BACKGROUND: Nitric Oxide (NO) has been discovered to be an important endothelium-derived relaxing factor. The exogenous inhaled NO may diffuse from the alveoli to pulmonary vascular smooth muscle and produce pulmonary vasodilation, but any NO that diffuses into blood will be inactivated before it can produce systemic effects. To examine the effects of NO on pulmonary and systemic hemodynamics, NO was inhaled by experimental dogs in an attempt to reduce the increase in pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) induced by hypoxia in dogs. METHODS: Eight mongrel dogs were studied while inhaling 1)50% O2 (baseline), 2)12% O2 in N2 (hypoxia), 3)followed by the same hypoxic gas mixture of O2 and N2 containing 20, 40 and 80 ppm of NO, respectively. RESULTS: Breathing at FIO2 0.12 nearly doubled the pulmonary vascular resistance from 173 56dyn sec cm-5 to 407 139dyn sec cm-5 and significantly increased the mean pulmonary artery pressure from 16 3mmHg to 22 4mmHg. After adding 20~80 ppm NO to the inspired gas while maintaining the FIO2 at 0.12, the mean pulmonary artery pressure decreased (p<0.05) to the level when breathing oxygen at FIO2 0.5 while the PaO2 and PaCO2 were unchanged. The pulmonary vascular resistance decreased significantly and the right ventricular stroke work index returned to a level similar to breathing at FIO2 0.5 by addition of NO into the breathing circuit. Pulmonary hypertension resumed within 3~5 minutes of ceasing NO inhalation. In none of our studies did inhaling NO produce systemic hypotension and elevate methemoglobin levels. CONCLUSIONS: Inhalation of 20~80 ppm NO selectively induced pulmonary vasodilation and reversed hypoxic pulmonary vasoconstriction without causing systemic vasodilation and bronchodilation. Methemoglobin and NO2 were within normal limit during the study.
Animals ; Anoxia ; Dogs ; Endothelium-Dependent Relaxing Factors ; Hemodynamics* ; Hypertension, Pulmonary ; Hypotension ; Inhalation* ; Methemoglobin ; Muscle, Smooth, Vascular ; Nitric Oxide* ; Oxygen ; Pulmonary Artery ; Respiration ; Stroke ; Vascular Resistance ; Vasoconstriction* ; Vasodilation

BACKGROUND: Naringin, one of the flavonoids in citrus fruit peels, is known to have antioxidant and hepatotonic effects in animal studies. We evaluated the effect of naringin on 1) blood lipid profiles, 2) regression of fatty streak of aorta, and 3) liver toxicity in diet-induced hypercholesterolemic rabbits. METHODS: New Zealand White Rabbits (2.0 - 2.5 Kg) were divided to three groups; group without treatment, group treated with 100 mg/kg/d or 500 mg/kg/d naringin, and group treated with 1 mg/kg/d or 20 mg/kg/d lovastatin. They were fed on 0.25% or 1.0% cholesterol-containing diet for 8 weeks and then sacrificed. Blood samples were collected for measurement of total cholesterol, HDL-cholesterol, triglyceride, serum GOT and GPT. Aortas and livers were harvested for evaluation of fatty streak and pathologic examination. RESULTS: 1)Feeding of 1% cholesterol diet for eight weeks significantly increased the cholesterol level upto 20 folds. Neither lovastatin nor naringin did lower these marked hypercholesterolemia. But both naringin (500 mg/kg/d) and lovastatin (1 mg/kg/d) significantly reduced the area of fatty streak by 75% and 58%, respectively. Naringin was more effective in inhibition of fat infiltration into liver than lovastatin which showed hepatotoxicity as increase of serum GPT level (p=0.01). 2)Feeding of 0.25% cholesterol diet for eight weeks significantly increased the cholesterol level upto 17 folds. Total cholesterol and triglyceride levels tended to decrease by treatment with naringin (500 mg/kg/d) and lovastatin (20 mg/kg/d), but this decreases were not statistically significant. However, areas of fatty streak significantly decreased by treatment with naringin and lovastatin by 64 and 82%, respectively (p<0.05). Microscopic analysis revealed that foam cell infiltration into intima was significantly reduced by naringin and lovastatin. In contrast to lovastatin, naringin significantly reduced the level of serum GPT (p<0.05). CONCLUSION: Like lovastatin, naringin has strong antiatherogenic action which may not be associated with its very mild lipid lowering action. In contrast to lovastatin, naringin does have hepatoprotective effect.
Animals ; Aorta ; Cholesterol ; Citrus ; Diet ; Flavonoids ; Foam Cells ; Hypercholesterolemia ; Liver ; Lovastatin ; Rabbits* ; Triglycerides

BACKGROUND AND OBJECTIVES: The causative role of serum uric acid has been controversial in Benign paroxysmal positional vertigo (BPPV). The aim of this study was vto determine the role of serum uric acid in developing idiopathic BPPV. MATERIALS AND METHODS: We recruited 168 consecutive patients with a confirmed diagnosis of idiopathic BPPV. The patients comprised 116 women (age range: 29~70 years, mean+/-SD: 55.8+/-9.7 years) and 52 men (age range: 32~70 years, mean+/-SD: 55.2+/-10.9 years). The serum uric acid levels of the patients were compared with those of 194 controls (age range: 20~70 years, mean+/-SD: 55.5+/-7.8 years) without a history of dizziness. RESULTS: The serum uric acid levels were decreased in patients with BPPV compared with those in normal controls (4.8+/-1.3 vs 5.3+/-1.3, p=0.001). However, multiple logistic regression analyses adjusted for age, sex, alcohol, smoking, hyperphosphatemia and osteopenia/osteoporosis did not demonstrate that the hypouricemia is an independent risk factor for BPPV. CONCLUSION: This study suggests that serum uric acid level is not a risk factor for developing idiopathic BPPV.
Dizziness ; Female ; Humans ; Hyperphosphatemia ; Logistic Models ; Male ; Risk Factors ; Smoke ; Smoking ; Uric Acid ; Vertigo

Migrainous vertigo is one of common recurrent vestibular disorders. Because the diagnostic criteria have not been yet settled internationally, we have a difficulty in both diagnosis and research in migraineurs with vertigo. Literature about the diagnostic criteria of migrainous vertigo and its differential diagnosis were reviewed. Until now, the criteria proposed by Neuhauser et al. is regarded as most adequate in diagnosis of migrainous vertigo. Differential diagnosis of migrainous vertigo should be guided by distinction of vestibular symptoms and nonvestibular dizziness and consider the common causes of recurrent vertigo. Just like migraine itself, migrainous vertigo is diagnosed on the basis of history and exclusion of other vestibular disorders mimicking migrainous vertigo. Therefore, delicate history taking is the most important in diagnosis and management of patients with migrainous vertigo.
Diagnosis, Differential ; Dizziness ; Humans ; Migraine Disorders ; Vertigo

No abstract available.
Carcinoma, Renal Cell* ; Prognosis*

No abstract available.
Carcinoma, Renal Cell* ; Prognosis*

No abstract available.
Humans

BACKGROUND: Extracellular ATP, released from platelets and nerve endings, plays significant roles in the regulation of circulation. The effects of ATP depend on the location of the vessels and the species of experimental animals. Until now, studies were limited to arteries, so we compared the effects of ATP in rat vena cava with those in the aorta and attempted to identify the characteristics of their receptors. METHODS: Vascular rings were isolated from the rat inferior vena cava and descending thoracic aorta. Endothelial cells were preserved or removed by gentle rubbing. The isometric contractions were recorded on polygraph using a force transducer. RESULTS: In the vena cava ring precontracted by 100 nM norepinephrine (NE), ATP elicited relaxations in a dose-dependent manner. These effects were abolished by removal of the endothelium or pretreatment with a nitric oxide synthase inhibitor. Relaxations to ATP in the vena cava (EC50 :9.9 microM) were less potent than those in the aorta (1.7 microM). The relative order of potencies was ADP>ATP>AMP>adenosine, but the maximal relaxation to ADP was smaller than to ATP. ATP-induced vasorelaxation was blocked by suramin, a nonselective antagonist for P2 purinoceptor and reactive blue-2, a P2Y blocker. At basal tension, ATP contracted the vena cava dose-dependently and these effects were potentiated by endothelium-removal. Contractions in the vena cava were also less potent than in the aorta, and the order of potencies was alpha, beta-MeATP>UTP>ATP>ADP>AMP=adenosine. ATP-induced vasoconstriction was blocked by suramin and alpha, beta-MeATP, a desensitizing antagonist of P2X purinoceptor, and potentiated by pretreatment with UTP. CONCLUSION: These results suggest that ADP and ATP acts on P2Y1- and P2Y2-purinoceptor in the endothelium, respectively and induces vasorelaxation of the vena cava, which is mediated by nitric oxide. Since ATP and UTP induced vasoconstriction in endothelium-denuded condition, it may be mediated by the activation of the P2X and P2Y4, 6 purinoceptor on smooth muscles, respectively.
Adenosine Diphosphate ; Adenosine Triphosphate ; Animals ; Aorta ; Aorta, Thoracic ; Arteries ; Endothelial Cells ; Endothelium ; Isometric Contraction ; Muscle, Smooth ; Nerve Endings ; Nitric Oxide ; Nitric Oxide Synthase ; Norepinephrine ; Rats* ; Receptors, Purinergic P2 ; Receptors, Purinergic P2X ; Receptors, Purinergic* ; Relaxation ; Suramin ; Transducers ; Uridine Triphosphate ; Vasoconstriction ; Vasodilation ; Vena Cava, Inferior*

Only a few tests can evaluate the function of the saccule and inferior vestibular nerve. Vestibular-evoked myogenic potentials (VEMP) are inhibitory potentials recorded in the contracting muscles, usually in the sternocleidomastoids (SCM), when sound stimuli are applied. A disynaptic pathway originating in the saccule is known to mediate VEMP. The main pathway of saccule-induced inhibitory postsynaptic potentials to ipsilateral SCM motoneurons seems to be the medial vestibulospinal tract which descends within the medial longitudinal fasciculus. VEMP have been applied to determine saccular function in many disorders involving the peripheral vestibular apparatus. However, the characteristics and the diagnostic values of VEMP require further exploration in central vestibulopathies. In this review, the basic principles and recording methods of VEMP are overviewed. We will also review VEMP responses found in central as well as peripheral vestibular disorders. Despite several issues that need further elucidation, such as the exact neural pathway mediating VEMP, aging effects on VEMP, and normalization of the muscle contraction during the recording, VEMP allows us exclusive information on the function of saccule and its neural pathway, which cannot be provided by other vestibular function tests.
Aging ; Brain Stem ; Cerebellum ; Contracts ; Inhibitory Postsynaptic Potentials ; Muscle Contraction ; Muscles ; Negotiating ; Neural Pathways ; Saccule and Utricle ; Vertigo ; Vestibular Function Tests ; Vestibular Nerve ; Vestibule, Labyrinth