Biomedical subjects

H C Lin

Publications and source records attributed to H C Lin.

At least 127 records · Page 7Linked to original sources

PubMed1999

Effects of vasopressin on portal-systemic collaterals in portal hypertensive rats: role of nitric oxide and prostaglandin.

This study investigated the effect of vasopressin on portal-systemic collaterals in portal hypertensive rats and the influence of nitric oxide (NO) and prostaglandin on the responsiveness of collateral vessels to vasopressin. The vascular responsiveness to graded concentrations of vasopressin was tested with or without the incubation of n(omega)-nitro-L-arginine (NNA) (100 micromol/L) and/or indomethacin (10 micromol/L) in perfused collateral vascular beds of rats with portal hypertension induced by partial portal vein ligation. In addition, concentration-response curves to vasopressin with incubation of a vasopressin V(1) receptor antagonist d(CH(2))(5)Tyr(Me) arginine vasopressin and concentration-response curves to a V(2) receptor agonist 1-desamino-8-D-arginine vasopressin were performed. Vasopressin significantly increased the perfusion pressure of collaterals, and this effect was suppressed by the addition of the V(1) receptor antagonist. Perfusion with the V(2) receptor agonist had no effect on the collaterals. Incubation with NNA, indomethacin, or both significantly potentiated the response of collaterals to vasopressin. In addition, the pressor response to vasopressin in the combination group was significantly higher than that in the NNA-alone group. The results show that vasopressin produces a direct vasoconstrictive effect on the portal-systemic collaterals of portal hypertensive rats. This effect is mediated by the vasopressin V(1,) but not V(2), receptors. The attenuation of the response to vasopressin by NO and prostaglandin suggest a function role of both mediators in the regulation of the portal-systemic collateral circulation in portal hypertensive rats.

Animals↗

PubMed1999

The ileal brake: a fifteen-year progress report.

The "ileal brake" is the primary inhibitory feedback mechanism to control transit of a meal through the gastrointestinal tract in order to optimize nutrient digestion and absorption. Neurohormonal factors mediating this response continue to be identified. Recently, additional brakes that fine-tune transit have been described. When gut traffic control is disrupted, pathologic states characterized by malabsorption and impaired drug bioavailability manifest as diarrhea and malnutrition. An understanding of the importance of these nutrient-triggered brakes provides essential clues to future treatments of chronic diarrhea, malnutrition, and drug malabsorption.

Digestive System Physiological Phenomena↗

PubMed1999

Modulation of cardiovascular effects produced by nitric oxide and ionotropic glutamate receptor interaction in the nucleus tractus solitarii of rats.

Both nitric oxide (NO) and glutamate in the brain stem nuclei are involved in central cardiovascular regulation. In the present study, we investigated possible functional interactions between NO and glutamate in the modulation of cardiovascular function in the nucleus tractus solitarii (NTS) of anesthetized rats. In Sprague-Dawley rats, intra-NTS unilateral microinjections of L-glutamate (0.1 nmol/60 nl) and its ionotropic agonists NMDA (5 pmol) and AMPA (2 pmol) resulted in significant decreases in mean blood pressure (MBP) and heart rate (HR). The cardiovascular effects of L-glutamate, NMDA and AMPA were significantly blocked by prior administration of the neuronal NO synthase (nNOS) inhibitor, 7-nitroindazole (7-NI, 0.5 nmol), or by the soluble guanylyl cyclase (sGC) inhibitor, 1H-[1.2.4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ, 0.03-1 pmol). Conversely, a depressor and bradycardic effect was elicited by microinjection of either the NO precursor L-arginine (10 nmol) or the NO donor sodium nitroprusside (SNP, 0.2 nmol) into the NTS. Prior administration of the NMDA receptor antagonists MK-801 (0.1-1 nmol) and APV (0.1-4 nmol) significantly attenuated these effects of L-arginine. Similarly, cardiovascular responses to L-arginine in the NTS were inhibited by pre-injections with the non-NMDA receptor antagonists CNQX (10-330 pmol) and NBQX (2-10 pmol). Furthermore, APV (4 nmol) and CNQX (330 pmol) attenuated the depressor and bradycardic effects of SNP, respectively. This study demonstrates that baroreflex-like responses to microinjections of L-glutamate and its ionotropic agonists into the NTS involve synthesis of NO and activation of sGC. Reciprocally, central cardiovascular effects of NO also depend on responsive ionotropic glutamate receptors.

Animals↗

PubMed1999

Increased progenitor cell proliferation in the peripheral blood of patients with bronchial asthma: the role of nitric oxide.

BACKGROUND: Asthma exacerbation is associated with increased numbers of circulating CD34(+) progenitor cells, which may migrate to airways and develop into mature cells under the effects of cytokines and hematopoietic factors. Nitric oxide (NO) generation is enhanced in asthma and is known to suppress human hematopoiesis. OBJECTIVES: We studied circulating progenitor cells in the blood of patients with varying severity of asthma and examined the contribution of NO to their proliferation into eosinophil-forming colonies ex vivo. METHODS: With use of multiparameter flow cytometric analyses, the cell numbers and intracellular inducible NO synthase (iNOS) immunoreactivity of circulating CD34(+) cells in peripheral blood was measured. The serum level of GM-CSF or IL-5 was also determined. The colonies grown from progenitor cells were cultured in methylcellulose either in the presence or absence of growth factors, including GM-CSF, stem cell factor, and IL-3. RESULTS: A significantly greater number of circulating CD34(+) cells increased together with higher intracellular iNOS immunoreactivity in moderate asthmatics compared with mild intermittent asthmatics and healthy subjects. There was no significant difference in iNOS immunoreactivities or CD34(+) progenitor cell numbers between healthy subjects and those with mild intermittent asthma. Serum levels of GM-CSF or IL-5 were significantly higher in all asthmatics compared with healthy subjects and correlated with circulating CD34(+) cells. A greater number of colonies was grown either in the presence or absence of growth factors with a higher percentage of cells of eosinophil lineage in asthmatics than in health subjects. N(G)-nitro-L-arginine methyl ester potentiated and sodium nitroprusside inhibited the colony growth in both asthmatic and healthy subjects without a significant change in the percentage of eosinophil lineage. CONCLUSIONS: The production of NO from progenitor cells or other circulating cells may act in an autocrine or paracrine fashion to regulate progenitor cell growth and colony formation. However, this is not sufficient to control the increased proliferation of progenitor cells observed in asthma.

Adult↗

PubMed1999

Effects of sustained-release lanreotide on hemodynamics in rats with portal vein stenosis.

BACKGROUND/AIMS: Somatostatin and its analogue have been shown to provide beneficial effects in the management of portal hypertension and hyperdynamic circulation. The current study was undertaken to evaluate the effects of lanreotide, a sustained-release somatostatin analogue, on hemodynamics in rats with portal hypertension. METHODS: Immediately after portal vein stenosis, rats were randomly assigned to receive vehicle or a single intramuscular injection of lanreotide 10 mg/kg. Hemodynamic measurements (radioactive microsphere technique) with portal systemic shunts determinations were performed on the 4th and 8th day after surgery, respectively. RESULTS: On the 4th day after surgery, rats treated with lanreotide had significantly lower cardiac index and higher systemic vascular resistance than rats treated with vehicle, while these values were no different on the 8th day after portal vein stenosis. In contrast, the elevation of portal pressure, portal tributary blood flow, and splanchnic fraction of cardiac output had ameliorated following lanreotide administration associated with an increase in splanchnic arterial resistance. Portal systemic shunts were lower in rats receiving lanreotide than in rats receiving vehicle. CONCLUSION: The current study showed that a single injection of sustained-release lanreotide in rats with portal vein stenosis delayed the development of peripheral arterial vasodilatation and hyperdynamic circulation, while it modified the evolution of portal hypertension and splanchnic hyperemia. This treatment also prevents, in part, the development of portal systemic shunts in rats with portal vein stenosis.

Animals↗

PubMed1999

Evidence against a role for endotoxin in the hyperdynamic circulation of rats with prehepatic portal hypertension.

BACKGROUND/AIMS: Excessive formation of nitric oxide may mediate the generalized vasorelaxation and hyporesponsiveness to vasoconstrictors observed in portal hypertensive states. Endotoxin, released from the bowel and detoxified by the liver, could stimulate inducible nitric oxide synthase directly or indirectly via the cytokine cascade. This study investigated the effect of chronic intraperitoneal injection of polymyxin B, a neutralizing antagonist of endotoxin, on the hemodynamics of partially portal vein-ligated (PVL) rats. METHODS: Concomitantly with endotoxin (600 EU) and dactinomycin (80 microg), polymyxin B (0.1 mg) or normal saline (N/S) was administered via an intraperitoneal route to male Sprague-Dawley rats. Twenty-four hours later, mean arterial pressure was determined. In PVL rats polymyxin B (0.1 mg in 5 cc N/S) or N/S was given intraperitoneally twice daily from 2 days prior to operation until 5 days (short-term) or 14 days (long-term) after the operation. Long-term polymyxin B- or N/S-treated sham-operated rats were included as controls. Hemodynamic studies with a thermodilution technique were performed at the end of treatment. Blood samples were collected from another series of PVL rats with long-term treatment to determine plasma levels of endotoxin and tumor necrosis factor-alpha. Plasma levels of endotoxin and tumor necrosis factor-alpha were measured by Limulus assay and the ELISA method, respectively. RESULTS: With the dosage of 0.1 mg polymyxin B, hypotension in rats subjected to endotoxin and dactinomycin administration could be corrected (polymyxin B vs. placebo: 130.0+/-7.7 vs. 108.8+/-6.7 mm Hg, p<0.05). However, long-term or short-term treatment with the same dosage of polymyxin B failed to ameliorate the hyperdynamic circulation of PVL rats. In addition, long-term treatment with polymyxin B did not change systemic and portal hemodynamics in sham-operated rats. Plasma levels of endotoxin and tumor necrosis factor-alpha were comparable in PVL rats treated with long-term polymyxin B or N/S (p>0.05). CONCLUSIONS: Our findings do not support the role of endotoxin in the hyperdynamic circulation of PVL rats.

Animals↗

PubMed1999

D-amphetamine-induced depletion of energy and dopamine in the rat striatum is attenuated by nicotinamide pretreatment.

The present study examined the effects of nicotinamide on the D-amphetamine (AMPH)-induced dopamine (DA) depletion and energy metabolism change in the rat striatum. In chronic studies, co-administration of AMPH with desipramine, a drug that retards the metabolism of AMPH, (10 mg/kg, intraperitoneal [i.p.], respectively) caused a significant decrease of striatal DA content measured 7 days later. Pretreatment with nicotinamide (500 mg/kg, i.p.), the precursor molecule for the electron carrier molecule nicotinamide adenine dinucleotide (NAD), attenuated this effect of AMPH, whereas itself exerted no long-term effect on striatal DA content. In acute studies, a decrease in striatal adenosine triphospate/adenosine diphosphate (ATP/ADP) ratio was found 3 h after co-injection of AMPH and desipramine. However, nicotinamide pretreatment blocked the reduced striatal ATP/ADP ratio and resulted in a striking increase in striatal NAD content in AMPH-treated rats. Furthermore, nicotinamide was noted to increase striatal ATP/ADP ratio and NAD content in saline-treated rats. These findings suggest that nicotinamide protects against AMPH-induced DAergic neurotoxicity in the striatum of rats via energy supplement.

Animals↗

PubMed1999

Fat intolerance depends on rapid gastric emptying.

Patients with fat intolerance complain of early satiety, bloating, nausea, and vomiting. Since these symptoms are similar to those of patients with postgastrectomy dumping syndrome, we hypothesized that fat intolerance may be associated with early, rapid gastric emptying. Using a three-meal gastric emptying study, we compared gastric emptying in nine patients with a history of fat intolerance and nine normal volunteers. On three separate days, 500-ml radiolabeled test meals containing 0, 15, or 60 g of fat were studied. The percentages of the test meal emptied at 15 and 60 min were analyzed by repeated measures two-way ANOVA. At 15 min (p < 0.05) but not 60 min, gastric emptying was faster in patients than normals. Gastric emptying at 15 min (p < 0.001) and 60 min (p < 0.001) depended on the dose of fat. We conclude that fat intolerance is associated with early, rapid gastric emptying.

Adult↗

PubMed1999

Effect of anaemia on haemodynamics in patients with cirrhosis.

BACKGROUND: It has been suggested that increased blood haemoglobin attenuates splanchnic vasodilatation in portal-hypertensive rats by nitric oxide inactivation. However, the haemodynamic effect of anaemia in cirrhotic patients of varying severity has been rarely discussed. The aim of this study was to evaluate the influence of anaemia on systemic and splanchnic haemodynamics in cirrhotic patients of differing severity. METHODS: Two hundred and twenty-five cirrhotic patients were included in this study. All biochemical and haemodynamic results were utilized for analysis. Anaemia was defined as a haemoglobin level below the cut-off value of 12 g/dL, which might best predict low systemic vascular resistance. RESULTS: Compared with non-anaemic patients, anaemic patients had decreased mean arterial pressure (90 +/- 1 vs 95 +/- 1 mmHg, P = 0.002), and decreased systemic vascular resistance (1022 +/- 25 vs 1227 +/- 30, P < 0.0001), and increased cardiac index (4.3 +/- 0.1 vs 3.8 +/- 0.1 L/min per m2, P < 0.0001) and increased hepatic venous pressure gradient (16.7 +/- 0.5 vs 14.4 +/- 0.6 mmHg, P = 0.006). Haemoglobin concentration exerted an influence on the degree of vasodilatation in cirrhotic patients, with Child-Pugh's A class (but not in Child-Pugh's B and C classes), and in patients without ascites (but not in patients with ascites). CONCLUSIONS: It was concluded that anaemia has a negative effect on hyperdynamic circulation in patients with early cirrhosis which is not observed in patients with advanced cirrhosis.

Anemia↗

PubMed1999

Hypodense alveolar macrophages in patients with diabetes mellitus and active pulmonary tuberculosis.

SETTING: Alveolar macrophages (AM), a heterogeneous cell population, play a critical role in eliminating mycobacterial infections in collaboration with lymphocytes. Patients with diabetes mellitus (DM) show increased susceptibility to pulmonary tuberculosis (TB) infection. It is still uncertain whether there is a defect in T cell or AM activation in patients with DM against TB infection. OBJECTIVE: To study the difference in activation status of AM and T cells between patients with TB + DM and TB alone. METHOD: The heterogeneity of AM from 14 patients with TB + DM, 9 with TB alone, 10 normal subjects and 8 DM alone patients, was studied using Percoll density fractionation. The intracellular H2O2 production of AM before and after stimulation with phorbol myristate acetate (PMA) or F-Met-Leu-Phen (FMLP) was assayed by loading cells with 2',7'-dichlorofluorescin (DCFH) and analyzed by flow cytometry. Lymphocytes subsets (CD3, CD4, CD8) and their activation status (CD25) in bronchoalveolar lavage were also measured. RESULTS: The proportion of the least dense AM (< 1,030 g/ml) and the magnitude of DCFH oxidation of AM was higher in TB patients than in normal subjects, regardless of DM. Patients with TB + DM had a significantly lower proportion of the least density AM fraction than TB alone patients, regardless of disease extent. Among TB patients, the proportion of the least dense AM was inversely correlated with the bacterial load on sputum and the disease extent on chest radiograph. Stimulation of AM with PMA or FMLP induced an increase in the hypodense AM subpopulations and enhanced intracellular H2O2 generation in patients with TB + DM and to a similar extent in normal subjects, but not in patients with TB alone. There was no significant difference in CD3 numbers, CD4/CD8 ratio, and CD25+ cells between patients with TB alone and TB + DM. The activation status of AM or T lymphocytes from DM alone patients was not significantly different from those from normal subjects. CONCLUSION: Hypodense subpopulations of AM increase in active TB patients and are related to the disease severity as well as activation status of AM. AM in TB patients complicated with DM was less activated, and may be contributory to the susceptibility to mycobacterial infection.

Adult↗

PubMed1999

Aggregation inhibitory activity of minor acetophenones from Paeonia species.

Two minor acetophenones, 2,5-dihydroxy-4-methoxy-acetophenone (2) and 2,5-dihydroxy-4-methylacetophenone (7) from Paeonia species were found to selectively inhibit the aggregation of rabbit platelets induced by arachidonic acid. They were more potent than the major compound, paeonol (1), and 7 also inhibited the formation of TXA2 and PGD2 from arachidonic acid.

Acetophenones↗

PubMed1999

The rebleeding course and long-term outcome of esophageal variceal hemorrhage after ligation: comparison with sclerotherapy.

BACKGROUND: Endoscopic variceal ligation is widely accepted as the optimum endoscopic treatment for esophageal variceal hemorrhage. However, the rebleeding course and long-term outcome of patients with esophageal variceal hemorrhage after ligation have been poorly defined. Therefore, we conducted a long-term follow-up study to delineate the outcome of ligation and compare it with that after sclerotherapy. METHODS: One hundred and eighty-five liver cirrhotic patients with endoscopically proven esophageal variceal hemorrhage were randomized to undergo endoscopic variceal sclerotherapy or ligation. These patients received regular follow-up and detailed clinical assessment. RESULTS: Two patients developed hepatoma within 6 months of entry in each group and were excluded. Another six patients in the sclerotherapy group and seven patients in the ligation group were excluded because of poor compliance or lost to follow-up. Therefore, 84 patients in each group were analyzed. In this long-term follow-up (55.3 +/- 12.5 months) the rebleeding rate for ligation was lower than that for sclerotherapy, regardless of whether the rebleeding was analyzed by patient number or Kaplan-Meier analysis. With regard to the rebleeding risk of various periods, the sclerotherapy risk was higher than that of ligation within 4 weeks of the initial endoscopic treatment or before variceal eradication. Multifactorial analysis showed hematemesis, poor hepatic function, and sclerotherapy were the risk factors determining rebleeding. The annual hepatocellular carcinoma incidence was 4.9%. There was no difference in survival between sclerotherapy and ligation. Multifactorial analysis showed that poor hepatic function was the only factor determining survival. CONCLUSIONS: The rebleeding risk was higher in sclerotherapy than in ligation before variceal eradication, especially within 4 weeks of the initial endoscopic treatment. Long-term survival was dependent on hepatic reserve regardless of the treatment method.

Chi-Square Distribution↗

PubMed1999

Spider angiomas in patients with liver cirrhosis: role of alcoholism and impaired liver function.

BACKGROUND: Spider angioma is a common sign in patients with liver cirrhosis, but the pathogenesis is still unclear. Alcohol and hyperestrogenemia are both possible etiologies. This study was designed to investigate the relationship of spider angiomas in patients with liver cirrhosis to alcohol, liver function test results, and plasma levels of sex hormones. METHODS: Eighty-two patients with liver cirrhosis and 18 healthy subjects were enrolled in this study. The number, size, and location of the spider angiomas were recorded for all subjects. Plasma levels of estradiol and testosterone were measured. RESULTS: Cirrhotic patients had significantly higher estradiol/testosterone ratios (26.8 +/- 5.1 x 10(-3) versus 8.8 +/- 2.0 x 10(-3); P = 0.002) than healthy controls. Twenty-seven (33%) of the 82 cirrhotic patients had spider angiomas. Cirrhotic patients with spider angiomas were younger (56 +/- 3 versus 66 +/- 1 years; P = 0.002) and had higher serum bilirubin levels (3.3 +/- 0.6 versus 1.7 +/- 0.2 mg/dl; P = 0.002), longer prothrombin time (16.8 +/- 0.8 versus 14.8 +/- 0.4 sec; P = 0.01), and higher prevalence of alcoholism (41% versus 20%; P = 0.04) than those without. Stepwise logistic regression showed that alcoholism and serum bilirubin level were the only significant and independent predictors associated with the presence of spider angiomas in cirrhotic patients (odds ratio = 3.5; 95% confidence interval = 1.2-10.8; P = 0.03, and odds ratio = 2.8; 95% confidence interval = 1.3-5.7; P = 0.006, respectively). CONCLUSIONS: Alcoholism and impaired liver function are important predictors of the presence of spider angiomas in patients with liver cirrhosis.

Aged↗

PubMed1999

Serum uric acid levels in patients with cirrhosis: a reevaluation.

It has been reported that the serum uric acid levels in patients with cirrhosis were decreased compared with healthy subjects. These studies suggested that the lower serum uric acid levels in cirrhotic patients were attributed mainly to an increased effective vascular volume, and consequently to an excessive renal clearance of uric acid. However, the previous observations are challenged by a recent hypothesis for the pathogenesis of hyperdynamic circulation and formation of ascites in cirrhosis. The current study was undertaken to reevaluate serum uric acid levels in patients with cirrhosis. Ninety-eight cirrhotic patients with normal renal functions were included in this study. All biochemical and hemodynamic data were utilized for analysis. The mean serum uric acid level (mean, 6.1+/-1.2 mg/dL; range, 2.7-9.1 mg/dL) was higher than that of the age- and sex-matched healthy control subjects (mean, 5.5+/-1.3 mg/dL; range, 2.9-8.1 mg/dL; p = 0.018). Using multiple regression analysis it was determined that the serum uric acid level was not related to the severity of liver disease, cardiac index, systemic vascular resistance, and hepatic venous pressure gradient but was related closely to age (r = 0.210, p = 0.026) and effective renal plasma flow (r = -0.677, p < 0.0001). Compared with cirrhotic patients without ascites, those with ascites had a significantly higher serum uric acid level (6.7+/-1.6 mg/dL vs. 5.6+/-1.7 mg/dL, p < 0.05) and lower effective renal plasma flow (396+/-125 mL/min vs. 445+/-149 mL/min, p < 0.05). In conclusion, for cirrhotic patients with normal serum creatinine levels, the current study shows that the mean serum uric acid level is higher than that of healthy control subjects. It is not related to the severity of liver failure and systemic and portal hemodynamics, but is related closely to renal functions, especially the renal plasma flow.

Adult↗

PubMed1999

Portal hypotensive effects of combined terlipressin and DL-028, a synthetic alpha 1 adrenoceptor antagonist administration on anesthetized portal hypertensive rats.

AIMS/BACKGROUND: The purpose of this study was to investigate the therapeutic effects of terlipressin, alone or in combination with DL-028, a synthetic alpha 1-adrenoceptor antagonist on anesthetized portal hypertensive rats. METHODS: Portal hypertension was induced by either partial portal vein ligation (PVL) or bile duct ligation (BDL) in Sprague-Dawley rats. Each portal hypertensive rat received only one of the two regimens: vehicle plus terlipressin or DL-028 plus terlipressin. Terlipressin dosage was 0.017 mg/kg/min infused for 3 min, while vehicle or DL-028 (0.50 microgram/kg/min) was continuously infused for 40 min, starting 10 min before terlipressin infusion. RESULTS: In PVL rats, infusions of vehicle plus terlipressin induced significant, maximum reduction of portal venous pressure (PVP, -11.0 +/- 1.8%) and prominent elevation of mean arterial pressure (MAP, 50.3 +/- 9.0%) from baseline. Infusions of DL-028 plus terlipressin induced maximum PVP reduction (-17.5 +/- 2.8%) and MAP elevation (39.8 +/- 7.4%). In BDL rats, infusion of vehicle plus terlipressin also induced significant, maximum reduction of PVP (-6.8 +/- 2.1%) and prominent elevation of MAP (61.4 +/- 7.8%) from baseline. Infusions of DL-028 plus terlipressin induced maximum PVP reduction (-17.9 +/- 2.2%) and MAP elevation (47.9 +/- 7.4%). Compared to vehicle plus terlipressin, DL-028 significantly enhanced portal hypotensive effects of and attenuated systemic pressor effects of terlipressin in both PVL and BDL rats. CONCLUSIONS: Our results suggest that terlipressin, alone or in combination with DL-028, induced portal hypotensive effects in portal hypertensive rats. The combination of terlipressin with DL-028 was beneficial in enhancing the portal hypotensive effects and ameliorating the systemic pressor effects of terlipressin.

Adrenergic alpha-Antagonists↗

PubMed1999

Effects of octreotide on central hemodynamics and systemic oxygen use in patients with viral cirrhosis.

OBJECTIVE: Octreotide has potentially beneficial effects in patients with cirrhosis. However, the effects of octreotide on central hemodynamics and oxygen use have not been established. The present study was undertaken to evaluate the effect of octreotide on central hemodynamics and oxygen use in patients with viral cirrhosis. METHODS: Twenty-five patients with cirrhosis were enrolled in the study. They were randomly assigned to receive either placebo (n = 10) or a continuous infusion of 100 microg/h of octreotide after an initial 100-microg bolus (n = 15). Hemodynamic measurements and oxygenation values were obtained before and 60 min after octreotide or placebo administration. RESULTS: Placebo administration did not have any effect on hemodynamic and oxygenation values. In patients who received octreotide, systemic hemodynamic values including cardiac index, mean arterial pressure, and systemic vascular resistance were not affected. The mean pulmonary arterial pressure tended to increase after octreotide administration but was statistically insignificant. There was a significant increase in pulmonary arterial vascular resistance, whereas the pulmonary capillary wedge pressure and right atrial pressure were significantly decreased. Arterial oxygen tension, systemic oxygen uptake, and oxygen extraction ratio were significantly decreased after octreotide administration, whereas oxygen transport as well as arterial and mixed venous oxygen contents remained unchanged. CONCLUSIONS: In patients with viral cirrhosis, octreotide administration exerted a significant effect on pulmonary circulation. It also resulted in a decrease in systemic oxygen uptake and oxygen extraction ratio. These results suggested that octreotide may impair tissue oxygenation in patients with viral cirrhosis.

Aged↗

PubMed1999

Role of substance P in the pathogenesis of spider angiomas in patients with nonalcoholic liver cirrhosis.

OBJECTIVE: Cutaneous spider angioma is a common sign observed in patients with liver cirrhosis, but its pathogenesis is still unclear. Increased plasma levels of estrogen, vascular dilation, and neovascularization are possible etiologies. This study was designed to investigate the relationship of spider angiomas in patients with nonalcoholic liver cirrhosis to the plasma levels of sex hormones and various vasodilators and hemodynamic parameters. METHODS: A total of 60 patients with nonalcoholic liver cirrhosis and 20 healthy subjects were included in this study. The number, size, and location of the spider angiomas were recorded. Plasma levels of estradiol, testosterone, substance P, calcitonin gene-related peptide, and nitrate/nitrite and forearm hemodynamics were measured. RESULTS: Cirrhotic patients showed higher plasma estradiol/testosterone ratios (28.3+/-47.2 x 10(-3), median 10.5 x 10(-3) vs 8.2+/-8.3 x 10(-3), median 5.7 x 10(-3), p = 0.003) and levels of nitrate/ nitrite (29.9+/-17.5, median 23.8 vs 21.4+/-10.0, median 20.6 micromol/L, p = 0.01) and substance P (47.5+/-62.5, median 29.2 vs 15.2+/-7.7, median 12.3 pg/ml, p < 0.001) than healthy controls. Sixteen (27%) of the 60 cirrhotic patients had spider angiomas. Cirrhotic patients with spider angiomas disclosed higher plasma levels of substance P (84.7+/-105.3, median 53.1 vs 34.5+/-30.7, median 25.8 pg/ml, p = 0.006) and serum levels of bilirubin (3.9+/-3.8, median 1.9 vs 1.9+/-1.9, median 1.2 mg/dl, p = 0.02) than those without. Stepwise logistic regression showed substance P was the only significant and independent predictor associated with the presence of spider angiomas in cirrhotic patients (odds ratio = 3.0, 95% confidence interval = 1.4-6.6, p = 0.01). CONCLUSION: Plasma levels of substance P are elevated in patients with nonalcoholic cirrhosis and may play an important role in the pathogenesis of spider angiomas.

Aged↗

PubMed1999

Intestinal fat-induced inhibition of meal-stimulated gastric acid secretion depends on CCK but not peptide YY.

Fat in small intestine decreases meal-stimulated gastric acid secretion and slows gastric emptying. CCK is a mediator of this inhibitory effect (an enterogastrone). Because intravenously administered peptide YY (PYY) inhibits acid secretion, endogenous PYY released by fat may also be an enterogastrone. Four dogs were equipped with gastric, duodenal, and midgut fistulas. PYY antibody (anti-PYY) at a dose of 0.5 mg/kg or CCK-A receptor antagonist (devazepide) at a dose of 0.1 mg/kg was administered alone or in combination 10 min before the proximal half of the gut was perfused with 60 mM oleate or buffer. Acid secretion and gastric emptying were measured. We found that 1) peptone-induced gastric acid secretion was inhibited by intestinal fat (P < 0.0001), 2) inhibition of acid secretion by intestinal fat was reversed by CCK-A receptor antagonist (P < 0.0001) but not by anti-PYY, and 3) slowing of gastric emptying by fat was reversed by CCK-A antagonist (P < 0. 05) but not by anti-PYY. We concluded that inhibition of peptone meal-induced gastric acid secretion and slowing of gastric emptying by intestinal fat depended on CCK but not on circulating PYY.

Animals↗