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Joan Rodés - One of the best experts on this subject based on the ideXlab platform.
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Effects of ritanserin, a selective and specific S2-Serotonergic Antagonist, on portal pressure and splanchnic hemodynamics in rats with long-term bile duct ligation
Hepatology (Baltimore Md.), 1993Co-Authors: Mercedes Fernández, Jaime Bosch, Pilar M Pizcueta, Juan Carlos García-pagán, Faust Feu, Isabel Cirera, Joan RodésAbstract:This study investigated the short-term effects of ritanserin, a selective and specific S2-Serotonergic Antagonist, in an experimental model of cirrhosis and intrahepatic portal hypertension caused by long-term bile duct ligation and division and in normal control rats. The rats subjected to bile duct ligation were randomized under blind conditions into two groups to receive ritanserin (0.7 mg/kg body wt, intravenously; n = 10) or the same volume of placebo (isotonic saline solution; n = 10). We performed hemodynamic studies with radiolabeled microspheres 60 min after drug administration. Two groups of normal rats (n = 6) were studied after they received ritanserin or placebo. Ritanserin administration to rats subjected to bile duct ligation significantly reduced portal pressure (from 16.2 ± 1.3 mm Hg to 12.3 ± 0.7 mm Hg; mean decrease, 22% ± 5%; p < 0.05). This reduction was associated with lower portal venous resistance (4.3 ± 0.5 mm Hg ± min. 100 gm/ml in the placebo group vs. 3.1 ± 0.3 mm Hg. min. 100 gm/ml in rats given ritanserin; mean decrease, 28%; p = 0.069), but we saw no changes in portal vein inflow (3.9 ± 0.5 ml/min ± 100 gm vs. 4.4 ± 0.4 ml/min ± 100 gm), mean arterial pressure (110 ± 9 mm Hg vs. 102 ± 9 mm Hg) and cardiac index (32.9 ± 2.7 ml/min ± 100 gm vs. 40.5 ± 6.7 ml/min ± 100 gm). Hepatic arterial and kidney blood flows were not modified by ritanserin. Ritanserin had no systemic or splanchnic effects in normal rats. Our results demonstrate that ritanserin infusion decreases portal pressure without any systemic hemodynamic change in rats with secondary biliary cirrhosis and portal hypertension. These findings provide further support for a role of serotonin in the pathogenesis of portal hypertension and suggest a potential use of ritanserin (alone or associated with other agents) in the pharmacological treatment of portal hypertension. (HEPATOLOGY 1993;18:389–393).
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effects of ritanserin a selective and specific s2 Serotonergic Antagonist on portal pressure and splanchnic hemodynamics in portal hypertensive rats
Hepatology, 1991Co-Authors: Frederik Nevens, Mercedes Fernández, Jaime Bosch, Pilar M Pizcueta, Joan RodésAbstract:Serotonergic mechanisms have recently been implicated in the pathogenesis of portal hypertension; this suggests that blockade of serotonin S2 receptors may be a new approach for the pharmacological therapy of portal hypertension. This study was aimed at investigating the effects of ritanserin, a selective S2-Serotonergic Antagonist, in portal-hypertensive rats whose condition was due to partial portal vein ligation. The animals were randomized under double-blind conditions into two groups: the first received ritanserin (0.7 mg/kg body wt, intravenously), and the second received the same volume of placebo (isotonic saline solution). The hemodynamic studies were performed using radiolabeled microspheres 60 min after drug administration. Ritanserin administration significantly reduced portal pressure (from 11.8 ± 0.8 mm Hg to 9.4 ± 0.6 mm Hg; p < 0.05). This was associated with lower portocollateral resistance (1.8 ± 0.2 mm Hg/ml/min 100 gm in the ritanserin group vs. 2.3 ± 0.2 mm Hg/ml/min 100 gm in rats receiving placebo; not significant), but we saw no changes in portal-vein inflow (5.5 ± 0.7 ml/min 100 gm vs. 5.4 ± 0.5 ml/min 100 gm), mean arterial pressure (95.9 ± 3.5 mm Hg vs. 94.0 ± 4.0 mm Hg) and cardiac index (31.9 ± 3.5 ml/min 100 gm vs. 28.5 ± 2.6 ml/min 100 gm). Hepatic arterial and kidney blood flows were not modified by ritanserin. In summary, our results demonstrate that ritanserin infusion decreases portal pressure without causing systemic hemodynamic changes. This effect is probably due to a decrease in portocollateral resistance in portal-hypertensive rats. These results provide further for a role of serotonin in the pathogenesis of portal hypertension. (HEPATOLOGY 1991;14:1174–1178.)
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Effects of ritanserin, a selective and specific S2‐Serotonergic Antagonist, on portal pressure and splanchnic hemodynamics in portal hypertensive rats
Hepatology (Baltimore Md.), 1991Co-Authors: Frederik Nevens, M. Pilar Pizcueta, Mercedes Fernández, Jaime Bosch, Joan RodésAbstract:Serotonergic mechanisms have recently been implicated in the pathogenesis of portal hypertension; this suggests that blockade of serotonin S2 receptors may be a new approach for the pharmacological therapy of portal hypertension. This study was aimed at investigating the effects of ritanserin, a selective S2-Serotonergic Antagonist, in portal-hypertensive rats whose condition was due to partial portal vein ligation. The animals were randomized under double-blind conditions into two groups: the first received ritanserin (0.7 mg/kg body wt, intravenously), and the second received the same volume of placebo (isotonic saline solution). The hemodynamic studies were performed using radiolabeled microspheres 60 min after drug administration. Ritanserin administration significantly reduced portal pressure (from 11.8 ± 0.8 mm Hg to 9.4 ± 0.6 mm Hg; p < 0.05). This was associated with lower portocollateral resistance (1.8 ± 0.2 mm Hg/ml/min 100 gm in the ritanserin group vs. 2.3 ± 0.2 mm Hg/ml/min 100 gm in rats receiving placebo; not significant), but we saw no changes in portal-vein inflow (5.5 ± 0.7 ml/min 100 gm vs. 5.4 ± 0.5 ml/min 100 gm), mean arterial pressure (95.9 ± 3.5 mm Hg vs. 94.0 ± 4.0 mm Hg) and cardiac index (31.9 ± 3.5 ml/min 100 gm vs. 28.5 ± 2.6 ml/min 100 gm). Hepatic arterial and kidney blood flows were not modified by ritanserin. In summary, our results demonstrate that ritanserin infusion decreases portal pressure without causing systemic hemodynamic changes. This effect is probably due to a decrease in portocollateral resistance in portal-hypertensive rats. These results provide further for a role of serotonin in the pathogenesis of portal hypertension. (HEPATOLOGY 1991;14:1174–1178.)
Frederik Nevens - One of the best experts on this subject based on the ideXlab platform.
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effects of ritanserin a selective and specific s2 Serotonergic Antagonist on portal pressure and splanchnic hemodynamics in portal hypertensive rats
Hepatology, 1991Co-Authors: Frederik Nevens, Mercedes Fernández, Jaime Bosch, Pilar M Pizcueta, Joan RodésAbstract:Serotonergic mechanisms have recently been implicated in the pathogenesis of portal hypertension; this suggests that blockade of serotonin S2 receptors may be a new approach for the pharmacological therapy of portal hypertension. This study was aimed at investigating the effects of ritanserin, a selective S2-Serotonergic Antagonist, in portal-hypertensive rats whose condition was due to partial portal vein ligation. The animals were randomized under double-blind conditions into two groups: the first received ritanserin (0.7 mg/kg body wt, intravenously), and the second received the same volume of placebo (isotonic saline solution). The hemodynamic studies were performed using radiolabeled microspheres 60 min after drug administration. Ritanserin administration significantly reduced portal pressure (from 11.8 ± 0.8 mm Hg to 9.4 ± 0.6 mm Hg; p < 0.05). This was associated with lower portocollateral resistance (1.8 ± 0.2 mm Hg/ml/min 100 gm in the ritanserin group vs. 2.3 ± 0.2 mm Hg/ml/min 100 gm in rats receiving placebo; not significant), but we saw no changes in portal-vein inflow (5.5 ± 0.7 ml/min 100 gm vs. 5.4 ± 0.5 ml/min 100 gm), mean arterial pressure (95.9 ± 3.5 mm Hg vs. 94.0 ± 4.0 mm Hg) and cardiac index (31.9 ± 3.5 ml/min 100 gm vs. 28.5 ± 2.6 ml/min 100 gm). Hepatic arterial and kidney blood flows were not modified by ritanserin. In summary, our results demonstrate that ritanserin infusion decreases portal pressure without causing systemic hemodynamic changes. This effect is probably due to a decrease in portocollateral resistance in portal-hypertensive rats. These results provide further for a role of serotonin in the pathogenesis of portal hypertension. (HEPATOLOGY 1991;14:1174–1178.)
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Effects of ritanserin, a selective and specific S2‐Serotonergic Antagonist, on portal pressure and splanchnic hemodynamics in portal hypertensive rats
Hepatology (Baltimore Md.), 1991Co-Authors: Frederik Nevens, M. Pilar Pizcueta, Mercedes Fernández, Jaime Bosch, Joan RodésAbstract:Serotonergic mechanisms have recently been implicated in the pathogenesis of portal hypertension; this suggests that blockade of serotonin S2 receptors may be a new approach for the pharmacological therapy of portal hypertension. This study was aimed at investigating the effects of ritanserin, a selective S2-Serotonergic Antagonist, in portal-hypertensive rats whose condition was due to partial portal vein ligation. The animals were randomized under double-blind conditions into two groups: the first received ritanserin (0.7 mg/kg body wt, intravenously), and the second received the same volume of placebo (isotonic saline solution). The hemodynamic studies were performed using radiolabeled microspheres 60 min after drug administration. Ritanserin administration significantly reduced portal pressure (from 11.8 ± 0.8 mm Hg to 9.4 ± 0.6 mm Hg; p < 0.05). This was associated with lower portocollateral resistance (1.8 ± 0.2 mm Hg/ml/min 100 gm in the ritanserin group vs. 2.3 ± 0.2 mm Hg/ml/min 100 gm in rats receiving placebo; not significant), but we saw no changes in portal-vein inflow (5.5 ± 0.7 ml/min 100 gm vs. 5.4 ± 0.5 ml/min 100 gm), mean arterial pressure (95.9 ± 3.5 mm Hg vs. 94.0 ± 4.0 mm Hg) and cardiac index (31.9 ± 3.5 ml/min 100 gm vs. 28.5 ± 2.6 ml/min 100 gm). Hepatic arterial and kidney blood flows were not modified by ritanserin. In summary, our results demonstrate that ritanserin infusion decreases portal pressure without causing systemic hemodynamic changes. This effect is probably due to a decrease in portocollateral resistance in portal-hypertensive rats. These results provide further for a role of serotonin in the pathogenesis of portal hypertension. (HEPATOLOGY 1991;14:1174–1178.)
Mercedes Fernández - One of the best experts on this subject based on the ideXlab platform.
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Effects of ritanserin, a selective and specific S2-Serotonergic Antagonist, on portal pressure and splanchnic hemodynamics in rats with long-term bile duct ligation
Hepatology (Baltimore Md.), 1993Co-Authors: Mercedes Fernández, Jaime Bosch, Pilar M Pizcueta, Juan Carlos García-pagán, Faust Feu, Isabel Cirera, Joan RodésAbstract:This study investigated the short-term effects of ritanserin, a selective and specific S2-Serotonergic Antagonist, in an experimental model of cirrhosis and intrahepatic portal hypertension caused by long-term bile duct ligation and division and in normal control rats. The rats subjected to bile duct ligation were randomized under blind conditions into two groups to receive ritanserin (0.7 mg/kg body wt, intravenously; n = 10) or the same volume of placebo (isotonic saline solution; n = 10). We performed hemodynamic studies with radiolabeled microspheres 60 min after drug administration. Two groups of normal rats (n = 6) were studied after they received ritanserin or placebo. Ritanserin administration to rats subjected to bile duct ligation significantly reduced portal pressure (from 16.2 ± 1.3 mm Hg to 12.3 ± 0.7 mm Hg; mean decrease, 22% ± 5%; p < 0.05). This reduction was associated with lower portal venous resistance (4.3 ± 0.5 mm Hg ± min. 100 gm/ml in the placebo group vs. 3.1 ± 0.3 mm Hg. min. 100 gm/ml in rats given ritanserin; mean decrease, 28%; p = 0.069), but we saw no changes in portal vein inflow (3.9 ± 0.5 ml/min ± 100 gm vs. 4.4 ± 0.4 ml/min ± 100 gm), mean arterial pressure (110 ± 9 mm Hg vs. 102 ± 9 mm Hg) and cardiac index (32.9 ± 2.7 ml/min ± 100 gm vs. 40.5 ± 6.7 ml/min ± 100 gm). Hepatic arterial and kidney blood flows were not modified by ritanserin. Ritanserin had no systemic or splanchnic effects in normal rats. Our results demonstrate that ritanserin infusion decreases portal pressure without any systemic hemodynamic change in rats with secondary biliary cirrhosis and portal hypertension. These findings provide further support for a role of serotonin in the pathogenesis of portal hypertension and suggest a potential use of ritanserin (alone or associated with other agents) in the pharmacological treatment of portal hypertension. (HEPATOLOGY 1993;18:389–393).
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effects of ritanserin a selective and specific s2 Serotonergic Antagonist on portal pressure and splanchnic hemodynamics in portal hypertensive rats
Hepatology, 1991Co-Authors: Frederik Nevens, Mercedes Fernández, Jaime Bosch, Pilar M Pizcueta, Joan RodésAbstract:Serotonergic mechanisms have recently been implicated in the pathogenesis of portal hypertension; this suggests that blockade of serotonin S2 receptors may be a new approach for the pharmacological therapy of portal hypertension. This study was aimed at investigating the effects of ritanserin, a selective S2-Serotonergic Antagonist, in portal-hypertensive rats whose condition was due to partial portal vein ligation. The animals were randomized under double-blind conditions into two groups: the first received ritanserin (0.7 mg/kg body wt, intravenously), and the second received the same volume of placebo (isotonic saline solution). The hemodynamic studies were performed using radiolabeled microspheres 60 min after drug administration. Ritanserin administration significantly reduced portal pressure (from 11.8 ± 0.8 mm Hg to 9.4 ± 0.6 mm Hg; p < 0.05). This was associated with lower portocollateral resistance (1.8 ± 0.2 mm Hg/ml/min 100 gm in the ritanserin group vs. 2.3 ± 0.2 mm Hg/ml/min 100 gm in rats receiving placebo; not significant), but we saw no changes in portal-vein inflow (5.5 ± 0.7 ml/min 100 gm vs. 5.4 ± 0.5 ml/min 100 gm), mean arterial pressure (95.9 ± 3.5 mm Hg vs. 94.0 ± 4.0 mm Hg) and cardiac index (31.9 ± 3.5 ml/min 100 gm vs. 28.5 ± 2.6 ml/min 100 gm). Hepatic arterial and kidney blood flows were not modified by ritanserin. In summary, our results demonstrate that ritanserin infusion decreases portal pressure without causing systemic hemodynamic changes. This effect is probably due to a decrease in portocollateral resistance in portal-hypertensive rats. These results provide further for a role of serotonin in the pathogenesis of portal hypertension. (HEPATOLOGY 1991;14:1174–1178.)
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Effects of ritanserin, a selective and specific S2‐Serotonergic Antagonist, on portal pressure and splanchnic hemodynamics in portal hypertensive rats
Hepatology (Baltimore Md.), 1991Co-Authors: Frederik Nevens, M. Pilar Pizcueta, Mercedes Fernández, Jaime Bosch, Joan RodésAbstract:Serotonergic mechanisms have recently been implicated in the pathogenesis of portal hypertension; this suggests that blockade of serotonin S2 receptors may be a new approach for the pharmacological therapy of portal hypertension. This study was aimed at investigating the effects of ritanserin, a selective S2-Serotonergic Antagonist, in portal-hypertensive rats whose condition was due to partial portal vein ligation. The animals were randomized under double-blind conditions into two groups: the first received ritanserin (0.7 mg/kg body wt, intravenously), and the second received the same volume of placebo (isotonic saline solution). The hemodynamic studies were performed using radiolabeled microspheres 60 min after drug administration. Ritanserin administration significantly reduced portal pressure (from 11.8 ± 0.8 mm Hg to 9.4 ± 0.6 mm Hg; p < 0.05). This was associated with lower portocollateral resistance (1.8 ± 0.2 mm Hg/ml/min 100 gm in the ritanserin group vs. 2.3 ± 0.2 mm Hg/ml/min 100 gm in rats receiving placebo; not significant), but we saw no changes in portal-vein inflow (5.5 ± 0.7 ml/min 100 gm vs. 5.4 ± 0.5 ml/min 100 gm), mean arterial pressure (95.9 ± 3.5 mm Hg vs. 94.0 ± 4.0 mm Hg) and cardiac index (31.9 ± 3.5 ml/min 100 gm vs. 28.5 ± 2.6 ml/min 100 gm). Hepatic arterial and kidney blood flows were not modified by ritanserin. In summary, our results demonstrate that ritanserin infusion decreases portal pressure without causing systemic hemodynamic changes. This effect is probably due to a decrease in portocollateral resistance in portal-hypertensive rats. These results provide further for a role of serotonin in the pathogenesis of portal hypertension. (HEPATOLOGY 1991;14:1174–1178.)
Nishikant K. Subhedar - One of the best experts on this subject based on the ideXlab platform.
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Effect of alpha-melanocyte stimulating hormone on locomotor recovery following spinal cord injury in mice: Role of Serotonergic system.
Neuropeptides, 2010Co-Authors: Ashish P. Bharne, Manoj A. Upadhya, Dadasaheb M. Kokare, Nishikant K. SubhedarAbstract:Abstract The present study underscores the effect of Serotonergic Antagonist on alpha-melanocyte stimulating hormone (α-MSH) induced neuronal regeneration. Swiss-albino mice were subjected to experimental spinal cord injury (ESCI) and treated with Serotonergic Antagonist, ritanserin, alone or in combination with α-MSH, and the locomotor recovery was investigated. ESCI was induced at thoracic T 10–12 level by compression method. Motor function score (0–10) of each mouse was monitored prior to, and on days 1, 4, 7, 10 and 14 following ESCI. Untreated ESCI animals showed almost normal hind limb motor function by 14days. Similar degree of recovery was observed on day 10 in animals given α-MSH or ritanserin. However, in animals treated with both agents, comparable recovery was observed on day 4. While histological examination of the spinal cord following ESCI showed demyelination, necrosis and cyst formation, treatment with ritanserin, alone and in combination with α-MSH, significantly prevented the tissue damage. We suggest that early antagonism of Serotonergic 5-HT 2a/2c receptors may potentiate the neurotropic and locomotor recovery activity of α-MSH.
Jaime Bosch - One of the best experts on this subject based on the ideXlab platform.
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Effects of ritanserin, a selective and specific S2-Serotonergic Antagonist, on portal pressure and splanchnic hemodynamics in rats with long-term bile duct ligation
Hepatology (Baltimore Md.), 1993Co-Authors: Mercedes Fernández, Jaime Bosch, Pilar M Pizcueta, Juan Carlos García-pagán, Faust Feu, Isabel Cirera, Joan RodésAbstract:This study investigated the short-term effects of ritanserin, a selective and specific S2-Serotonergic Antagonist, in an experimental model of cirrhosis and intrahepatic portal hypertension caused by long-term bile duct ligation and division and in normal control rats. The rats subjected to bile duct ligation were randomized under blind conditions into two groups to receive ritanserin (0.7 mg/kg body wt, intravenously; n = 10) or the same volume of placebo (isotonic saline solution; n = 10). We performed hemodynamic studies with radiolabeled microspheres 60 min after drug administration. Two groups of normal rats (n = 6) were studied after they received ritanserin or placebo. Ritanserin administration to rats subjected to bile duct ligation significantly reduced portal pressure (from 16.2 ± 1.3 mm Hg to 12.3 ± 0.7 mm Hg; mean decrease, 22% ± 5%; p < 0.05). This reduction was associated with lower portal venous resistance (4.3 ± 0.5 mm Hg ± min. 100 gm/ml in the placebo group vs. 3.1 ± 0.3 mm Hg. min. 100 gm/ml in rats given ritanserin; mean decrease, 28%; p = 0.069), but we saw no changes in portal vein inflow (3.9 ± 0.5 ml/min ± 100 gm vs. 4.4 ± 0.4 ml/min ± 100 gm), mean arterial pressure (110 ± 9 mm Hg vs. 102 ± 9 mm Hg) and cardiac index (32.9 ± 2.7 ml/min ± 100 gm vs. 40.5 ± 6.7 ml/min ± 100 gm). Hepatic arterial and kidney blood flows were not modified by ritanserin. Ritanserin had no systemic or splanchnic effects in normal rats. Our results demonstrate that ritanserin infusion decreases portal pressure without any systemic hemodynamic change in rats with secondary biliary cirrhosis and portal hypertension. These findings provide further support for a role of serotonin in the pathogenesis of portal hypertension and suggest a potential use of ritanserin (alone or associated with other agents) in the pharmacological treatment of portal hypertension. (HEPATOLOGY 1993;18:389–393).
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effects of ritanserin a selective and specific s2 Serotonergic Antagonist on portal pressure and splanchnic hemodynamics in portal hypertensive rats
Hepatology, 1991Co-Authors: Frederik Nevens, Mercedes Fernández, Jaime Bosch, Pilar M Pizcueta, Joan RodésAbstract:Serotonergic mechanisms have recently been implicated in the pathogenesis of portal hypertension; this suggests that blockade of serotonin S2 receptors may be a new approach for the pharmacological therapy of portal hypertension. This study was aimed at investigating the effects of ritanserin, a selective S2-Serotonergic Antagonist, in portal-hypertensive rats whose condition was due to partial portal vein ligation. The animals were randomized under double-blind conditions into two groups: the first received ritanserin (0.7 mg/kg body wt, intravenously), and the second received the same volume of placebo (isotonic saline solution). The hemodynamic studies were performed using radiolabeled microspheres 60 min after drug administration. Ritanserin administration significantly reduced portal pressure (from 11.8 ± 0.8 mm Hg to 9.4 ± 0.6 mm Hg; p < 0.05). This was associated with lower portocollateral resistance (1.8 ± 0.2 mm Hg/ml/min 100 gm in the ritanserin group vs. 2.3 ± 0.2 mm Hg/ml/min 100 gm in rats receiving placebo; not significant), but we saw no changes in portal-vein inflow (5.5 ± 0.7 ml/min 100 gm vs. 5.4 ± 0.5 ml/min 100 gm), mean arterial pressure (95.9 ± 3.5 mm Hg vs. 94.0 ± 4.0 mm Hg) and cardiac index (31.9 ± 3.5 ml/min 100 gm vs. 28.5 ± 2.6 ml/min 100 gm). Hepatic arterial and kidney blood flows were not modified by ritanserin. In summary, our results demonstrate that ritanserin infusion decreases portal pressure without causing systemic hemodynamic changes. This effect is probably due to a decrease in portocollateral resistance in portal-hypertensive rats. These results provide further for a role of serotonin in the pathogenesis of portal hypertension. (HEPATOLOGY 1991;14:1174–1178.)
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Effects of ritanserin, a selective and specific S2‐Serotonergic Antagonist, on portal pressure and splanchnic hemodynamics in portal hypertensive rats
Hepatology (Baltimore Md.), 1991Co-Authors: Frederik Nevens, M. Pilar Pizcueta, Mercedes Fernández, Jaime Bosch, Joan RodésAbstract:Serotonergic mechanisms have recently been implicated in the pathogenesis of portal hypertension; this suggests that blockade of serotonin S2 receptors may be a new approach for the pharmacological therapy of portal hypertension. This study was aimed at investigating the effects of ritanserin, a selective S2-Serotonergic Antagonist, in portal-hypertensive rats whose condition was due to partial portal vein ligation. The animals were randomized under double-blind conditions into two groups: the first received ritanserin (0.7 mg/kg body wt, intravenously), and the second received the same volume of placebo (isotonic saline solution). The hemodynamic studies were performed using radiolabeled microspheres 60 min after drug administration. Ritanserin administration significantly reduced portal pressure (from 11.8 ± 0.8 mm Hg to 9.4 ± 0.6 mm Hg; p < 0.05). This was associated with lower portocollateral resistance (1.8 ± 0.2 mm Hg/ml/min 100 gm in the ritanserin group vs. 2.3 ± 0.2 mm Hg/ml/min 100 gm in rats receiving placebo; not significant), but we saw no changes in portal-vein inflow (5.5 ± 0.7 ml/min 100 gm vs. 5.4 ± 0.5 ml/min 100 gm), mean arterial pressure (95.9 ± 3.5 mm Hg vs. 94.0 ± 4.0 mm Hg) and cardiac index (31.9 ± 3.5 ml/min 100 gm vs. 28.5 ± 2.6 ml/min 100 gm). Hepatic arterial and kidney blood flows were not modified by ritanserin. In summary, our results demonstrate that ritanserin infusion decreases portal pressure without causing systemic hemodynamic changes. This effect is probably due to a decrease in portocollateral resistance in portal-hypertensive rats. These results provide further for a role of serotonin in the pathogenesis of portal hypertension. (HEPATOLOGY 1991;14:1174–1178.)
