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Biomedical subjects

H Shigemori

Publications and source records attributed to H Shigemori.

At least 37 records · Page 2Linked to original sources
PubMed1996

Effect of vasopressin on esophageal varices blood flow in patients with cirrhosis: comparisons with the effects on portal vein and superior mesenteric artery blood flow.

BACKGROUND/AIMS: Vasopressin reduces portal pressure which may be due to decreased portal inflow. However, it remains unclear whether vasopressin is able to selectively reduce esophageal varices blood flow. The aim of this study was to address this question. METHODS: Fifteen patients with cirrhosis and esophageal varices were included in this prospective study. Portal vein and superior mesenteric artery flow velocity were measured with a percutaneous echo-Doppler. Esophageal varices flow velocity was measured using a transesophageal echo-Doppler technique. Mean arterial pressure and heart rate were also recorded. These measurements were performed at baseline condition and 15 min after observer blind drug administration. In this study, two groups, six patients receiving placebo and nine patients receiving 0.3 U/min of vasopressin, were randomized according to the coded number. RESULTS: Placebo administration had no effect on systemic and splanchnic circulation. In contrast, vasopressin administration increased mean arterial pressure (p < 0.05) associated with a bradycardia (p < 0.01). In splanchnic circulation, vasopressin decreased portal vein (-32 +/- 3%, p < 0.01), superior mesenteric artery (-30 +/- 2%, p < 0.01), and esophageal varices flow velocity (-48 +/- 5%, p < 0.01). When the magnitude of these reductions was compared, ANOVA showed a significant difference (p < 0.01). Furthermore, the reduction in esophageal varices flow velocity was significantly higher than that in portal vein flow velocity (p < 0.01) and that in superior mesenteric artery flow velocity (p < 0.01). CONCLUSIONS: These data support the view that vasopressin is able to selectively reduce esophageal varices blood flow. This effect, in addition to its well-established portal pressure reducing action, may play a role in its therapeutic efficacy in the treatment of variceal bleeding.

Aged↗
PubMed1996

Echo-Doppler measurements of portal vein and superior mesenteric artery blood flow in humans: inter- and intra-observer short-term reproducibility.

The reproducibility of echo-Doppler measurements of portal vein and superior mesenteric artery blood flow has not been extensively studied. In the present study, two groups of subjects were examined to test inter- and intra-observer reproducibility. Each study population consisted of 15 nonportal hypertensive and 15 portal hypertensive subjects. With a standardized technique, the crosssectional area and velocity of blood flow in the portal vein and superior mesenteric artery were recorded in triplicate by skilled operators. The flow volume of each vessel was calculated by multiplying the cross-sectional area by the velocity of blood flow. The measurements were performed in a blind fashion over a 60 min period. The reproducibility of measurements was assessed by calculation of intraclass correlation coefficients and coefficients of variation. The intra-observer intraclass correlation coefficient was 0.77 for portal vein blood flow and 0.84 for superior mesenteric artery blood flow, suggesting good reproducibility. The intra-observer coefficient of variation was 11 and 9%, respectively. In contrast, the interobserver intraclass correlation coefficient was calculated to be 0.49 for portal blood vein blood flow and 0.57 for superior mesenteric artery blood flow, indicating fair reproducibility. In addition, the interobserver coefficients of variation were calculated to be 20 and 18%, respectively. These data suggest that intra-observer reproducibility in echo-Doppler measurements of portal vein and superior mesenteric artery blood flow is acceptable but inter-observer reproducibility is not. Examination by a single operator, rather than multiple operators, is therefore advisable. Even when measurements are performed by a single investigator an approximate variance of 10% in the measurement in a single subject should be expected.

Adult↗
PubMed1996

Vasopressin plus oxygen vs vasopressin alone in cirrhotic patients with portal-hypertensive gastropathy: effects on gastric mucosal haemodynamics and oxygenation.

The effects of vasopressin plus oxygen and vasopressin alone on gastric mucosal perfusion and oxygenation were studied using reflectance spectrophotometry and laser Doppler velocimetry in 23 cirrhotic patients with portal-hypertensive gastropathy. The measurements were performed under basal conditions and after double-blinded administration of placebo (n = 7), vasopressin (0.3 U/min; n = 8) or vasopressin (0.3 U/min) plus nasal oxygen (4 L/min; n = 8). No significant effects on gastric mucosal haemodynamics and oxygenation were observed after placebo. In contrast, vasopressin and vasopressin plus oxygen induced a similar reduction in haemoglobin content (-26 +/- 2 and -21 +/- 4%, respectively P < 0.01), and laser Doppler signal (-23 +/- 2 and -22 +/- 2%, respectively, P < 0.01). Although each treatment induced a significant reduction in oxygen saturation (-21 +/- 2 and -7 +/- 1%, respectively P < 0.01), the effect was less pronounced in patients receiving the combination than in those receiving vasopressin alone (P < 0.01). These data suggest that vasopressin and vasopressin plus oxygen reduce gastric mucosal hyperaemia and that the oxygen supplement partially protects against gastric mucosal hypoxia during vasopressin infusion in cirrhotic patients with portal-hypertensive gastropathy.

Aged↗
PubMed1996

Distinctive portal venographic pattern in patients with sclerotherapy resistant oesophageal varices.

We performed prophylactic sclerotherapy in 350 patients with 'high risk' oesophageal varices (F2 or F3 with a moderate or severe red colour sign). Of these patients, eight exhibited sclerotherapy resistance (i.e. no significant reduction in the size of varices after five sessions of sclerotherapy). Thus, the prevalence of sclerotherapy resistant varices was 2%. Of 350 patients, 97 underwent haemodynamic investigation before sclerotherapy. This group consisted of seven patients with sclerotherapy resistant varices and 90 patients with non-resistant varices. Portal pressure, assessed by portal venous pressure gradient, was similar in these two groups (21.5 +/- 4.8 vs 19.8 +/- 5.0 mmHg, respectively; NS). However, the prevalence of the 'pipe-line' form of variceal feeding pattern (a large dilated left gastric vein running up the oesophagus) was higher in patients with resistant varices than in those with non-resistant varices (100 vs 3%, respectively; P < 0.01) and the diameter of the left gastric vein was larger in patients with resistant varices than in those with non-resistant varices (12.4 +/- 2.0 vs 7.8 +/- 2.3 mm, respectively; P < 0.01). Moreover, the extravariceal portosystemic shunt was poorly developed in patients with resistant varices compared with non-resistant varices (0 vs 52%, respectively; P < 0.05). We conclude that the pipe-line pattern, fed by a large left gastric vein and associated with poorly developed extravariceal portosystemic shunt, is a distinctive portal venographic feature of sclerotherapy resistant varices.

Esophageal and Gastric Varices↗
PubMed1996

Hepatic artery hemodynamic responsiveness to altered portal blood flow in normal and cirrhotic livers.

PURPOSE: To compare hepatic artery hemodynamic response to altered portal blood flow in normal and cirrhotic livers. MATERIALS AND METHODS: The portal blood flow and hepatic artery pulsatility index were measured by means of duplex ultrasound before and after subjects (eight control subjects and 10 cirrhotic patients) ingested a 500-kcal mixed-liquid meal and during intravenous infusion of vasopressin at a rate of 0.3 U/min (nine control and nine cirrhotic subjects). The hepatic artery buffer index (ratio of maximum change from baseline in hepatic artery pulsatility index to maximum change from baseline in portal blood flow) was also calculated. RESULTS: Meal consumption increased the portal blood flow and hepatic artery pulsatility index in all subjects. The hepatic artery buffer index, however, was significantly lower in cirrhotic than in control subjects (0.67 min/L +/- 0.06 [standard error of the mean] vs 1.54 min/L +/- 0.20, respectively; P < .01). Vasopressin infusion decreased the portal blood flow and hepatic artery pulsatility index in all subjects. Again, the hepatic artery buffer index was significantly lower in cirrhotic than in control subjects (0.28 min/L +/- 0.07 vs 0.50 min/L +/- 0.04, respectively; P < .05). CONCLUSION: Hepatic artery vascular responsiveness to altered portal blood flow is blunted in cirrhotic livers.

Fasting↗
PubMed1995

Effects of exercise-induced sympathoadrenergic activation on portal blood flow.

We examined the relationship between portal venous blood flow and sympathoadrenergic activation after muscle exercise. For this purpose, we used echo Doppler and measured plasma noradrenaline concentration before and after mild (7 metabolic units, N = 8) and maximal exercise (14 metabolic units, N = 8) in 16 patients without significant disease. Portal venous flow did not change after mild exercise. In contrast, a significant reduction in portal venous flow was observed after maximal exercise (P < 0.01). This was due to reductions in both cross-sectional area of the portal vein (P < 0.01) and portal venous velocity (P < 0.01). Overall, there were significant inverse relationships between the change in plasma noradrenaline concentration and that in cross-sectional area of the portal vein [r = -0.44, P < 0.01 (absolute change); r = -0.47, P < 0.01 (relative change)], that in portal venous velocity (r = -0.63, P < 0.01; r = -0.61, P < 0.01), and that in portal venous flow (r = -0.54, P < 0.01; r = -0.59, P < 0.01). These results suggest that the reduction in portal venous flow after exercise is related to the degree of sympathoadrenergic activation. This reduction may be due mainly to splanchnic vasoconstriction.

Adult↗
PubMed1995

Omeprazole administration does not impair gastrointestinal mucosal perfusion, oxygenation, and hexosamine generation.

Omeprazole is a potent antisecretory drug that acts by inhibiting the gastric proton pump. In the present study, we have observed the effects of this drug on gastrointestinal mucosal perfusion, oxygenation, and hexosamine generation in humans. Sixteen healthy volunteers were included. Gastrointestinal mucosal perfusion and oxygenation (duodenum, antrum, and corpus) were assessed by laser-Doppler flowmetry and reflectance spectrophotometry. Biopsy specimens were also taken from each location to determine hexosamine content as a quantitative indicator of mucus generation. In addition, serum gastrin level was measured. After baseline data were obtained, subjects were randomly assigned to receive 20 mg of oral omeprazole once daily for 7 days (n = 8) or placebo (n = 8). All measurements were performed again after double-blinded drug administration. No effect was found after placebo administration. In contrast, omeprazole administration significantly increased serum gastrin level (p < .05), suggesting an inhibition of acid secretion. However, this drug did not alter either laser-Doppler signal or oxygen saturation at each location. In addition, no change in mucosal hexosamine content was observed at each location. We conclude that oral omeprazole, despite its well-established antisecretory effect, has no adverse effect on the mucosal defense in humans.

Adult↗
PubMed1995

Xestobergsterol C, a new pentacyclic steroid from the Okinawan marine sponge Ircinia Sp. and absolute stereochemistry of xestobergsterol A.

A new pentacyclic steroid, xestobergsterol C [1], possessing a cis C/D ring junction, has been isolated together with two known compounds, xestobergsterols A [2] and B [3], from the Okinawan marine sponge Ircinia sp., and the structure determined on the basis of spectral data. Reexamination of the nmr data of xestobergsterols A [2] and B [3] resulted in revision of the configuration at C-23 and of the conformation of ring D in 2 and 3. The absolute stereochemistry of xestobergsterol A [2] was established by the cd exciton chirality method.

Animals↗
PubMed1995

Supplemental oxygen during endoscopic variceal ligation: effects on arterial oxygenation and cardiac arrhythmia.

OBJECTIVES: Endoscopic variceal ligation may affect cardiopulmonary function. The aim of this study was to determine the effect of either nasal oxygen (2 L/min) or no oxygen on arterial oxygenation and cardiac arrhythmia during variceal ligation. METHODS: A prospective, endoscopy team-blinded, randomized, cross-over study (first session vs second session) was conducted in 30 cirrhotic patients undergoing variceal ligation. Oxygen saturation (SaO2) and cardiac arrhythmia were assessed by a pulse oximeter. In this study, 15 patients received supplemental oxygen in the first sessions, and 15 received oxygen in the second sessions. RESULTS: Oxygen desaturation (nadir SaO2 < 90%) occurred in 23% of patients breathing room air but was prevented by oxygen (p < 0.01), and the nadir SaO2 was significantly lower in patients breathing room air than in those receiving oxygen (93.2 +/- 0.7% vs 98.3 +/- 0.3%, p < 0.01). During the procedure, premature ventricular contraction was more frequently observed in patients breathing room air than in those receiving oxygen (14.0 +/- 3.2/h vs 5.4 +/- 1.5/r, p < 0.05). CONCLUSIONS: These data suggest that oxygen desaturation and cardiac arrhythmia are common in patients undergoing variceal ligation and that low flow nasal oxygen can alleviate these events. Supplemental oxygen is therefore advisable to avoid potential serious cardiopulmonary accidents in patients undergoing variceal ligation.

Administration, Intranasal↗
PubMed1994

Effects of propranolol on gastric mucosal perfusion and serum gastrin level in cirrhotic patients with portal hypertensive gastropathy.

Gastric mucosal hyperemia associated with elevated serum gastrin level has been suggested in cirrhotic patients with portal hypertensive gastropathy (PHG). Clinical evidence has shown that these patients may benefit from propranolol administration. The aim of this study was to investigate effect of propranolol on gastric mucosal perfusion and serum gastrin level in cirrhotic patients with portal hypertensive gastropathy. Gastric mucosal perfusion was assessed by laser Doppler flowmetry. Measurements were performed under basal conditions and after observer-blind administration of propranolol (30-60 mg/day, N = 9) or placebo (N = 9) for seven days. Placebo had no effect on either gastric mucosal perfusion or serum gastrin level. In contrast, propranolol administration significantly decreased both antrum gastric mucosal perfusion (from 0.88 +/- 0.28 to 0.73 +/- 0.26 V, P < 0.05) and corpus gastric mucosal perfusion (from 0.94 +/- 0.35 to 0.78 +/- 0.25 V, P < 0.05). However, this drug had no effect on serum gastrin level. We conclude that chronic propranolol administration in cirrhotic patients with portal hypertensive gastropathy may reduce gastric mucosal perfusion without changing serum gastrin level.

Double-Blind Method↗
PubMed1994

Wedged hepatic venous pressure reflects portal venous pressure during vasoactive drug administration in nonalcoholic cirrhosis.

Hepatic venous catheterization is widely used to assess portal pressure. However, it remains unclear whether wedged hepatic venous pressure is a close indicator of portal venous pressure during vasoactive drug administration in nonalcoholic cirrhosis. To address this issue, we analyzed the data from our previous published studies. Forty patients with nonalcoholic cirrhosis (HBV infection in five, HCV infection in 28, and cryptogenic in seven) were available in this analysis. A vasoconstrictor (N = 14), vasodilator (N = 10), or combination (N = 16) was administered. The agreement of the changes between portal and wedged hepatic venous pressures during pharmacological manipulation was assessed by an intraclass correlation coefficient. The intraclass correlation coefficient in each subgroup was more than 0.60 (0.62 in vasoconstrictor group, 0.87 in vasodilator group, and 0.73 in combination group). When the analysis was performed according to the cause of liver disease, the values were 0.67 in HBV infection, 0.73 in HCV infection, and 0.74 in cryptogenic cirrhosis. These results suggest that wedged hepatic venous pressure reflects portal venous pressure during vasoactive drug administration in patients with nonalcoholic cirrhosis.

Female↗
PubMed1994

Portal pressure after prophylactic sclerotherapy in patients with high-risk varices.

Portal hemodynamics and transhepatic portal venographic findings were studied before and after prophylactic sclerotherapy (mean duration = 40 +/- 14 days) in 16 patients with high-risk esophageal varices. Portal pressure, evaluated by the portal venous pressure gradient, increased by a mean of 21% in eight patients (50%) and decreased by a mean of 20% in eight patients (50%) with no statistically significant change overall. The two groups were further analyzed separately to identify the mechanism of the change in portal pressure. Intrahepatic vascular resistance did not change significantly in either group. However, the prevalence of extravariceal portosystemic shunts was greater in patients with decreased portal pressure than in those with increased portal pressure (88% vs. 25%, p < 0.05). Further, the enlargement of extravariceal portosystemic shunts was more marked in patients with decreased portal pressure than in those with increased portal pressure (88% vs. 0%, p < 0.01). In addition, liver function, assessed by intrinsic clearance, was not modified in the two groups. We conclude that prophylactic sclerotherapy increases or decreases portal pressure without modifying liver function. Although the mechanism of these portal pressure changes is not clear, intrahepatic vascular resistance does not play an important role and the presence of extravariceal portosystemic shunts may prevent further increases in portal pressure.

Esophageal and Gastric Varices↗
PubMed1994

Portal vein hemodynamics in cirrhotic patients with portal hypertensive gastropathy: an echo-Doppler study.

Portal hypertensive gastropathy is a major complication of cirrhosis. The aims of this study were to characterize portal vein hemodynamics and sympathetic nervous activity in cirrhotic patients with gastropathy. Forty-seven cirrhotics (mild gastropathy in 7) and 25 controls were included in this study. Portal vein hemodynamics was assessed by echo-Doppler, and sympathetic nervous activity by plasma adrenaline and noradrenaline concentrations. Portal blood flow was similar in cirrhotics and controls. However, the congestion index of the portal vein (calculated as the ratio of cross-sectional area and blood velocity) was significantly higher in the former than in the latter. Furthermore, the congestion index of the portal vein paralleled the severity of the gastropathy (ANOVA, p < 0.05). Plasma adrenaline and noradrenaline concentrations were higher in cirrhotics than in controls. However, there was no linear relationship between plasma adrenaline (ANOVA, NS) and noradrenaline (ANOVA, NS) concentrations and the severity of gastropathy. These results suggest a relative contribution of "passive congestion" in the pathogenesis of gastropathy.

Aged↗
PubMed1994

Cardiovascular responsiveness after isotonic exercise in cirrhotic patients: study on sympathoadrenergic and renin-angiotensin systems.

OBJECTIVES: The aim of this study was to evaluate cardiovascular responsiveness after isotonic exercise in cirrhotic patients. METHODS: Included were 11 cirrhotic patients and 10 age-matched normal subjects, who served as controls. Hemodynamic data were obtained on each subject before and after muscle exercise on a treadmill (7 metabolic units). Plasma noradrenaline concentration and plasma renin activity also were determined. RESULTS: In both groups, isotonic exercise increased heart rate and systolic arterial pressure, whereas diastolic arterial pressure was not modified. The increase in heart rate and systolic arterial pressure did not differ significantly between the two groups. Plasma noradrenaline concentration and plasma renin activity also were increased. The changes in plasma noradrenaline concentration and plasma renin activity was higher in cirrhotic patients than in controls (p < 0.05, p < 0.05), although the differences were not significant when calculated as a percentage. CONCLUSIONS: Cardiovascular responsiveness to isotonic exercise is almost intact in cirrhotic patients. However, supernormal activation of the sympathoadrenergic and renin-angiotensin systems is required to maintain cardiovascular homeostasis in these patients.

Adult↗
PubMed1993

Reduced portosystemic hemodynamic responsiveness after orthostasis in patients with cirrhosis.

We studied portosystemic hemodynamic responsiveness after 1 min orthostasis in nine patients with cirrhosis and nine age-matched normal subjects. Orthostasis increased diastolic arterial pressure, which is a close indicator of arterial tone, in normal subjects (+17%, P < 0.01). In contrast, no significant change in diastolic arterial pressure was observed in patients with cirrhosis (-3%, NS). The increase in heart rate was less in patients with cirrhosis than in normal subjects (+15% vs +28%, P < 0.05). Orthostasis also decreased portal blood flow, which was assessed by an echo-Doppler flowmetry, in normal subjects (-27%, P < 0.01), but in patients with cirrhosis it was not modified (-3%, NS). Plasma noradrenaline concentration showed similar increase in both groups (normal vs cirrhosis; +61% vs +55%, NS). Although the change in plasma noradrenaline concentration was related with that in diastolic arterial pressure (r = 0.71, P < 0.05) and inversely with that in portal blood flow (r = -0.69, P < 0.05) in normal subjects, no such significant correlation was found in patients with cirrhosis. We conclude that (1) a reduced hemodynamic responsiveness to sympathetic stimulation exists on both systemic and portohepatic vascular beds and (2) such a blunted baroreflex function is probably located at the receptor or effector level in patients with cirrhosis.

Adult↗