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101.
Hoka S Takeshita A Aishima K Higashi H Takahashi S Yoshitake J 《Journal of anesthesia》1987,1(2):143-147
Adenosine triphosphate as well as sodium nitroprusside has been used for hypotensive anesthesia. The purpose of this study was to examine the possibility that two hypotensive drugs may exert different effects on venous capacitance during controlled hypotension. In rats anesthetized with ketamine, mean arterial pressure was lowered to 50mmHg by intravenous infusion of adenosine triphosphate or sodium nitroprusside. Venous capacitance was assessed before and during induced hypotension by measuring the mean circulatory filling pressure (MCFP). MCFP was measured after briefly arresting the circulation by inflating an indwelling balloon in the right atrium. MCFP was lower during adenosine triphosphate-induced as well as sodium nitroprusside-induced hypotension as compared with the respective value at control (P < 0.01 for adenosine triphosphate and sodium nitroprusside). However, the decrease in MCFP by adenosine triphosphate (0.8 ± 0.1mmHg) was less (P < 0.01) than that by sodium nitroprusside (2.3 ± 0.3mmHg). These results suggest that at a comparable level of arterial hypotension venodilator effect of adenosine triphosphate was less than that of sodium nitroprusside. Less venodilatation during adenosine triphosphate-induced hypotension may contribute to the maintenance of cardiac output during hypotensive anesthesia.(Hoka S, Takeshita A, Aishima K et al.: Venodilator effects of adenosine triphosphate and sodium nitroprusside; comparisons during controlled hypotension. J Anesth 1: 144–147, 1987) 相似文献
102.
Expression of a 72-kDa heat shock protein, and its cytoprotective function, in gastric mucosa in cirrhotic rats 总被引:8,自引:0,他引:8
Watanabe D Otaka M Mikami K Yoneyama K Goto T Miura K Ohshima S Lin JG Shibuya T Segawa D Kataoka E Konishi N Odashima M Sugawara M Watanabe S 《Journal of gastroenterology》2004,39(8):724-733
Background Portal hypertensive gastropathy (PHG) is a clinical entity that is observed frequently in patients with liver cirrhosis. In PHG, gastric mucosa is highly susceptible to mucosal injury caused by noxious agents. Many studies, including ours, have reported that a 72-kDa heat shock protein (HSP72) has a crucial cytoprotective function in gastric mucosa. In this study, we investigated the expression and cytoprotective effect of HSP72 on gastric mucosa in portal hypertensive rats.Methods PHG was produced by bile duct ligation (BDL) or carbon tetrachloride administration in male Sprague-Dawley rats. The expression of HSP72 in the gastric mucosa was evaluated by Western blotting. Induction of gastric mucosal HSP72 by 6-h water-immersion stress was compared between cirrhotic and control rats. Also, mucosal protective abilities against hydrochloric acid (HCl; 0.6N) following pretreatment with water-immersion stress to induce HSP72 were studied in both groups.Results Portal venous pressure was significantly higher in cirrhotic rats compared with control rats (P < 0.05). Baseline expression (before water-immersion stress) of mucosal HSP72 was significantly lower in cirrhotic rats compared with control rats. HCl-induced gastric mucosal lesions were significantly suppressed in control rats compared with cirrhotic rats, especially when HSP72 was preinduced by water-immersion stress.Conclusions These findings suggest that HSP72 in the gastric mucosa plays a crucial role with respect to cytoprotection; the induction of HSP72 may provide therapeutic strategies for protection against mucosal injury in PHG. 相似文献
103.
Michael H. Chase Sumio Enomoto Toshiki Murakami Yoshio Nakamura Masato Taira 《Experimental neurology》1981,71(1):226-233
Intracellular records were obtained in the chronic cat from neurons of the nucleus reticularis gigantocellularis (NGC) during naturally occurring sleep and wakefulness. When wakefulness and quiet sleep was compared with active sleep, the membrane potential level of NGC neurons gradually decreased; a depolarized membrane potential was maintained tonically and selectively throughout active sleep. These data support the concept that NGC neurons assist in the generation of somatic atonia during active sleep and suggest that this state-dependent inhibitory function may be controlled by the nucleus pontis oralis as part of the general phenomenon of reticular response reversal. 相似文献
104.
105.
Shigeo Koido Toshifumi Ohkusa Kosaburo Nakae Tetsuji Yokoyama Tomoyoshi Shibuya Naoto Sakamoto Kan Uchiyama Hiroshi Arakawa Taro Osada Akihito Nagahara Sumio Watanabe Hisao Tajiri 《World journal of gastroenterology : WJG》2014,20(22):6961-6967
AIM:To evaluate significant risk factors for incomplete colonoscopy at a Japanese academic hospital.METHODS:A total of 11812 consecutive Japanese people were identified who underwent a colonoscopy at an academic hospital.A multiple logistic regression model was used to evaluate retrospectively the significant risk factors for incomplete colonoscopy.RESULTS:The cecal intubation rate was 95.0%.By univariate analysis,age,female sex,poor bowel cleansing,and a history of abdominal or pelvic surgery were significant risk factors for incomplete colonoscopy(P<0.001).Moreover,age-and sex-adjusted analysis showed that significant risk factors for incomplete colonoscopy were female sex(OR=1.38,95%CI:1.17-1.64,P=0.0002),age≥60 years old(OR=1.44,95%CI:1.22-1.71,P<0.0001),a history of prior abdominal or pelvic surgery(OR=1.55,95%CI:1.28-1.86,P<0.0001),poor bowel cleansing(OR=4.64,95%CI:3.69-5.84,P<0.0001),and inflammatory bowel disease(IBD)(OR=1.48,95%CI:1.13-1.95,P=0.0048).In Japanese men,by age-adjusted analysis,IBD(OR=1.69,95%CI:1.18-2.43,P=0.005)was an independent risk factor for incomplete colonoscopy.CONCLUSION:Several characteristics in the Japanese population were identified that could predict technical difficulty with colonoscopy. 相似文献
106.
107.
Tachikawa M Fukaya M Terasaki T Ohtsuki S Watanabe M 《The European journal of neuroscience》2004,20(1):144-160
The creatine/phosphocreatine shuttle system, as catalysed reversibly by creatine kinases, is thought to be essential for the storing and buffering of high phosphate-bound energy in tissues with high energy demand. In the present study, we aimed to clarify the cellular system of creatine biosynthesis and its energy metabolism in the mouse brain by immunohistochemistry for creatine biosynthetic enzyme S-adenosylmethionine:guanidinoacetate N-methyltransferase (GAMT), ubiquitous mitochondrial creatine kinase (uCK-Mi) and brain-type cytoplasmic creatine kinase (CK-B). GAMT was expressed highly in oligodendrocytes and olfactory ensheathing glia and moderately in astrocytes, whereas GAMT was very low in neurons and microglia. By contrast, uCK-Mi was expressed selectively in neurons and localized in their mitochondria in dendrites, cell bodies, axons and terminals. The distinct and almost complementary distribution of GAMT and uCK-Mi suggests that the creatine in neuronal mitochondria is derived not only from the circulation, but also from local glial cells associated with these neuronal elements. By contrast, CK-B was selective to astrocytes among glial populations, and was exclusive to inhibitory neurons among neuronal populations. Interestingly, these cells with high CK-B immunoreactivity are known to be highly resistant to acute energy loss, such as hypoxia and hypoglycemia. Considering that phosphocreatine generates ATP much faster than the processes of glycolysis and oxidative phosphorylation, the highly regulated cellular expressions of creatine biosynthetic and metabolic enzymes suggest that the creatine/phosphocreatine shuttle system plays a role in brain energy homeostasis through a novel neuron-glial relationship. 相似文献
108.
Although steatohepatitis can be induced by an excessive intake of alcohol, it can also arise through various other causes, in which case it is known as non-alcoholic fatty liver disease (NAFLD). NAFLD is classified into two categories:simple fatty liver with a favorable clinical outcome, and non-alcoholic steatohepatitis (NASH), which is intractable and progressive. Recently in Japan, there has been an increase in the number of individuals at risk of lifestyle-related diseases, due to increased insulin resistance and visceral fat obesity. The metabolic syndrome (MS) is associated with several risk factors for atherosclerosis, including diabetes mellitus (DM), hypertension, and hyperlipidemia. Visceral fat obesity is the prime cause of NASH in the liver, and is therefore considered to be one of the phenotypic features of MS. Furthermore, most chronic liver diseases are associated with hepatitis C virus (HCV) infection. Fatty degeneration of hepatocytes is often observed in the liver of HCV-infected individuals, and results from viral suppression of mitochondrial beta-oxidation of fatty acid. The natural outcome of HCV infection is worse in patients with lifestyle-related high insulin resistance and visceral fat obesity. In this review, we describe the recent advances in research on progressive liver diseases that are the result of fat accumulation in the liver, with special reference to MS. 相似文献
109.
Horikawa Y Otaka M Komatsu K Jin M Odashima M Wada I Matsuhashi T Ohba R Oyake J Hatakeyama N Dubois RN Watanabe S 《Digestive diseases and sciences》2007,52(10):2757-2765
Resistance to chemotherapeutic agents is one of the distinct features of cancer cells. We evaluate the role of activated MEK-ERK
signaling in Camptotecin/irinotecan (CPT-11)-induced cell death using constitutively activated MEK1-transfected normal rat
intestinal epithelial cells (IEC-caMEK cells). A CPT-11-induced inhibitory concentration of 50% was determined by WST assay.
Apoptosis was evaluated by DNA staining and fragmented DNA analysis. Protein expressions were analyzed by western blotting.
We also examined the role of cyclooxygenase-2 in the cell systems. IEC-caMEK cells possessed survival advantages compared
to control cells. Apoptosis was remarkably suppressed in IEC-caMEK cells. Western blot analysis revealed increased expression
of Bcl-2, Bcl-xL, Mcl-1, and COX-2 and decreased expression of Bak in IEC-caMEK cells. The COX-2 selective inhibitor ameliorated
the antiapoptotic nature of IEC-caMEK cells. MEK activation suppressed CPT-11-induced apoptosis in IEC-caMEK cells via a COX-2-
dependent mechanism. Therefore, MEK-ERK signaling may contribute to the drug-resistant nature of cancer cells. 相似文献
110.
Kogoro Kasahara MD Yuichi Yamashita Hisao Ishibashi Takashi Fukumoto Sumio Tenmoku Akiyoshi Kashii Kyotaro Kanazawa 《Surgery today》1987,17(6):445-454
Preoperative patients with periampullary cancer had a higher mean Σ IRI value than that of normal controls, and also had a
delayed pattern of insulin response and a lower insulinogenic index during oral-GTT. Σ IRI levels after pancreatoduodenectomy
were similar to those of normal controls when the pancreatic remnants were histologically intact at the time of surgery. Postoperative
Σ IRI levels could not be predicted based on the extent of histological fibrosis of the distal pancreas at the time of surgery.
Patency of pancreatojejunostomy was obtained with the modified Warren's method in 39 out of 40 patients, and Σ IRI levels
were maintained up to 5 years postoperatively. No significant difference was found in Σ IRI levels between pancreatoduodenectomised
patients with the conventional Roux-en-Y procedure and those with the inverted Roux-en-Y with jejunal interposition. The mean
insulin peak value and Σ IRI level were higher in pancreatoduodenectomised patients than in normal controls, and higher in
gastrectomised patients than in pancreatoduodenectomised patients. Pancreatoduodenectomy with superior mesenteric arterial
dissection resulted in remarkably low Σ IRI levels. 相似文献