Portal Hypotensive Effects of Tetrandrine and Verapamil in Portal Hypertensive Rats

Liu, Tsun-Bin; H, Lin; Huang, Yo-Ping; Sun, Changming; Hong, Chuang‐Ye

doi:10.1111/j.2042-7158.1997.tb06757.x

Cited by 16 publications

(16 citation statements)

References 13 publications

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“…Our pilot chronic study also indicated that such regimens induced portal hypotensive effects. In our previous acute intravenous study [9], we found that tetrandrine was less potent than verapamil in reducing portal venous pressure. However, in our pilot chronic oral study, we observed that tetrandrine was equipotent to verapamil in portal pressure reduction in portal vein li gated rats.…”

Section: Resultsmentioning

confidence: 99%

“…It has been reported as a blocker of the voltage-activated, L-type Ca2+ channel in vascular smooth muscle cells [6,7], In hypertensive as well as normotensive rats, intravenous injection of tetrandrine induces a dose-dependent decrease of mean arterial pressure [8], However, the potential role of tetrandrine in portal hypertension therapy has yet to be assessed. Recently, we have observed that tetrandrine induced a dosedependent reduction of portal venous pres sure after acute intravenous infusion in portal Introduction hypertensive rats [9], In this study, we aimed to investigate the chronic hemodynamic ef fects of tetrandrine on portal hypertensive rats. Recently, it has been recognized that combination therapy of portal hypertension with drugs of different mechanisms of action does have the favorable advantages of both reducing side effects and enhancing portal hy potensive effects [2,3], In this study, we also evaluated whether the combination of tetran drine and propranolol achieved better results than either drug alone in portal hypertensive rats.…”

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confidence: 99%

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Hemodynamic Effects of Chronic Tetrandrine and Propranolol Administration on Portal Hypertensive Rats

et al. 1997

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The purpose of this study was to investigate the therapeutic effects of tetrandrine and propranolol, alone or in combination, on portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation in Sprague-Dawley rats. Animals were allocated into one of the four groups: vehicle group (0.1 N HC1, 0.7 ml/day), tetrandrine group (50 mg/kg/ day), propranolol group (30 mg/kg/day), and tetrandrine (50 mg/kg/day) plus propranolol (30 mg/kg/day) group. Drug or vehicle was administered by gavage for consecutive 9 days. After 9 days of treatment, the portal venous pressure and mean arterial pressure in each treatment group were significantly lower than those in the vehicle group. The cardiac index was not changed by tetrandrine alone, but reduced in the two groups receiving propranolol alone or in combination. Total peripheral resistance was significantly decreased in the tetrandrine group and significantly increased in the tetrandrine plus propranolol group as compared with the vehicle group. Our results suggested that tetrandrine or propranolol alone induced portal hypotensive effects, with propranolol achieving better antihyperdynamic effects in terms of cardiac index, and in combination propranolol effects predominated over those of tetrandrine.

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Section: Resultsmentioning

confidence: 99%

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Hemodynamic Effects of Chronic Tetrandrine and Propranolol Administration on Portal Hypertensive Rats

et al. 1997

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“…In this context, the potency of DL-028 and prazosin (dose range in micrograms ) is far greater than that of tetrandrine and verapamil (dose range in milligrams), two calcium channel antagonists, as reported in our previous paper [6]. Moreover, reduction of PVP by DL-028 and prazosin was much longer in duration (130 min) than that by tetrandrine and verapamil [6]. There are mainly two types of pharmacological approach to reduce portal hypertension: by decreasing portal blood flow or by decreasing portal vascular resistance (PVR).…”

Section: Discussionmentioning

confidence: 87%

“…Nevertheless, severe systemic or coronary vasoconstriction is the major drawback of vasopressin [2,4], while about one third of cirrhotic patients do not respond to propranolol [3]. In this context, efforts were made in trying to find some potential portal hypotensive drugs [5,6].…”

Section: Introductionmentioning

confidence: 99%

Portal Hypotensive Effects of DL-028 and Prazosin on Portal Hypertensive Rats

Huang¹,

Lin²,

Chern

et al. 1998

Pharmacology

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The portal hypotensive effects of prazosin and DL-028 (chem- ical name: 3-[[4-(2-methoxyphenyl)piperazin-1-yl]methyl]- 2,3-dihydroimidazo[1,2-c]quinazolin-5(6H)-one(27b)), a synthetic α₁-adrenoceptor antagonist, were assessed in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation in Sprague-Dawley rats. Two weeks after ligation, when the hyperdynamic state was stabilized the rats were anesthetized after an overnight fast and cannulated for measuring mean arterial pressure (MAP), portal venous pressure (PVP), cardiac index (CI) and heart rate (HR). Both DL-028 and prazosin (1, 3.3 and 10 µg/kg) induced dose-dependent decreases of PVP and MAP after intravenous infusion, with effects lasting for longer than 30 min. The maximum percentage reduction of PVP after DL-028 was 10, 10 and 15%, respectively, for the dosages given (1, 3.3 and 10 µg/kg), and 5, 12 and 25%, respectively, after prazosin. CI was not changed by either drug. HR was not changed by either drug except DL-028 at 10.0 µg/kg with a bradycardiac effect. Our results showed that both DL-028 and prazosin reduced PVP in portal hypertensive rats.

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“…In rats with liver cirrhosis and portal hypertension, Tet could reduce liver cell damage and fibroses, and lower the serum ALT, alkaline phosphatase (ALP) and total bilirubin (STB) to normal [4] . Tet could also lower the portal pressure and systemic arterial pressure in portal hypertensive rats [5] . In comparison with the traditional antifibrotic drug colohicine, Tet had more or less similar effects in reducing serum procollagen III peptide (P III P), HA and intrahepatic inflammation and had better effect than colohicine and less toxic side-effects [6] in suppression of proliferation and transformation of FSCs as well as the degree of collagen deposition.…”

Section: Effect Of Tetrandrine On Experimental Hepatofibrosis In Ratsmentioning

confidence: 99%

Progress in studies of tetrandrine against hepatofibrosis

Li¹

1998

WJG

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Subject headings liver cirrhosis/therapy; liver cirrhosis/pathology; liver cirrhosis, expremental/therapy; tetrandrine/therapeutic use Tetrandrine (Tet) is the main alkaloid isolated from the lumpy root of Stephania tetrandra s. Moore. Its molecular formula is C 33 H 42 N 2 O 6 and its chemical structure belongs to a dibenzy-isoquindine. Modern pharmacological studies have proved that Tet is a Ca 2+ antagonist, which acts mainly on the calcium channel of cell to block the cross-membrane transportation of calcium ions as well as their intracellular distribution and utilization. In recent years, the actions of Tet in preventing and treating hepatofibrosis have gradually attracted attention of more investigators. With the establishment of the technique of liver cell isolation and culture and advance in technology of molecular biology, studies of the antihepafibrotic effects of Tet have probed into the cellular, subcellular and molecular levels. This article is to give a brief review of such researches over the past few years. EFFECT OF TETRANDRINE ON EXPERIMENTAL HEPATOFIBROSIS IN RATSThe effects of Tet on CC l4 induced rat hepatofibrosis model showed that the serum contents of hyaluronic acid (HA) and serum ALT activities among the Tet treated groups in different stages were all lower than those in the untreated control model (P < 0.01). At the end of the 3rd week, the degrees of liver cell degeneration and necroses and inflammatory cell unvasion in the treated group were all lower than those of the control model. At the end of the 12th week, the control model rats showed an increase in fibroblast proliferation to grade 2.8 with pseudolobule formation on HE and VG staining; however in the corresponding treatment group, the lobular structure was still fairly well preserved, although there were some proliferation of fibroblasts and increase in collagen. These indicate that Tet may improve liver function, reduce liver damage and inhibit the extracellular matrix ( ECM ) formation [1] . Tet could suppress the proliferation and transformation of fat storing cells (FSC or Ito cells), reduce the deposition of type IV collagen and remarkably decrease the number of FSCs in rat with hepatofibrosis, as compared with the saline treated controls (P < 0.01). Moreover, the area of rough endoplasmic neticulum of FSCs in the treated group was less than that of the control group (P < 0.05) [2,3] . In rats with liver cirrhosis and portal hypertension, Tet could reduce liver cell damage and fibroses, and lower the serum ALT, alkaline phosphatase (ALP) and total bilirubin (STB) to normal [4] . Tet could also lower the portal pressure and systemic arterial pressure in portal hypertensive rats [5] . In comparison with the traditional antifibrotic drug colohicine, Tet had more or less similar effects in reducing serum procollagen III peptide (P III P), HA and intrahepatic inflammation and had better effect than colohicine and less toxic side-effects [6] in suppression of proliferation and transformation of FSCs as well as the degree of c...

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Portal Hypotensive Effects of Tetrandrine and Verapamil in Portal Hypertensive Rats

Cited by 16 publications

References 13 publications

Hemodynamic Effects of Chronic Tetrandrine and Propranolol Administration on Portal Hypertensive Rats

Hemodynamic Effects of Chronic Tetrandrine and Propranolol Administration on Portal Hypertensive Rats

Portal Hypotensive Effects of DL-028 and Prazosin on Portal Hypertensive Rats

Progress in studies of tetrandrine against hepatofibrosis

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