, cytologic atypism, infiltrative growth pattern and type of initial therapy may be correlated with biologic behavior.
Acinar Cells* ; Biopsy ; Biopsy, Fine-Needle ; Carcinoma, Acinar Cell* ; Female ; Humans ; Male ; Middle Aged ; Neck Dissection ; Salivary Glands* ; Young Adult

The present study was designed: (1) to determine whether or not hypoxia stimulates the release of endothelium-derived relaxing factors (EDRFs) from endothelial cells, and (2) to examine whether or not the hypoxia-induced EDRFs release is further augmented by previous hypoxia-reoxygenation, using vessel and rabbit carotid artery without endothelium as a bioassay test ring. The test ring was contracted by prostaglandin F2alpha, (3 X 10-6 M/L), which was added to the solution perfuming through the aortic segment. Hypoxia was evoked by switching the solution aerated with 95% 02/5% CO2 mixed gas to one aerated with 95% N2/5% CO2 mixed gas. When the contraction induced by prostaglandin F2alpha reached a steady state, the solution was exchanged for hypoxic one. And then, hypoxia and reoxygenation were interchanged at intervals of 2 minutes (intermittent hypoxia). The endothelial cells were also exposed to single 10-minute hypoxia (continuous hypoxia). When the bioassay ring was superfused with the perfusate through intact aorta, hypoxia relaxed the precontracted bioassay test ring markedly. Whereas, when bioassay ring was superfused with the perfusate through denuded aorta or polyethylene tubing, hypoxia relaxed the precontracted ring slightly. The relaxation was not inhibited by indomethacin but by nitro-L-arginine or methylene blue. The hypoxia-induced relaxation was further augmented by previous hypoxia-reoxygenation and the magnitude of the relaxation by intermittent hypoxia was significantly greater than that of the relaxation by continuous hypoxia. The results suggest that hypoxia stimulates EDNO release from endothelial cells and that the hypoxia-induced EDNO release is further augmented by previous hypoxia-reoxygenation.
Anoxia* ; Aorta ; Biological Assay ; Carotid Arteries ; Dinoprost ; Endothelial Cells ; Endothelium* ; Endothelium-Dependent Relaxing Factors ; Indomethacin ; Methylene Blue ; Nitric Oxide ; Polyethylene ; Relaxation

BACKGROUND: Extracellular K+ concentration ([K+]o) can be increased within several mM by the efflux of intracellular K+. To investigate the effect of an increase in [K+]o on vascular contractility, we attempted to examine whether extracellular K+ might modulate vascular contractility, endothelium-dependent relaxation (EDR) and intracellular Ca2+ concentration ([Ca2+]i) in endothelial cells (EC). MATERIAL AND METHOD: We observed isometric contractions in rabbit carotid, superior mesentery, basilar arteries and mouse aorta. [Ca2+]i was recorded by microfluorimeter using Fura-2/AM in EC. RESULT: No change in contractility was recorded by the increase in [K+]o from 6 to 12 mM in conduit artery such as rabbit carotid artery. whereas resistant vessels, such as basilar and branches of superior mesenteric arteries (SMA), were relaxed by the increase. In basilar artery, the relaxation by the increase in [K+]o from 1 to 3 mM was bigger than that by the increase from 6 to 12 mM. In contrast, in branches of SMA, the relaxation by the increase in [K+]o from 6 to 12 mM is bigger than that by the increase from 1 to 3 mM. Ba2 (30microM) did not inhibit the relaxation by the increase in [K+]o from 1 to 3 mM but did inhibit the relaxation by the increase from 6 to 12 mM. In the mouse aorta without the endothelium or treated with NG-nitro-L-arginine (30microM), nitric oxide synthesis blocker, the increase in [K+]o from 6 to 12 mM did not change the magnitude of contraction induced either norepinephrine or prostaglandin F2alpha. The increase in [K+]o up to 12 mM did not induce contraction of mouse aorta but the increase more than 12 mM induced contraction. In the mouse aorta, EDR was completely inhibited on increasing [K+]o from 6 to 12 mM. In cultured mouse aorta EC, [Ca2+]i was increased by acetylcholine or ATP application and the increased [Ca2+]i was reduced by the increase in [K+]o reversibly and concentration-dependently. In human umbilical vein EC, similar effect of extracellular K+ was observed. Ouabain, a Na+-K+ pump blocker, and Ni2 , a Na+-Ca2+ exchanger blocker, reversed the inhibitory effect of extracellular K+. CONCLUSION: In resistant arteries, the increase in [K+]o relaxes vascular smooth muscle and the underlying mechanisms differ according to the kinds of the arteries; Ba2 -insensitive mechanism in basilar artery and Ba2 -sensitive one in branches of SMA. It also inhibits [Ca2+]i increase in EC and thereby EDR. The initial mechanism of the inhibition may be due to the activation of Na+-K+ pump.
Acetylcholine ; Adenosine Triphosphate ; Animals ; Aorta ; Arteries ; Basilar Artery ; Calcium ; Carotid Arteries ; Dinoprost ; Endothelial Cells ; Endothelium ; Endothelium-Dependent Relaxing Factors ; Humans ; Isometric Contraction ; Mesenteric Artery, Superior ; Mesentery ; Mice ; Muscle, Smooth, Vascular* ; Nitric Oxide ; Nitroarginine ; Norepinephrine ; Ouabain ; Potassium ; Relaxation* ; Umbilical Veins ; Vasodilation

PURPOSE: To characterize the MR findings for a differential diagnosis and to make a plan for treatment by interventional technique of the vascular masses with/without hypertrophic feeding vessels of the head and neck. SUBJCETS AND METHODS: Seven patients with vascular masses of the head and neck proved by pathology, angiography, clinical findings were included. Vascular masses included 4 venous malformations, a capillary hemangioma, and a hemangiopericytoma, a hemangioma combined with arteriovenous malformation. 7 patients had MR studies with 1.0T and 1.5T using routine TI-, T2- weighted spin echo sequences, and contrast enhancement. 4 MR angiography, 3 inversion recovery, and 6 contrast angiography were studied from 7 patients RESULTS: All vascular masses demonstrated higher than muscle signal intensity on Tl-weighted images, bright signal intensity on T2-weighted images, and prominent enhancement, except AV hemangioma combined with prominent arteriovenous malformation on postcontrast scan. Three hemangiomas demonstrated distinct serpiginous signal voids. Venous malformations demonstrated venous lakes seen as homogenous regions of high signal intensity and phleboliths seen as low signal foci on images. Inversion recovery was the best pulse sequence for evaluation of the extent of lesion. CONCLUSION: MR findings of the vascular masses of the head and neck are useful in delineating the extent of the disease, differentiating venous malformation or cavernous hemangioma from other hemangiomatous lesions including hypertrophic feeding vessels, and making a plan for treatment by interventional technique also.
Angiography ; Arteriovenous Malformations ; Diagnosis, Differential* ; Head* ; Hemangioma ; Hemangioma, Capillary ; Hemangioma, Cavernous ; Hemangiopericytoma ; Humans ; Lakes ; Neck* ; Pathology

Deteriorated mental status and new neurological deficits after head trauma signify the formation of intracranial hematoma or brain edema. In a case of head trauma accompanied by basal skull fracture, even if without intracranial hematoma formation or edema, we should be alert to the possibility of injury of the petrosal carotid artery which needs prompt diagnostic evaluation and management. We report a case of traumatic cerebral infarction due to injury of the petrosal internal carotid artery and review the literatures.
Brain Edema ; Carotid Arteries ; Carotid Artery, Internal* ; Cerebral Infarction* ; Craniocerebral Trauma* ; Edema ; Head* ; Hematoma ; Skull Fractures

PURPOSE: Among many pathophysiologic mechanisms of hypoxic-ischemic brain injury, reactive oxygen species (ROS) cause or contribute to brain damage relates to their ability to attack the fatty acid moiety of plasma and subcellular membranes. Because ROS are generated by hypoxia-ischemia especially during reperfusion period of recovery, repetitive hypoxia-reoxygenation in newborn brain may result in more severe damage than a similar single insult. It is to determine whether repetitive hypoxia-reoxygenation may produce more ROS than a similar single insult in newborn rat brain. METHODS: We compared the production of lipid peroxidation in 3 days old rat brain following normoxia, repetitive hypoxia-reoxygenation and an equal duration of sustained hypoxia-reoxygenation by measuring 8-isoprostane-F2alpha. 8-isoprostane-F2alpha is free radical catalyzed metabolites of arachidonic acid, which is produced independent of cyclooxygenase. RESULTS: Compared to a single duration hypoxia-reoxygenation, repetitive hypoxia- reoxygenation produce more ROS (8-isoprostane-F2alpha) in newborn rat brain (P < 0.005). CONCLUSION: It can be speculated that repetitive hypoxia is more detrimental than equal duration of single insult in new born rat brain. Relations between increased ROS production and brain injury following repetitive hypoxia-reoxygenation should be evaluated.
Animals ; Anoxia* ; Arachidonic Acid ; Brain Injuries ; Brain* ; Humans ; Infant, Newborn* ; Lipid Peroxidation* ; Membranes ; Plasma ; Prostaglandin-Endoperoxide Synthases ; Rats* ; Reactive Oxygen Species ; Reperfusion