RGM1, a cell line derived from normal gastric mucosa of rat.
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Animals↗
Biomedical subjects
T Kamada
Publications and source records attributed to T Kamada.
Collateral channels that develop after an acute myocardial infarction prevent subsequent left ventricular dilation.
OBJECTIVES: We sought to evaluate the effect of collateral channels that develop late after a first anterior myocardial infarction on left ventricular dilation and function. BACKGROUND: Collateral channels in an infarct-related artery may develop long after occlusion of the artery. Well visualized collateral channels that appear immediately after a myocardial infarction reduce infarct size and preserve left ventricular function. However, the functional significance of collateral channels that develop late after myocardial infarction has not been evaluated in terms of left ventricular function. METHODS: We studied 21 patients with a first anterior myocardial infarction and an infarct-related artery that remained totally occluded after reperfusion therapy and did not reopen within 1 month of infarction. No collateral channels were observed during the acute period. Patients were classified into two groups according to the extend of collateral formation 1 month after infarction: group C, patients with well developed collateral channels (n = 11), and group NC, patients with absent or poorly developed collateral channels (n = 10). Infarct size was determined by peak creatine kinase activity and thallium-201 single-photon emission computed tomography. Global and regional left ventricular function and left ventricular volumes were assessed by left ventriculography. These measurements were identical in both groups 1 month after infarction. Left ventricular function was reevaluated after 2.12 +/- 0.79 years (mean +/- SD). RESULTS: There were no significant changes in global and regional left ventricular function between the two groups during the long-term follow-up period. However, the end-diastolic volume index of group NC increased from 71 +/- 14 to 85 +/- 19 ml/m2, whereas that of group C decreased from 64 +/- 18 to 59 +/- 12 ml/m2. This important change during the long-term follow-up period resulted in a significant difference (p = 0.0006) in the end-diastolic volume index between the groups 2 years after onset (p = 0.002), whereas 1 month after infarction the difference was not significant (p = 0.36). A similar pattern was observed for the end-systolic volume index (group C: 38 +/- 16 to 35 +/- 14 ml/m2; group NC: 45 +/- 12 to 58 +/- 18 ml/m2, p = 0.018). The power of the tests to detect the observed differences showing nonsignificant results ranged from 0.05 to 0.38, whereas the power of the tests indicating a significant difference in end-diastolic and end-systolic volume indexes was >0.88. CONCLUSIONS: Collateral channels that develop after a myocardial infarction do not reduce the infarct size or prevent left ventricular dilation within 1 month of infarction. In contrast, such collateral channels prevent subsequent ventricular dilation and the deterioration of left ventricular function over 2 years. However, our results may have been biased because of the small number of patients.
Aged↗
Role of nitric oxide in regulation of coronary blood flow during myocardial ischemia in dogs.
OBJECTIVES: This study was undertaken to examine whether nitric oxide released in ischemic myocardium decreases the coronary vascular resistance and attenuates the severity of contractile and metabolic dysfunction. BACKGROUND: Endothelium-derived relaxing factor, recently identified as nitric oxide, is a potent relaxant of coronary smooth muscle. METHODS: The left anterior descending coronary artery was perfused through an extracorporeal bypass tube placed in the carotid artery in 56 open chest dogs. After hemodynamic stabilization, we occluded this bypass tube to decrease coronary blood flow to one third of the control flow. Thereafter, we maintained a constant coronary perfusion pressure (40.9 +/- 3.1 mm Hg). RESULTS: Under ischemic conditions, the coronary arteriovenous differences in nitrate and nitrite (end products of nitric oxide) increased (from 3.5 +/- 0.4 [mean +/- SEM] to 12.9 +/- 2.1 mumol/liter, p < 0.01). NG-Monomethyl L-arginine (3 micrograms/kg body weight per min, intracoronary) decreased the coronary arteriovenous differences in nitrate and nitrite (5.0 +/- 0.9 mumol/liter, p < 0.05) and coronary blood flow (from 29.8 +/- 0.5 to 18.1 +/- 1.1 ml/100 g per min, p < 0.001). Fractional shortening (from 3.7 +/- 1.0 to -1.3 +/- 0.7%, p < 0.001) and lactate extraction ratio (from -44.0 +/- 4.1 to -59.2 +/- 4.9%, p < 0.005) of the perfused area also decreased. These values were restored by the concomitant administration of L-arginine. Blood flow to the endomyocardium was decreased relative to the epimyocardium. A reduction in coronary blood flow and worsening of myocardial contractile and metabolic functions due to the administration of NG-monomethyl L-arginine during ischemia were observed in denervated hearts. A reduction in coronary blood flow in ischemic myocardium was observed with the administration of NW-nitro-L-arginine methyl ester as well, although neither NW-nitro-L-arginine methyl ester nor NG-monomethyl L-arginine changed coronary blood flow and myocardial contractile and metabolic functions in the nonischemic myocardium. The cyclic guanosine monophosphate content of epicardial coronary artery increased due to myocardial ischemia; this increase was attenuated with NG-monomethyl L-arginine treatment. CONCLUSIONS: We conclude that endogenous nitric oxide predominantly decreases the coronary vascular resistance of ischemic endomyocardium, thereby improving myocardial contractility and metabolic function.
Animals↗
Detection of patients with sick sinus syndrome by use of low amplitude potentials early in filtered P wave.
OBJECTIVES: This study sought to determine whether patients with sick sinus syndrome could be detected by analyzing the initial portion of the signal-averaged P wave corresponding to the electrical activity of the perinodal atrial myocardial cells. BACKGROUND: In sick sinus syndrome, pathophysiologic abnormalities have been shown not only in the sinus node, but also in the atrial muscle, especially the perinodal portion. METHODS: The study included 41 patients with sick sinus syndrome and 140 age-matched control subjects. Eighteen of 41 patients with sick sinus syndrome had paroxysmal atrial fibrillation. Signal-averaged P wave electrocardiograms (ECGs) were recorded through a bandpass filter of 40 to 300 Hz with a P wave-triggering technique. Signals of the orthogonal bipolar leads were combined into a spatial magnitude. The root mean square voltage for the initial 30 ms (EP30) and the duration of initial low amplitude signals < 4 microV (ED4) of the filtered P wave were measured. The root mean square voltage for the last 20 ms (LP20) and the duration of the filtered P wave were also measured. RESULTS: EP30 was significantly lower and ED4 was significantly longer in patients with sick sinus syndrome than in the control subjects (EP30 [mean +/- SD]: 2.18 +/- 0.90 vs. 3.94 +/- 1.45 microV, p < 0.0001; ED4: 31.7 +/- 14.5 vs. 14.0 +/- 7.4 ms, p < 0.0001), although there was no significant difference in LP20 between patients with sick sinus syndrome without paroxysmal atrial fibrillation and the control subjects. The duration of the filtered P wave was significantly but minimally longer in patients with sick sinus syndrome than in the control subjects (139.8 +/- 18.8 vs. 127.3 +/- 13.6 ms, p < 0.0001). The criteria of EP30 < 3.0 microV and ED4 > 22 ms as atrial early potential gave a sensitivity of 76%, a specificity of 91%, a positive predictive value of 74% and a negative predictive value of 93% for identification of patients with sick sinus syndrome. CONCLUSIONS: These results suggest that the long, low amplitude signals early in the filtered P wave on the signal-averaged ECGs are characteristic of sick sinus syndrome. Thus, the atrial early potential could be a useful marker to identify patients with sick sinus syndrome.
Adult↗
Ultrasonic myocardial tissue characterization in patients with dilated cardiomyopathy: value in noninvasive assessment of myocardial fibrosis.
Dilated cardiomyopathy (DCM) is usually diagnosed from the left ventricular functional viewpoint by the detection of dilated ventricular cavity and depressed myocardial contractility. Although histologic analysis of the myocardium no doubt provides clinically important information, it is possible only with microscopic examination of biopsy specimen of the myocardium. The objective of this particular study is to clarify the comparative values of the measures of ultrasonic tissue characterization, that is, calibrated myocardial integrated backscatter (IB) and the magnitude of cyclic variation in IB, with conventional echocardiographic parameters in assessing histologic condition of the myocardium. The magnitude of cyclic variation in IB and myocardial IB at end-diastole calibrate with the power of Doppler signals from the blood were measured in addition to conventional echocardiographic parameters in 14 patients with DCM. Calibrated myocardial IB was higher in patients with more fibrosis in the biopsy specimen of the heart tissue, whereas the magnitude of variation in IB or conventional echocardiographic parameters did not significantly correlate with a histologic estimate of myocardial fibrosis. Calibrated myocardial IB provides information about the myocardial fibrosis that cannot be assessable with conventional echocardiographic parameters. Calibrated myocardial IB and the magnitude of cyclic variation of IB are likely to reflect somewhat different acoustic properties of the myocardium.
Adult↗
Endothelial dysfunction in the early stage of atherosclerosis precedes appearance of intimal lesions assessable with intravascular ultrasound.
The objective of this study was to clarify whether morphologic evaluation of the in vivo artery with intravascular ultrasound provides as sensitive a marker as endothelial dysfunction or microscopic histologic assessment. Endothelial dysfunction assessed with the changes in the vessel diameter during acetylcholine infusion has been used as a more sensitive marker of atherosclerosis than the angiographic estimates of morphologic structure of the vessel. Recent advent of intravascular ultrasound has provided such high-resolution images of the vessels that morphologic changes in the vessel structure are sensitively and accurately detected. Twenty-two rabbits were divided into three groups: six rabbits fed a cholesterol-rich diet for 2 weeks as the hypercholesterolemia group, eight rabbits fed with the diet for 8 weeks as the atherosclerosis group, and eight rabbits fed a normal diet as the normal group. After evaluating the atherosclerotic lesions by intravascular ultrasound, the cross-sectional area was measured in the baseline and during the infusion of acetylcholine (0.05, 0.5, and 5 micrograms/kg/min) and nitroglycerin (5 micrograms/kg/min). No atherosclerotic lesions were detectable with intravascular ultrasound in any rabbit despite the presence of microscopic intimal lesions in the vessels in the rabbits of the atherosclerosis group. The cross-sectional area increased during acetylcholine infusion in the rabbits of the normal and the hypercholesterolemia groups. In contrast, in the rabbits of the atherosclerosis group, the cross-sectional area did not significantly increase during acetylcholine infusion at the rate of 0.5 microgram/kg/min and even tended to decrease at the rate of 5 micrograms/kg/min (-3.8% +/- 3.7%, P < 0.05 vs the normal group). Dilating responses to nitroglycerin infusion were similar among all three groups. In conclusion, impairment of the endothelium-dependent vasodilating response assessed with intravascular ultrasound in the in vivo vessel precedes the appearance of echographic atherosclerotic findings. Thus intravascular ultrasound, if used in combination with drug intervention to assess endothelial function, would provide even more accurate assessment of the vessels than conventional intravascular ultrasound alone.
Acetylcholine↗
Myocardial integrated ultrasonic backscatter in patients with old myocardial infarction: comparison with radionuclide evaluation.
The purpose of our study was to clarify whether the abnormalities in integrated backscatter may be used to assess myocardial viability in patients with old myocardial infarction by comparing these integrated backscatter parameters with conventional radionuclide and echocardiographic estimates of myocardial viability. Two myocardial integrated backscatter parameters, the magnitude of cyclic variation in integrated backscatter and the myocardial integrated backscatter calibrated with the power of Doppler signals from the blood along the same ultrasound beam (calibrated myocardial integrated backscatter), were measured in 21 normal persons and 33 patients with old anteroseptal myocardial infarction. Calibrated myocardial integrated backscatter was higher and the magnitude of cyclic variation in integrated backscatter was lower in the infarct septum compared with the septum of normal subjects. Percent thallium uptake, as assessed in scintigraphic images taken at rest or after reinjection, correlated well with the calibrated myocardial integrated backscatter (r = -0.72, p < 0.01) and more weakly but significantly with the magnitude of cyclic variation in integrated backscatter (r = 0.55, p < 0.05) in 16 of 33 patients. The measurement of calibrated myocardial integrated backscatter, in addition to the magnitude of cyclic variation of integrated backscatter, may likely be valuable in the noninvasive assessment of myocardial viability.
Adult↗
Portal insulin delivery is superior to peripheral delivery in handling of portally delivered glucose.
It is still controversial as to whether physiological portal insulin delivery has metabolic advantages over peripheral insulin delivery. To clarify this issue, glycemic regulation during intravenous (IVGTT) and oral (OGTT) glucose tolerance tests and hyperglycemic clamp studies with either peripheral or portal glucose infusion was investigated in left-segmentally pancreatectomized dogs with portal ([PPx] n = 7) or systemic ([Tx] n = 7) venous drainage of the remaining pancreas. In Tx dogs, systemic diversion of pancreatic venous effluent was accomplished by gastroduodenal-caval shunt. Data obtained were compared with those in normal control dogs ([NC] n = 7). The loss of pancreatic beta-cell mass in PPx dogs decreased insulin responses to peripheral and portal glucose loads. In contrast, Tx dogs showed insulin responses comparable to those of NC dogs to glucose loads via both routes. Against peripheral glucose loads (IVGTT and hyperglycemic clamp with peripheral glucose infusion), PPx and Tx dogs showed deteriorated glucose handling. Against portal glucose loads (OGTT and hyperglycemic clamp with portal glucose infusion), deteriorated glucose handling was observed in Tx dogs, but not in PPx dogs. Deterioration in glycemic regulation against portal glucose loads in left-segmentally pancreatectomized dogs with peripheral insulin delivery but not in pancreatectomized dogs with portal delivery indicates that intraportal hyperglycemia and hyperinsulinemia are essential for promoting hepatic glucose handling.
Animals↗
Fas antigen expression in liver tissues of patients with chronic hepatitis B.
BACKGROUND: Hepatitis B virus-infected cells can be eliminated by the cytotoxic T cell-mediated immune reaction. Fas ligand, recently detected on the surface of cytotoxic T cell, is thought to induce cells to apoptosis by adhering to Fas antigen. AIMS/METHODS: To evaluate the role of Fas antigen and apoptosis in chronic hepatitis B, we immunohistochemically studied Fas antigen and HBsAg expression in liver samples from patients with hepatitis B virus infection. RESULTS: In samples from 56 HBV patients, Fas antigen was mainly expressed in the cytoplasm (partly at the membrane) of hepatocytes, and these positive cells were detected especially at the periportal region near "piecemeal necrosis". According to Knodell's HAI scoring system, the scores of periportal inflammation and necrosis (category I) and the scores of intralobular inflammation and necrosis (category II) were similarly higher in Fas antigen-positive cases than in Fas antigen-negative cases (p < 0.01), and there was a positive correlation between these scores and the degree of Fas antigen expression. In normal cases, Fas antigen was not detected. In patients with HBV infection, Fas antigen expression was closely correlated with the activity of the viral hepatitis. HBsAg was expressed by the majority of hepatocytes. However, Fas antigen was expressed by fewer hepatocytes than the number of HBsAg-positive cells. CONCLUSIONS: These findings suggest that the expression of Fas antigen may not be triggered only by HBV infection, and immunological interaction may be needed for the expression and for apoptosis to occur.
Adolescent↗
NSAIDS and the microcirculation of the stomach.
In this article, the effect of NSAIDs on the gastric mucosal microcirculation was reported. Although the precise mechanism of NSAID-induced ulcerogenesis is still unknown, most NSAIDs have been shown to impair gastric mucosal microcirculation and cause gastric mucosal damage.
Animals↗
Evidences for involvement of cyclooxygenase-2 in proliferation of two gastrointestinal cancer cell lines.
Cyclooxygenase (COX) consists of two isozymes, COX-1 and COX-2. The roles of these isozymes in the gastrointestinal tract are unknown. We investigated messenger RNA expression of the COX-1 and COX-2 genes in the gastrointestinal cancer cell lines MKN28, MKN45, KATO III CACO-2, DLD-1 and LoVo. These cell lines expressed comparable levels of COX-1 mRNA, although their expression of COX-2 varied. Therefore, we studied the effects of NS-398 and indomethacin, specific and non-specific inhibitors for COX-2, on proliferation of the cell lines. Both of the inhibitors suppressed proliferation of the two cell lines that highly expressed COX-2 (MKN45 and CACO-2). However, these inhibitors exerted minimal effects on proliferation of the other cell lines, which expressed significantly lower levels of COX-2. Therefore, it was proposed that COX-2 participates in proliferation of cancer cells because of over expression of the COX-2 gene.
Cell Division↗
Role of basal release of nitric oxide in the presence of acute left ventricular dysfunction: comparative study with normal condition.
The basal release of nitric oxide (NO) plays an important role in the regulation of vascular circulation in the presence of acute left ventricular dysfunction. It is not clear, however, whether the role is as important in the presence of acute left ventricular dysfunction as it is in the normal condition. In addition, the effects of flow rate on the role of basal NO have not been clarified in the presence of acute left ventricular dysfunction. This in vivo study was attempted to compare the contribution of the basal release of NO to the regulation of vascular circulation and the effects of a mechanically reduced basal flow rate on the contribution of basally released NO between the normal condition and acute left ventricular dysfunction. In eight anesthetized dogs, the responses of femoral artery blood flow to NG-monomethyl-L-arginine (L-NMMA, 10(-5)M) were observed with and without a reduction in basal flow. The same observation was performed after the production of acute left ventricular dysfunction by coronary microembolization. Without the reduction in basal flow, the L-NMMA-induced decrease in femoral artery flow was significantly larger in acute left ventricular dysfunction than in the normal condition (-40 +/- 12% vs-17 +/- 6%, P < .01). Under the reduction in basal flow, there was no significant change in flow during the infusion of L-NMMA in the normal condition and only a small decrease in acute left ventricular dysfunction. There was no significant difference in the L-NMMA-induced changes in flow between these conditions. The contribution of basally released NO to the regulation of vascular circulation is larger in the presence of acute left ventricular dysfunction than in the normal condition; however, the role of basal NO is reduced with a decrease in basal flow rate.
Acetylcholine↗
Inhibition of TGF-beta 1 expression by antisense oligonucleotides suppressed extracellular matrix accumulation in experimental glomerulonephritis.
Overproduction of transforming growth factor-beta 1 (TGF-beta 1) has been implicated in the pathogenesis of fibrotic diseases. TGF-beta 1 plays a crucial role in the accumulation of extracellular matrix (ECM) in human and experimental glomerular diseases. However, it remains unclear whether inhibition of TGF-beta 1 overproduction would suppress TGF-beta 1-induced ECM accumulation. To inhibit the overproduction of TGF-beta 1 in experimental glomerulonephritis induced by anti-Thy 1.1 antibody, we introduced antisense oligodeoxynucleotides (ODN) for TGF-beta 1 into the nephritic kidney by the HVJ-liposome-mediated gene transfer method. Sense, scrambled or reverse ODN were also introduced as controls. Transfected ODN accumulated mainly in the nuclei of mesangial cells in the glomeruli of transfected kidneys. In the antisense ODN-transfected rats, a marked decrease in expression of TGF-beta 1 mRNA was confirmed by Northern analysis. Consequently, the expression of TGF-beta 1 protein in the glomerulus was markedly reduced in the antisense ODN-transfected kidney with a comparable effect in preventing glomerular ECM expansion in experimental glomerulonephritis. In contrast, sense, scrambled and reverse ODNs failed to suppress TGF-beta 1 expression and ECM accumulation. Thus, these results suggested that inhibition of TGF-beta 1 overproduction could suppress progression to glomerulosclerosis.
Animals↗
Expression of betaine transporter mRNA: its unique localization and rapid regulation in rat kidney.
Betaine is a major compatible osmolyte in the renal medulla. It is taken up into cells via the betaine gamma-amino-n-butyric acid transporter (BGT-1). We investigated the localization of BGT-1 mRNA and its acute regulation by NaCl and furosemide administration. In situ hybridization revealed that BGT-1 mRNA is predominantly present in the outer medulla and papilla. Less intense signals were seen in the inner medulla and no signals were found in the cortex. Microscopic examination suggested that intense signals were present in the medullary thick ascending limbs of Henle's loop (MTAL) and the inner medullary collecting ducts (IMCD). A reverse transcription and polymerase chain reaction assay of individual microdissected segments along the nephron confirmed its localization. Intraperitoneal administration of NaCl rapidly increased the signal in the MTAL, and furosemide prevented the increase in BGT-1 mRNA by NaCl loading. In contrast, BGT-1 mRNA in the IMCD is less sensitive to these kinds of acute regulation. These results suggest that BGT-1 expression in the MTAL is rapidly regulated in response to the magnitude of NaCl absorption, as suggested for the expression of Na+/myo-inositol cotransporter.
Aldehyde Reductase↗
Exposure of astrocytes to hypoxia/reoxygenation enhances expression of glucose-regulated protein 78 facilitating astrocyte release of the neuroprotective cytokine interleukin 6.
Astrocytes exposed to hypoxia (H) or hypoxia/ reoxygenation (H/R) maintain cell viability and display changes in protein biosynthesis. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of metabolically labeled astrocytes exposed to H showed induction of an approximately 78-kDa polypeptide that demonstrated sequence identity with glucose-regulated protein (GRP) 78. Cell lysates from H/R astrocytes displayed induction of neuroprotective interleukin (IL) 6, which was present in a high-molecular-weight complex also containing GRP78, suggesting that GRP78 might be functioning as a chaperone during cellular stress consequent on H/R. Introduction of antisense oligonucleotide to GRP78 into astrocytes prevented expression of the protein and suppressed H/R-induced astrocyte release of IL-6 by approximately 50%. These data indicate that modulation of astrocyte properties during oxygen deprivation results, in part, from intracellular glucose depletion and subsequent expression of GRP78, which sustains generation of neuroprotective IL-6 under the stress of H/R.
Animals↗
Quantitative analysis of antibody to hepatitis C virus envelope 2 glycoprotein in patients with chronic hepatitis C virus infection.
The significance of circulating antibody to hepatitis C virus (HCV) envelope glycoprotein 2 (E2)/nonstructural protein 1 (NS1) glycoprotein was studied in 83 patients with chronic HCV infection diagnosed by polymerase chain reaction (PCR). E2/NS1 antibody was quantitatively examined by a passive hemagglutination test using recombinant E2/NS1 glycoprotein encompassing amino acids 388 to 664 of the HCV-H strain. The results were correlated with clinical and virological features such as genotypes and viremic levels assessed by a competitive reverse-transcription PCR assay. E2/NS1 antibody was found in 73 patients (88%), and its occurrence was related to viremic levels. E2/NS1 antibody titers were low in asymptomatic HCV carriers with low levels of viral replication; 9 of 17 such patients tested positive for E2/NS1 antibody (53%), compared with 64 of 66 chronic hepatitis C patients (97%) (P < .01). A significant direct relationship was observed between viremic levels and E2/NS1 antibody titers (r = .52, P < .01). Of the 13 patients with low viremic levels of < 10(6) copies/mL, only 5 tested positive for E2/NS1 antibody (38%), whereas 68 of the 70 patients with viremic levels of > or = 10(6) copies/mL had it (97%) (P < .01). As for the relation to HCV genotypes, no difference was seen in E2/NS1 antibody titers among genotypes examined (1b, 2a, and 2b). These findings suggest that the E2/NS1 antibody tested exhibits no neutralizing activity in chronic HCV infection but may serve as a serological indicator of active virus replication.
Adult↗
Lipopolysaccharide increases cell surface-associated fibronectin in fibroblasts in vitro.
This study assessed the fibronectin expression by fibroblasts derived from noninflamed and inflamed gingiva by measuring the amount of cell surface-associated fibronectin and fibronectin released into the medium. The effects of added lipopolysaccharide from Porphyromonas gingivalis, Prevotella nigrescens and Escherichia coli on both types of fibroblasts were also studied. In the absence of lipopolysaccharide, the amounts of the two types of fibronectin were significantly larger in the fibroblasts from inflamed than from noninflamed gingiva. The specific lipopolysaccharide had no effect on the amount of fibronectin released into the medium by either fibroblast type. The amount of cell surface-associated fibronectin increased significantly when lipopolysaccharide (0.1 and 1 microgram/ml) was added to the cells from the noninflamed gingiva (the effect was evident in the order: P. gingivalis>P.nigrescens>E. coli). Lipopolysaccharide from P. gingivalis significantly increased the cell surface-associated fibronectin even at a low concentration of lipopolysaccharide (0.01 microgram/ml). In fibroblasts from the inflamed gingiva, only the lipopolysaccharide from P. gingivalis was effective in increasing the amount of cell surface-associated fibronectin. Our findings showed that the fibronectin expression was increased in the fibroblasts from inflamed gingiva and that lipopolysaccharide from P. gingivalis increased the cell surface-associated fibronectin.
Analysis of Variance↗
Gastric mucosal energy metabolism and intracellular mucin content changes in patients with liver cirrhosis.
Biopsy samples from patients with liver cirrhosis were investigated for changes in gastric mucosal energy metabolism and intracellular mucin content using high performance liquid chromatography and an image analysing system. The test group consisted of eight non-cirrhotic patients with endoscopically normal mucosa (controls) and eight cirrhotic patients with oesophageal varices. The amount of ATP, energy charge level and intracellular mucin content were all significantly decreased in cirrhotic patients when compared with those of the controls. The decrease in energy charge also correlated well with the decrease in intracellular mucin content in the gastric mucosa. The results indicate that gastric mucosal energy metabolism is impaired in cirrhotic patients concomitantly with a decrease in the intracellular mucin content in the gastric mucosa. These changes may weaken defensive mechanisms against acid and NSAID, resulting in gastric mucosal injury in cirrhotic patients.
Adenosine Diphosphate↗