Search PubMed⌕ Search

Biomedical subjects

H C Lin

Publications and source records attributed to H C Lin.

At least 235 records · Page 13Linked to original sources

Laparoscopic surgical approach and anatomy of the abdomen in llamas.

OBJECTIVE: To describe 3 laparoscopic approaches for, and the normal laparoscopic anatomy of, the abdomen in adult llamas and to evaluate the effects of laparoscopy in those llamas. DESIGN: Prospective clinical trial. ANIMALS: Six adult castrated male llamas. PROCEDURE: After induction of general anesthesia, 3 surgical approaches to the abdomen were performed: left paralumbar, ventral midline, and right paralumbar. The abdomen was systematically examined, and anatomic features described. After recovery from anesthesia, all llamas were examined daily for 10 days and CBC was repeated 24, 72, and 120 hours after laparoscopy. RESULTS: Laparoscopy was successfully performed in all llamas by use of the ventral midline and right paralumbar approaches. The laparoscope was inadvertently placed into the left retroperitoneal space in 1 of the 6 llamas when the left paralumbar approach was used. Also, hemorrhage into the abdomen limited the view from the left side in another llama. Various approaches allowed viewing of the first and third forestomach compartments, liver, spleen, kidneys, small intestine, ileum, proximal loop of the ascending colon, spiral colon, and urinary bladder. Postoperative findings included subcutaneous emphysema and edema. Mean WBC count peaked 24 hours after surgery (mean, 23,500 cells/microliter). Generally, neutrophil count increased and lymphocyte count decreased during the 120 hours after surgery. CLINICAL IMPLICATIONS: Laparoscopy may be used for differentiation of medical and surgical lesions in the abdomen of llamas. The site for laparoscopy should be chosen on the basis of the most likely site of the suspected lesion.

Abdomen↗

Effects of long-term administration of octreotide in portal vein-stenosed rats.

The hemodynamic effects of long-term administration of octreotide in portal hypertension has not been established. In addition, whether long-term octreotide treatment prevents the development of portosystemic shunts has not yet been evaluated. Hence, the current study was undertaken to evaluate the effects of long-term administration of octreotide in rats with portal vein stenosis. Immediately after portal vein stenosis or sham operation, rats were given either a long-term octreotide administration of 100 micrograms/kg or a placebo every 12 hours by subcutaneous injection for 14 consecutive days. Systemic hemodynamics and regional blood flows, degree of mesenteric-systemic shunts, and plasma glucagon concentrations were measured after the final dose of octreotide or placebo. A fifth group of portal vein-stenosed rats received hemodynamic and plasma glucagon measurements after 1-day octreotide treatment given at 14 days after surgery. Long-term octreotide treatment modified the hyperdynamic circulation without affecting the degree of mesenteric-systemic shunts, and 1-day octreotide treatment decreased portal tributary blood flow without affecting the portal pressure, systemic hemodynamics, and degree of mesenteric-systemic shunts. Plasma glucagon levels were decreased in portal vein-stenosed rats receiving either long-term or 1-day octreodtide compared with rats receiving placebo. In contrast, chronic octreotide treatment did not affect any of the hemodynamic values or plasma glucagon levels in sham-operated rats. In conclusion, long-term administration of octreotide modified in part the development of portal hypertension and hyperdynamic circulation in portal vein-stenosed rats without affecting the degree of mesenteric-systemic shunts.

Analysis of Variance↗

Effect of beta 2-adrenoceptor agonists on plasma potassium and cardiopulmonary responses on exercise in patients with chronic obstructive pulmonary disease.

OBJECTIVE: The effect of beta 2-adrenoceptor agonist-induced hypokalaemia on cardiac arrhythmias might be exacerbated during exercise, especially in patients with more compromised airway function. METHODS: To evaluate the effect of beta 2-adrenoceptor agonists on plasma potassium and cardiopulmonary function during exercise, two identical submaximal treadmill exercise tests were performed, at least 48 h apart, by 13 patients with moderate to severe COPD (11 men and 2 women, mean age 66 y, mean FEV1/FVC ratio 48.9 (2.8)% 30 min after they had received nebulised fenoterol or salbutamol (2 mg). The experiment was done as a randomised, double-blind, crossover trial after an initial baseline study with vehicle (0.45% saline). Plasma potassium concentration, spirometry and the degree of breathlessness (Borg scale) were measured before treatment and immediately after exercise; oxygen saturation, QTc interval and cardiac rhythm were monitored continuously before, during and for 30 min after exercise. RESULTS: After the saline control, exercise caused an increase in Borg rating (of 4.9), a premature ventricular contractions (VPC) (2.8 beats/min), and a fall in oxygen saturation (-6.7%), but no significant change in plasma potassium (+0.04 mEq.dl-1), FEV1 or QTc interval. Inhalation of fenoterol and salbutamol did not affect QTc interval, Borg scale or VPC frequency at rest, but significantly increased the duration of exercise undertaken to reach the submaximal levels (786 s, versus 783 s) compared to the vehicle control. Following exercise, plasma potassium fell after fenoterol by 0.2 mEq.dl-1 and it increased after salbutamol by 0.1 mEq.dl-1 compared to baseline levels. Plasma potassium after exercise was significantly lower after fenoterol (3.2 mEq.dl-1) compared to the saline control (3.7 mEq.dl-1) and salbutamol (3.6 mEq.dl-1). Neither fenoterol nor salbutamol had any significant effect on the change in FEV1, oxygen saturation, Borg scale, frequency of VPCs or QTc interval during or after exercise compared to the saline control. CONCLUSION: When compared to salbutamol 2 mg, fenoterol 2 mg caused more marked hypokalaemia but no significant difference in cardiopulmonary response in patients with COPD during exercise.

Adrenergic beta-Agonists↗

Jejunal brake: inhibition of intestinal transit by fat in the proximal small intestine.

Optimal absorption of fat requires adequate time of contact with the absorptive sites of the small intestine. In order to prevent steatorrhea, intestinal transit must be slowed in response to the fat that has emptied into the small intestine. Intestinal transit is known to be inhibited by fat in the ileum via the ileal brake. This response has suggested that the regulation of intestinal transit is a function of the distal small intestine. However, clinical observations suggest that the ileal brake is not the only control mechanism for intestinal transit. In short bowel patients with resection of the ileum, the proportion of fecal fat recovery remained constant even after the fat intake was increased threefold. In these patients, optimal fat absorption based on the slowing of intestinal transit must have been triggered by an inhibitory mechanism located outside of the distal small intestine. To test the hypothesis that fat in the proximal small intestine inhibited intestinal transit, we compared intestinal transit during perfusion of the proximal half of the small intestine with 0 (buffer only), 15, 30, or 60 mM oleate in dogs equipped with duodenal and mid-intestinal fistula. Intestinal transit across a 150-cm test segment (between fistulas) was measured by counting for the recovery of a radioactive marker in the output of the mid-intestinal fistula during the last 30 min of a 90-min perfusion. We found that oleate inhibited intestinal transit in a load-dependent fashion (P < 0.005). Specifically, while the mean cumulative recovery of the transit marker was 95.5% during buffer perfusion, the recovery decreased when 15 mM (64.3%), 30 mM o(54.7%), or 60 mM oleate (38.7%) was perfused into the proximal half of the small intestine. We conclude that fat in the proximal small intestine inhibits intestinal transit as the jejunal brake.

Animals↗

Glutathione S-transferase and glutathione peroxidase are essential in the early stage of adriamycin resistance before P-glycoprotein overexpression in HOB1 lymphoma cells.

We have previously established Adriamycin-resistant HOB1 cell lines showing the multidrug resistance (MDR) phenotype. For further study, we analyzed the free-radical scavengers glutathione S-transferase (GST) and glutathione peroxidase (GPX) by enzyme assays and Northern blots. Three cell lines, HOB1/ADR0.1, HOB1/ADR1.0, and HOB1/ADR5.0, represented HOB1 cells resistant to 0.1, 1.0, and 5.0 microM Adriamycin, respectively. The mdr1 transcript was overexpressed in HOB1/ADR0.1 cells, and the amount of its expression reached a maximum between HOB1/ADR1.0 and HOB1/ADR5.0 cell lines. The increases in GST activity and GST-pi expression were observed only in high-level-resistant cell line (HOB1/ADR1.0 and HOB1/ADR5.0), which also showed increased GPX activity and expression. For investigation of the cytotoxic effect of Adriamycin on HOB1 cells prior to the mdr1 overexpression, an appropriate number of parental HOB1 cells were treated with 0.1 microM Adriamycin for 7 days, and the viable cells (HOB1/ADR) were isolated and subjected to analyses for mdr1, GST-pi, and GPX expression and for GST and GPX activity. In comparison with HOB1/ADR0.1 cells, HOB1/ADR cells did not show mdr1 overexpression but had significant increases in the activity and expression of GST and GPX. The current study suggests that in the early phase of Adriamycin treatment, GST and GPX are more important than P-glycoprotein for the development in HOB1 cells of resistance against Adriamycin.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Cytotoxic effects of anthrax lethal toxin on macrophage-like cell line J774A.1.

The cytotoxic effects of anthrax lethal toxin purified from an avirulent strain were examined on mouse macrophage-like J774A.1 cells. Cell death induced by high concentration of purified lethal toxin had the characteristics of necrosis. At lower concentrations, the toxin caused no morphological change and most of the cells were viable. Interestingly, apoptotic cells were observed when the cells were preincubated with a serine/threonine phosphatase inhibitor, calyculin A, and then exposed to a toxin concentration of 0.1 microg/ml. This is the first report that lethal toxin of the anthrax bacillus can induce both necrosis and apoptosis and that protein phosphatases are implicated in the regulation of bacterial toxin-induced apoptosis.

Animals↗

Decreased vascular reactivity of portal vein in rats with portal hypertension.

BACKGROUND/AIMS: Vascular hyporesponsiveness in portal hypertension is well documented in the arterial tissue. The present study aimed to investigate the possible changes in the portal vein from portal hypertensive rats. METHODS: Portal hypertension was induced by partial portal vein ligation. Fourteen days after surgery, portal veins were removed for contractile study and measurement of cAMP, cGMP and [Ca2+]i. RESULTS: In vitro tension preparation showed a decreased maximum response to norepinephrine in portal vein of portal vein ligated rats (38.3 +/- 4.1 vs. 23.4 +/- 1.5 mN/mm2). The pA2 values of WB4101 and yohimbine (alpha1- and alpha2-adrenoceptor antagonist, respectively) were not different between the two groups. Tissue cAMP (14.4 +/- 0.9 vs. 12.2 +/- 0.7 pmol/mg protein), but not cGMP, content was increased and intracellular calcium [Ca2+]i levels (247 +/- 9 vs. 281 +/- 13 nM) were decreased in portal vein ligated rats. CONCLUSIONS: These results showed that in portal vein from portal vein ligated rats, vascular hyporesponsiveness and an increase in basal cAMP content and a decrease in basal [Ca2+]i were observed.

Animals↗

Effect of octreotide on total effective vascular compliance in patients with posthepatitic cirrhosis.

BACKGROUND/AIMS: This study aimed to evaluate the effect of octreotide on total effective vascular compliance, measured during rapid volume expansion, in patients with posthepatitic cirrhosis. METHODS: Twenty-nine patients with posthepatitic cirrhosis were randomly assigned to receive a 100-micrograms/h infusion of octreotide after a 100-micrograms bolus (n = 15), or a placebo (n = 14). Hemodynamic measurements were recorded before and 30 min after drug administration. Thereafter, rapid volume expansion was performed in each patient and hemodynamic measurements were repeated immediately after volume expansion. RESULTS: Before volume expansion, placebo administration did not affect any of the hemodynamic values, while the hepatic blood flow was significantly decreased following octreotide administration. After volume expansion, the hemodynamic changes were similar between patients receiving octreotide and the placebo. However, the increase in right atrial pressure from the beginning to the end of volume expansion was higher and the total effective vascular compliance was lower in patients receiving octreotide (+3.5 +/- 0.3 mmHg, p = 0.05 and 1.69 +/- 0.16 ml.mmHg-1.kg-1, p < 0.05) compared to patients receiving placebo (+2.5 +/- 0.3 mmHg, 2.60 +/- 0.34 ml.mmHg-1.kg-1). CONCLUSIONS: The present study suggests that octreotide decreased total effective vascular compliance in patients with posthepatitic cirrhosis. It is possible that, in patients with posthepatitic cirrhosis, venoconstriction was induced following octreotide administration.

Aged↗

Spirometry in life-long non-smoking, healthy Chinese women in Taiwan.

To establish the spirometric values for normal, healthy Chinese women in Taiwan, the spirometry of 506 life-long non-smoking, healthy Chinese women was examined, including 140 subjects over the age of 60 years. Significant correlations among age, height and forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), FEV1/FVC%, peak expiratory flow (PEF), Vmax75, Vmax50, Vmax25 were found. However, there were no significant correlations between age and FEV1/FVC%, nor age and Vmax25 in the elderly group. FEV1 (FEV1*) and FVC (FVC*) were standardized to the overall mean height for elderly women using Cole's formula. The decline in FEV1* and FVC* with age were observed. The predicted value for the average 70-year-old woman with a height of 1.5 m derived from the present study is compared with those from other surveys of the elderly. The values from the present study are somewhat higher than the values from the Hong Kong study. The authors believe the fact that all of the present subjects were life-long non-smokers might explain the differences.

Adult↗

Increased production of hydrogen peroxide and expression of CD11b/CD18 on alveolar macrophages in patients with active pulmonary tuberculosis.

SETTING: Alveolar macrophages (AM) are important in host defense against Mycobacterium tuberculosis (TB). beta 2-integrins, especially CD11a/CD18 and CD11b/CD18, are implicated in leukocyte migration, antigen presentation, phagocytosis, and production of reactive oxygen species. OBJECTIVE: To explore the functional relevance of beta 2-integrin expression to intracellular H2O2 capacity of AM in TB patients. DESIGN: In a prospective study, AM retrieved from 18 active pulmonary TB patients and 18 normal subjects were assessed for beta 2-integrin expression and intracellular H2O2 metabolism capacity by loading with anti-CD11a/CD18, anti-CD11b/CD18 monoclonal antibodies and 2',7' dichlorofluorescein diacetate (DCFH-DA) respectively, and analyzed by flow cytometry. AM from 8 normal subjects were stimulated with tumor necrosis factor-alpha (TNF-alpha, 10(5) units/ml) to examine the relationship between H2O2 production and CD11b/CD18 expression. RESULTS: The magnitude of DCFH oxidation and CD11b/CD18 expression of AM was higher in TB patients than in normal subjects. The CD11b/CD18 expression was related to the magnitude of DCFH oxidation, but not to lymphocyte numbers or subpopulations (CD4, CD8, CD25). Stimulation of AM with TNF-alpha increased H2O2 production and CD11b/CD18 expression. Pretreatment with CD11b/CD18 monoclonal antibodies inhibited TNF-alpha-induced H2O2. CONCLUSION: AM in TB patients possessed a higher capacity of oxidant metabolism. The increased CD11b/CD18 expression may be related to the increased respiratory burst response in AM against mycobacterial invasion.

Adult↗

Novel antiplatelet constituents from formosan moraceous plants.

Sixteen constituents from Formosan Moraceous plants were tested for their antiplatelet activities in rabbit platelet suspension and human platelet-rich plasma. Cycloartocarpin A, cycloheterophyllin, broussochalcone A, kazinol A, broussoaurone A, and broussoflavonol F showed strong inhibition of arachidonic acid (AA)-induced platelet aggregation. Of the compounds tested, broussochalcone A exhibited the most potent inhibition of platelet aggregation induced by AA (IC50 = 6.8 microM). The antiplatelet effects of cycloheterophyllin, broussochalcone A, kazinol B, broussoaurone A, and broussoflavonol F are partially due to an inhibitory effect on cyclooxygenase.

Animals↗

Chronic administration of octreotide increases vascular responsiveness in rats with portal hypertension.

1. It has been reported that ortreotide partially corrects the hyperdynamic state in patients and animals with portal hypertension. The aim of the present study was to investigate whether chronic administration of octreotide can increase vascular responsiveness in rats with portal hypertension. 2. Portal hypertension was induced by partial portal vein ligation. Octreotide was given for 9 days subcutaneously (100 micrograms/kg every 12 h) starting 1 day before ligation. The aorta and mesenteric artery were then removed to study contraction after pressure recording. 3. Octreotide treatment significantly reduced portal pressure and plasma glucagon concentrations compared with the vehicle-treated group. Both phenylephrine and vasopressin induced concentration-dependent contractile responses in the aorta and mesenteric artery from both groups. The maximum contractile responses to phenylephrine and vasopressin in aorta and mesenteric artery were significantly greater in the octreotide-treated group than in the vehicle-treated group. The EC50 values for phenylephrine and vasopressin were significantly different in the aorta, but not in the mesenteric artery, but not in the mesenteric artery, between the two groups. In contrast, octreotide treatment did not alter the contractile responsiveness of arteries rom sham-operated rats. 4. These results show that, in rats with portal vein stenosis, octreotide increases arterial contractile responsiveness and reduces portal pressure.

Animals↗

Fat-induced ileal brake in the dog depends on peptide YY.

BACKGROUND & AIMS: Fat in the distal gut inhibits transit through the proximal small intestine as the ileal brake. Although the mediator of this response is not established, peptide YY (PYY) has been considered the most likely peptide candidate because inhibition of intestinal motility by fat in the distal gut correlated with the release of PYY but not other distal gut peptides such as enteroglucagon or neurotensin. Although intravenous administration of PYY inhibits intestinal transit, the role of this peptide remains to be confirmed because systemic PYY may not exert its effect by the same regulatory pathway as fat-induced ileal brake. The aim of this study was to definitively test the hypothesis that PYY mediates fat-induced ileal brake using the technique of peptide immunoneutralization. METHODS: In a fistulated dog model, intestinal transit during perfusion of the distal gut with 60 mmol/L oleate (ileal brake) was examined after intravenous administration of 0.5 mg/kg of PYY antibody (anti-PYY), nonspecific immunoglobulin G (control), or 0.15 mol/L NaCl. Intestinal transit result (cumulative percent recovery of 99mTc) was normalized within each animal against the transit result of the 0.15 mol/L NaCl experiment. RESULTS: Intestinal transit accelerated with PYY immunoneutralization, increasing cumulative percent recovery from 25.9 +/- 6.2 (control) to 81.2 +/- 6.3 (anti-PYY). CONCLUSIONS: Fat-induced ileal brake depends on PYY.

Animals↗

Protein absorption depends on load-dependent inhibition of intestinal transit in dogs.

Ileal perfusion of protein slows intestinal transit. Because optimal absorption of nutrients requires adequate time in contact with the mucosa, slowed intestinal transit may increase protein absorption by increasing the residence time of nutrients in the small intestine. Although protein supplements are routinely added to enteral feeding to correct protein malnutrition, little information is available on the effect of increasing the load of protein on intestinal transit and the efficiency of protein absorption. In six dogs equipped with duodenal and midintestinal fistulas, intestinal transit and the efficiency of protein absorption (percentage protein absorbed as estimated from the output of midintestinal fistula) were compared during intestinal perfusion with 0-, 50-, 100-, and 200-g/L solutions of a whey-based protein supplement. We found that intestinal transit slowed in a load-dependent fashion (P < 0.05); the amount of protein absorbed within the proximal one-half of the small intestine increased in a load-dependent fashion (P < 0.05) as intestinal transit slowed, and the percentage protein absorbed (reflecting the efficiency of protein absorption) was maintained at a high and nearly constant value of 66.5-72.5% across protein loads of 9-36 g. We conclude that enhanced protein absorption is associated with a load-dependent inhibition of intestinal transit.

Animals↗

Gastric secretion in Chinese patients with cirrhosis.

The role of gastric secretion has been controversial in patients with cirrhosis. Except for studies of gastric secretion in cirrhotic patients who underwent a shunt operation, there is no report correlating gastric secretion with portal pressure in patients with cirrhosis. In this study, we evaluated gastric secretion in cirrhotic patients and correlated it with hemodynamic parameters. Within 12 months, 20 normal volunteers and 16 cirrhotic patients were enrolled. Gastric secretion was assessed in all patients, but portal pressure hemodynamic studies were performed only in cirrhotic patients. We found that the median basal acid output, maximal acid output, and basal pepsin output in the controls (1.41 mmol/h, 9.2 mmol/h, and 0.02 mg/h, respectively) and in the cirrhotic patients (0.6 mmol/h, 7.84 mmol/h, and 1.5 mg/h, respectively) were not statistically different. However, maximal pepsin output was lower in the cirrhotic patients (1.5 mg/h) than in the normal subjects (5.14 mg/h) (p < 0.05). Gastric secretion correlated poorly with hepatic venous pressure gradient (HVPG) and the presence of congestive gastropathy in cirrhotic patients. The severity of congestive gastropathy correlated poorly with HVPG. Helicobacter pylori has difficulty replicating in the stomach when HVPG is > 14 mm Hg. We conclude that patients with cirrhosis have a lower maximal pepsin output than that of the healthy subjects. Gastric secretion correlates poorly with HVPG and the presence of congestive gastropathy in patients with cirrhosis.

Aged↗

Prevalence of gastric ulcer in cirrhotic patients and its relation to portal hypertension.

The prevalence of gastric ulcer and its relationship to the severity of cirrhosis and degree of portal hypertension was evaluated in 245 cirrhotic patients, and compared with 245 age- and sex-matched healthy subjects. Portal and systemic haemodynamic studies were performed in cirrhotic patients. The prevalence of gastric ulcer in cirrhotic patients was 20.8%, which was significantly higher than the 4.0% found in healthy controls. Using a multivariate logistic regression model, the hepatic venous pressure gradient was found to be the only predictor of the prevalence of gastric ulcer in cirrhotic patients to present with gastric ulcer. The hepatic venous pressure gradient was significantly higher in cirrhotic patients with gastric ulcer than in those without (17.3 +/- 4.4 vs 15.5 +/- 5.0 mmHg, P = 0.01). Other variables, including sex, smoking, cardiac output and severity or aetiology of cirrhosis did not show significant differences between the two patient groups. The prevalence of gastric ulcer in cirrhotic patients whose hepatic venous pressure gradient was below 12 mmHg (4.5%) was similar to that observed in the healthy controls (4.0%). However, when the hepatic venous pressure gradient was > 12 mmHg, the prevalence of gastric ulcer (24.4%) was significantly higher than that in control subjects. However, the incidence of gastric ulcer was not related to the degree of portal hypertension. In conclusion, the prevalence of gastric ulcer in cirrhotic patients was found to be significantly higher than in the age- and sex-matched healthy subjects. Portal hypertension with a hepatic venous pressure gradient > 12 mmHg may be an important factor contributing to the increased prevalence of gastric ulcer observed in patients with liver cirrhosis.

Case-Control Studies↗

Hyperglucagonaemia in cirrhotic patients and its relationship to the severity of cirrhosis and haemodynamic values.

Plasma glucagon concentrations were measured in 160 cirrhotic patients (Pugh's grade A in 52 patients, Pugh's grade B in 64 patients and Pugh's grade C in 44 patients). These values were compared with plasma glucagon concentrations in 57 age and sex-matched healthy subjects. Systemic and portal haemodynamic measurements, effective renal plasma flow and creatinine clearance were recorded for each patient. Plasma glucagon levels were significantly increased in cirrhotic patients compared with healthy subjects. In addition, plasma glucagon levels were higher in cirrhotic patients with ascites than in those without ascites and were increased in relation to the severity of cirrhosis as assessed by Pugh's score. Multiple linear regression found that only Child-Pugh's score was estimated to be an independent predictor of hyperglucagonaemia in cirrhotic patients. However, in patients with different degrees of oesophageal varices and in patients without oesophageal varices, plasma glucagon concentrations were no different among the different groups of patients, but were still higher than plasma glucagon concentrations in healthy subjects. In contrast, plasma glucagon levels were negatively correlated with mean arterial pressure and systemic vascular resistance. The results of the present study suggest that impairment of liver function plays, in part, a role in increased plasma glucagon levels observed in patients with cirrhosis. In addition, these data support the hypothesis that hyperglucagonaemia may contribute, at least in part, to the pathogenesis of peripheral arterial vasodilatation in cirrhosis with portal hypertension.

Adult↗

Plasma interleukin-8 levels in patients with post-hepatitic cirrhosis: relationship to severity of liver disease, portal hypertension and hyperdynamic circulation.

The present study investigated plasma levels of interleukin-8 (IL-8) in patients with post-hepatitic cirrhosis and correlated it with the severity of liver diseases and haemodynamic parameters. Plasma IL-8 levels were significantly higher in 57 post-hepatitic cirrhotic patients (7.5 +/- 1.8 pg/mL; P < 0.005) than those in 41 healthy subjects (2.0 +/- 0.2 pg/mL). Elevated (> 5 pg/mL) plasma IL-8 levels were found in up to 30% of cirrhotic patients. In cirrhotic patients, plasma IL-8 levels progressively increased in relation to the severity of liver dysfunction (4.5 +/- 1.0, 4.9 +/- 1.4 and 20.5 +/- 8.3 pg/mL for Pugh's class A, B and C, respectively; P < 0.005). A significant correlation was observed between plasma IL-8 levels and serum bilirubin levels (r = 0.72; P < 0.001). There were no differences in the hepatic venous pressure gradient (15.4 +/- 1.1 vs 15.1 +/- 0.9 mmHg; P > 0.05) and systemic vascular resistance (1119 +/- 118 vs 1199 +/- 54 dyn.s/cm5; P > 0.05) between cirrhotic patients with and without elevated plasma IL-8 levels. In addition, plasma IL-8 levels did not correlate with hepatic venous pressure gradient (r = 0.26; P > 0.05) and systemic vascular resistance (r = -0.24; P > 0.05). These results demonstrate that plasma IL-8 levels are increased in patients with post-hepatitic cirrhosis. The severity of liver cirrhosis is an important factor for the occurrence of enhanced IL-8 levels. IL-8 does not play a role in the hyperdynamic circulation observed in patients with post-hepatitic cirrhosis.

Bilirubin↗