Purpose
An organism receives internal and external stimuli successively. If the function of the organism become abnormal, the abnormality is projected on its body surface. Accordingly the condition of the organism's function can be grasped by palpation or other objective measuring methods.
Among these methods, we commonly put skin-electroresistance meters in clinical use.
However, the variation of the organism's function in a healthy condition has not been quantitatively grasped, while there are data on the variation of the values obtained from sick patients.
The purpose of this study is to investigate the variation of values obtained from subjects in a healthy condition in order to grasp the abnormal variation of values more exactly.
Method
Subjects were sixth-year pupils of Osaka Municial Elementary School of Higashi Awaji. Neurometory was sutomatically recorded at the regular points 0.75 second after the onset of the measurement, with a neurometer (Improved Model D-401; Noiro Ika Kogyo Inc.) adjusted at 12V, 200mV.
Result
Excited H₆ large intestine channels, and inhibited F₂ liver channels and F₆ stomach channels were frequently seen as in the same time of other years.
Unlike adult subjects, the current intensity was low in the Yong meridians of the hand (H4, 5, 6), and high in the Yin meridians of the hand and the foot (H1, 2, 3, F1, 2, 3).

PURPOSE: Patients treated with propranolol, a nonselective β-adrenoceptor antagonist, develop severe anaphylaxis, but the mechanism remains unknown. We determined effects of β₁- and β₂-adrenoceptor antagonists on the anaphylaxis-induced increase in vascular permeability in mice. METHODS: In anesthetized ovalbumin-sensitized C57BL mice, mean arterial blood pressure (MBP) was measured, and Evans blue dye extravasation and hematocrit (Hct) were assessed at 20 minutes after antigen injection. The following pretreatment groups (n=7/group) were studied: (1) sensitized control (non-pretreatment), (2) propranolol, (3) the selective β₂-adrenoceptor antagonist ICI 118,551, (4) the selective β₁-adrenoceptor antagonist atenolol, (5) adrenalectomy, (6) the selective β₂-adrenoceptor agonist terbutaline, and (7) non-sensitized groups. RESULTS: The antigen injection decreased MBP, and increased Hct and vascular permeability in the kidney, lung, mesentery, and intestine, but not in the liver or spleen. Pretreatment with ICI 118,551, propranolol and adrenalectomy, but not atenolol, reduced the survival rate and augmented the increases in Hct and vascular permeability in the kidney, intestine, and lung as compared with the sensitized control group. Pretreatment with terbutaline abolished the antigen-induced alterations. Plasma epinephrine levels were increased significantly in the sensitize control mice. CONCLUSIONS: Blockade of β₂-adrenoceptor can deteriorate systemic anaphylaxis by augmenting hyperpermeability-induced increase in plasma extravasation by inhibiting beneficial effects of epinephrine released from the adrenal glands in anesthetized mice.
Adrenal Glands ; Adrenalectomy ; Anaphylaxis ; Animals ; Arterial Pressure ; Atenolol ; Capillary Permeability ; Epinephrine ; Evans Blue ; Hematocrit ; Humans ; Intestines ; Kidney ; Liver ; Lung ; Mesentery ; Mice ; Mice, Inbred C57BL ; Plasma ; Propranolol ; Spleen ; Survival Rate ; Terbutaline

PURPOSE: Anaphylactic shock is sometimes accompanied by local interstitial edema due to increased vascular permeability. We performed magnetic resonance imaging (MRI) to compare edema in the larynx and brain of anesthetized rats during anaphylactic hypotension versus vasodilator-induced hypotension. METHODS: Male Sprague Dawley rats were subjected to hypotension induced by the ovalbumin antigen (n=7) or a vasodilator sodium nitroprusside (SNP; n=7). Apparent diffusion coefficient (ADC) and T2-relaxation time (T2RT) were quantified on MRI performed repeatedly for up to 68 min after the injection of either agent. The presence of laryngeal edema was also examined by histological examination. Separately, the occurrence of brain edema was assessed by measuring brain water content using the wet/dry method in rats with anaphylaxis (n=5) or SNP (n=5) and the non-hypotensive control rats (n=5). Mast cells in hypothalamus were morphologically examined. RESULTS: Mean arterial blood pressure similarly decreased to 35 mmHg after an injection of the antigen or SNP. Hyperintensity on T2-weighted images (as reflected by elevated T2RT) was found in the larynx as early as 13 min after an injection of the antigen, but not SNP. A postmortem histological examination revealed epiglottic edema in the rats with anaphylaxis, but not SNP. In contrast, no significant changes in T2RT or ADC were detectable in the brains of any rats studied. In separate experiments, the quantified brain water content did not increase in either anaphylaxis or SNP rats, as compared with the non-hypotensive control rats. The numbers of mast cells with metachromatic granules in the hypothalamus were not different between rats with anaphylaxis and SNP, suggesting the absence of anaphylactic reaction in hypothalamus. CONCLUSION: Edema was detected using the MRI technique in the larynx during rat anaphylaxis, but not in the brain.
Anaphylaxis ; Animals ; Arterial Pressure ; Brain ; Brain Edema ; Capillary Permeability ; Diffusion ; Edema ; Hypotension ; Hypothalamus ; Laryngeal Edema ; Larynx ; Magnetic Resonance Imaging ; Male ; Mast Cells ; Nitroprusside ; Ovalbumin ; Rats ; Rats, Sprague-Dawley

PURPOSE: Anaphylactic shock is sometimes accompanied by local interstitial edema due to increased vascular permeability. We performed magnetic resonance imaging (MRI) to compare edema in the larynx and brain of anesthetized rats during anaphylactic hypotension versus vasodilator-induced hypotension. METHODS: Male Sprague Dawley rats were subjected to hypotension induced by the ovalbumin antigen (n=7) or a vasodilator sodium nitroprusside (SNP; n=7). Apparent diffusion coefficient (ADC) and T2-relaxation time (T2RT) were quantified on MRI performed repeatedly for up to 68 min after the injection of either agent. The presence of laryngeal edema was also examined by histological examination. Separately, the occurrence of brain edema was assessed by measuring brain water content using the wet/dry method in rats with anaphylaxis (n=5) or SNP (n=5) and the non-hypotensive control rats (n=5). Mast cells in hypothalamus were morphologically examined. RESULTS: Mean arterial blood pressure similarly decreased to 35 mmHg after an injection of the antigen or SNP. Hyperintensity on T2-weighted images (as reflected by elevated T2RT) was found in the larynx as early as 13 min after an injection of the antigen, but not SNP. A postmortem histological examination revealed epiglottic edema in the rats with anaphylaxis, but not SNP. In contrast, no significant changes in T2RT or ADC were detectable in the brains of any rats studied. In separate experiments, the quantified brain water content did not increase in either anaphylaxis or SNP rats, as compared with the non-hypotensive control rats. The numbers of mast cells with metachromatic granules in the hypothalamus were not different between rats with anaphylaxis and SNP, suggesting the absence of anaphylactic reaction in hypothalamus. CONCLUSION: Edema was detected using the MRI technique in the larynx during rat anaphylaxis, but not in the brain.
Anaphylaxis ; Animals ; Arterial Pressure ; Brain ; Brain Edema ; Capillary Permeability ; Diffusion ; Edema ; Hypotension ; Hypothalamus ; Laryngeal Edema ; Larynx ; Magnetic Resonance Imaging ; Male ; Mast Cells ; Nitroprusside ; Ovalbumin ; Rats ; Rats, Sprague-Dawley

A 47-year-old male complaining of dyspnea and fever was admitted to our hospital and regurgitation of the aortic and mitral valves with mitral valve aneurysm due to infective endcarditis was diagnosed. The non-coronary and the right coronary cusps of the aortic valve had amount of vegetations, and also the anterior leaflet of the mitral valve had an aneurysm with vegetations. Both aortic and mitral valve replacement were performed. The postoperative clinical course was uneventful.