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H. Fritz - One of the best experts on this subject based on the ideXlab platform.
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The effects of Urapidil on thermoregulatory thresholds in volunteers.
Anesthesia & Analgesia, 2002Co-Authors: H. Fritz, Hansjoerg Hoff, Michael Hartmann, Waheedullah Karzai, Konrad R. G. SchwarzkopfAbstract:UNLABELLED In a previous study we have shown that the antihypertensive drug, Urapidil, stops postanesthetic shivering. One possible mechanism in the inhibition of postanesthetic shivering by Urapidil may be alterations in thermoregulatory thresholds. We therefore studied the effects of Urapidil on vasoconstriction and shivering thresholds during cold-induced shivering in volunteers. Seven healthy male volunteers were cooled by an infusion of saline at 4 degrees C on two study days separated by 48 h. Thermoregulatory vasoconstriction was estimated using forearm minus fingertip skin-temperature gradients, and values exceeding 0 degrees C were considered to represent significant vasoconstriction. The rectal core temperatures at the beginning of shivering and at vasoconstriction were considered the thermoregulatory thresholds. Before cooling, either 25 mg of Urapidil or placebo was administered randomly and blindly to each volunteer. When shivering occurred continuously for 10 min, another 25 mg of Urapidil was administered IV to completely stop shivering. Urapidil led to a decrease in core temperature at vasoconstriction and shivering threshold by 0.4 degrees C plus/minus 0.2 degrees C (P < 0.001) and 0.5 degrees C plus/minus 0.3 degrees C (P < 0.01), respectively. Oxygen consumption increased during shivering by 70% plus/minus 30% (P < 0.01) in comparison with baseline and decreased levels after shivering stopped, despite the continued low core temperature. Our investigation shows that Urapidil stops postanesthetic shivering by decreasing important thermoregulatory thresholds. This means that shivering, not hypothermia, is treated, and hypothermia will need more attention in the postanesthesia care unit. IMPLICATIONS In this study we show that the antihypertensive drug Urapidil stops cold-induced shivering and decreases normal thermoregulatory responses, i.e., the thresholds for vasoconstriction and shivering, in awake volunteers.
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a comparison between meperidine clonidine and Urapidil in the treatment of postanesthetic shivering
Anesthesia & Analgesia, 2001Co-Authors: K Schwarzkopf, Hansjoerg Hoff, Michael Hartmann, H. FritzAbstract:UNLABELLED Postanesthetic shivering can be treated with many types of drugs. We compared the effects of meperidine, clonidine, and Urapidil on postanesthetic shivering. Sixty patients shivering during recovery from general anesthesia were treated in a randomized, double-blinded fashion with 25 mg meperidine IV, 0.15 mg clonidine IV, or 25 mg Urapidil IV in three separate groups of 20 patients each. If shivering did not stop within 5 min, the treatment was repeated once; clonidine was replaced with saline for the second dose. Rectal temperature, arterial blood pressure, heart rate, SaO(2) and vigilance were monitored. Clonidine stopped shivering in all 20 patients. A single dose of meperidine stopped the shivering in 18 of 20 patients, with the other 2 patients needing a second dose. Urapidil was less effective: the first dose stopped the shivering in only six patients; the second dose was effective in another six; the drug was ineffective in 8 of 20 patients. Meperidine and clonidine were both nearly 100% effective in treating postanesthetic shivering without negative side effects. By comparison, Urapidil was only effective in 60% of patients treated (P <0.01). IMPLICATIONS Patients shivering during recovery from general anesthesia were treated in a randomized double-blinded fashion with meperidine, clonidine, or Urapidil. Meperidine and clonidine were both very effective, whereas Urapidil was only effective in 60% of patients treated.
Hansjoerg Hoff - One of the best experts on this subject based on the ideXlab platform.
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The Effects of Urapidil on Thermoregulatory Thresholds in Volunteers
2013Co-Authors: Harald G. Fritz, Hansjoerg Hoff, Michael Hartmann, Waheedullah Karzai, Konrad R. G. SchwarzkopfAbstract:In a previous study we have shown that the antihypertensive drug, Urapidil, stops postanesthetic shivering. One possible mechanism in the inhibition of postanesthetic shivering by Urapidil may be alterations in thermoregulatory thresholds. We therefore studied the effects of Urapidil on vasoconstriction and shivering thresholds during cold-induced shivering in volunteers. Seven healthy male volunteers were cooled by an infusion of saline at 4°C on two study days separated by 48 h. Thermoregulatory vasoconstriction was estimated using forearm minus fingertip skin-temperature gradients, and values exceeding 0°C were considered to represent significant vasoconstriction. The rectal core temperatures at the beginning of shivering and at vasoconstriction were considered the thermoregulatory thresholds. Before cooling, either 25 mg of urapidi
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The effects of Urapidil on thermoregulatory thresholds in volunteers.
Anesthesia & Analgesia, 2002Co-Authors: H. Fritz, Hansjoerg Hoff, Michael Hartmann, Waheedullah Karzai, Konrad R. G. SchwarzkopfAbstract:UNLABELLED In a previous study we have shown that the antihypertensive drug, Urapidil, stops postanesthetic shivering. One possible mechanism in the inhibition of postanesthetic shivering by Urapidil may be alterations in thermoregulatory thresholds. We therefore studied the effects of Urapidil on vasoconstriction and shivering thresholds during cold-induced shivering in volunteers. Seven healthy male volunteers were cooled by an infusion of saline at 4 degrees C on two study days separated by 48 h. Thermoregulatory vasoconstriction was estimated using forearm minus fingertip skin-temperature gradients, and values exceeding 0 degrees C were considered to represent significant vasoconstriction. The rectal core temperatures at the beginning of shivering and at vasoconstriction were considered the thermoregulatory thresholds. Before cooling, either 25 mg of Urapidil or placebo was administered randomly and blindly to each volunteer. When shivering occurred continuously for 10 min, another 25 mg of Urapidil was administered IV to completely stop shivering. Urapidil led to a decrease in core temperature at vasoconstriction and shivering threshold by 0.4 degrees C plus/minus 0.2 degrees C (P < 0.001) and 0.5 degrees C plus/minus 0.3 degrees C (P < 0.01), respectively. Oxygen consumption increased during shivering by 70% plus/minus 30% (P < 0.01) in comparison with baseline and decreased levels after shivering stopped, despite the continued low core temperature. Our investigation shows that Urapidil stops postanesthetic shivering by decreasing important thermoregulatory thresholds. This means that shivering, not hypothermia, is treated, and hypothermia will need more attention in the postanesthesia care unit. IMPLICATIONS In this study we show that the antihypertensive drug Urapidil stops cold-induced shivering and decreases normal thermoregulatory responses, i.e., the thresholds for vasoconstriction and shivering, in awake volunteers.
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a comparison between meperidine clonidine and Urapidil in the treatment of postanesthetic shivering
Anesthesia & Analgesia, 2001Co-Authors: K Schwarzkopf, Hansjoerg Hoff, Michael Hartmann, H. FritzAbstract:UNLABELLED Postanesthetic shivering can be treated with many types of drugs. We compared the effects of meperidine, clonidine, and Urapidil on postanesthetic shivering. Sixty patients shivering during recovery from general anesthesia were treated in a randomized, double-blinded fashion with 25 mg meperidine IV, 0.15 mg clonidine IV, or 25 mg Urapidil IV in three separate groups of 20 patients each. If shivering did not stop within 5 min, the treatment was repeated once; clonidine was replaced with saline for the second dose. Rectal temperature, arterial blood pressure, heart rate, SaO(2) and vigilance were monitored. Clonidine stopped shivering in all 20 patients. A single dose of meperidine stopped the shivering in 18 of 20 patients, with the other 2 patients needing a second dose. Urapidil was less effective: the first dose stopped the shivering in only six patients; the second dose was effective in another six; the drug was ineffective in 8 of 20 patients. Meperidine and clonidine were both nearly 100% effective in treating postanesthetic shivering without negative side effects. By comparison, Urapidil was only effective in 60% of patients treated (P <0.01). IMPLICATIONS Patients shivering during recovery from general anesthesia were treated in a randomized double-blinded fashion with meperidine, clonidine, or Urapidil. Meperidine and clonidine were both very effective, whereas Urapidil was only effective in 60% of patients treated.
Michael Hartmann - One of the best experts on this subject based on the ideXlab platform.
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The Effects of Urapidil on Thermoregulatory Thresholds in Volunteers
2013Co-Authors: Harald G. Fritz, Hansjoerg Hoff, Michael Hartmann, Waheedullah Karzai, Konrad R. G. SchwarzkopfAbstract:In a previous study we have shown that the antihypertensive drug, Urapidil, stops postanesthetic shivering. One possible mechanism in the inhibition of postanesthetic shivering by Urapidil may be alterations in thermoregulatory thresholds. We therefore studied the effects of Urapidil on vasoconstriction and shivering thresholds during cold-induced shivering in volunteers. Seven healthy male volunteers were cooled by an infusion of saline at 4°C on two study days separated by 48 h. Thermoregulatory vasoconstriction was estimated using forearm minus fingertip skin-temperature gradients, and values exceeding 0°C were considered to represent significant vasoconstriction. The rectal core temperatures at the beginning of shivering and at vasoconstriction were considered the thermoregulatory thresholds. Before cooling, either 25 mg of urapidi
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The effects of Urapidil on thermoregulatory thresholds in volunteers.
Anesthesia & Analgesia, 2002Co-Authors: H. Fritz, Hansjoerg Hoff, Michael Hartmann, Waheedullah Karzai, Konrad R. G. SchwarzkopfAbstract:UNLABELLED In a previous study we have shown that the antihypertensive drug, Urapidil, stops postanesthetic shivering. One possible mechanism in the inhibition of postanesthetic shivering by Urapidil may be alterations in thermoregulatory thresholds. We therefore studied the effects of Urapidil on vasoconstriction and shivering thresholds during cold-induced shivering in volunteers. Seven healthy male volunteers were cooled by an infusion of saline at 4 degrees C on two study days separated by 48 h. Thermoregulatory vasoconstriction was estimated using forearm minus fingertip skin-temperature gradients, and values exceeding 0 degrees C were considered to represent significant vasoconstriction. The rectal core temperatures at the beginning of shivering and at vasoconstriction were considered the thermoregulatory thresholds. Before cooling, either 25 mg of Urapidil or placebo was administered randomly and blindly to each volunteer. When shivering occurred continuously for 10 min, another 25 mg of Urapidil was administered IV to completely stop shivering. Urapidil led to a decrease in core temperature at vasoconstriction and shivering threshold by 0.4 degrees C plus/minus 0.2 degrees C (P < 0.001) and 0.5 degrees C plus/minus 0.3 degrees C (P < 0.01), respectively. Oxygen consumption increased during shivering by 70% plus/minus 30% (P < 0.01) in comparison with baseline and decreased levels after shivering stopped, despite the continued low core temperature. Our investigation shows that Urapidil stops postanesthetic shivering by decreasing important thermoregulatory thresholds. This means that shivering, not hypothermia, is treated, and hypothermia will need more attention in the postanesthesia care unit. IMPLICATIONS In this study we show that the antihypertensive drug Urapidil stops cold-induced shivering and decreases normal thermoregulatory responses, i.e., the thresholds for vasoconstriction and shivering, in awake volunteers.
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a comparison between meperidine clonidine and Urapidil in the treatment of postanesthetic shivering
Anesthesia & Analgesia, 2001Co-Authors: K Schwarzkopf, Hansjoerg Hoff, Michael Hartmann, H. FritzAbstract:UNLABELLED Postanesthetic shivering can be treated with many types of drugs. We compared the effects of meperidine, clonidine, and Urapidil on postanesthetic shivering. Sixty patients shivering during recovery from general anesthesia were treated in a randomized, double-blinded fashion with 25 mg meperidine IV, 0.15 mg clonidine IV, or 25 mg Urapidil IV in three separate groups of 20 patients each. If shivering did not stop within 5 min, the treatment was repeated once; clonidine was replaced with saline for the second dose. Rectal temperature, arterial blood pressure, heart rate, SaO(2) and vigilance were monitored. Clonidine stopped shivering in all 20 patients. A single dose of meperidine stopped the shivering in 18 of 20 patients, with the other 2 patients needing a second dose. Urapidil was less effective: the first dose stopped the shivering in only six patients; the second dose was effective in another six; the drug was ineffective in 8 of 20 patients. Meperidine and clonidine were both nearly 100% effective in treating postanesthetic shivering without negative side effects. By comparison, Urapidil was only effective in 60% of patients treated (P <0.01). IMPLICATIONS Patients shivering during recovery from general anesthesia were treated in a randomized double-blinded fashion with meperidine, clonidine, or Urapidil. Meperidine and clonidine were both very effective, whereas Urapidil was only effective in 60% of patients treated.
Henry Gozlan - One of the best experts on this subject based on the ideXlab platform.
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3h 5 methyl Urapidil labels 5 ht1a receptors and α1 adrenoceptors in the rat cns in vitro binding and autoradiographic studies
European Journal of Pharmacology, 1991Co-Authors: Anne Marie Laporte, Lee E Schechter, Daniel Vergé, Michel Hamon, F J Bolanos, Henry GozlanAbstract:Abstract The tritiated derivative of the potent antihypertensive agent, 5-methyl-Urapidil, was used as a radioligand in binding studies with rat brain membranes and tissue sections. Serotonin and prazosin inhibited [ 3 H]5-methyl-Urapidil binding to membranes from the rat hippocampus, cerebral cortex and brainstem biphasically, leading to the definition of serotomn high-affinity and prazosin high-affinity [ 3 H]5-niethyl-Urapidil binding sites. Comparison of these serotonin-sensitive [ 3 H]5-methyl-Urapidil binding sites with the 5-HT 1A sites labelled by [ 3 H]8-hydroxy-2-(di-n-propylamino)tetralin [ 3 H]8-oh-dpat) revealed striking similarities regarding pharmacological properties, respective densities and regional distribution. On the other hand, the prazosin-sensitive [ 3 H]5-methylUrapidil binding sites should correspond to the oiiA-subtype of adrenoceptors which has recently been defined. Detailed autoradiographic investigations allowed the detection of 5-HT.A sites labelled by both [ 3 H]5-methyl-Urapidil and [ 3 H]8-OH-DPAT in the posterior raphe nuclei (pallidus and obscurus) which are possibly involved in the hypotensive action of 5-methyl-Urapidil. These data demonstrate that [ 3 H]5-methyl-Urapidil is a useful radioligand for the visualization and quantification of both 5-HT 1A serotonin receptors and α-adrenoceptors in the central nervous system.
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[3H]5-methyl-Urapidil labels 5-HT1A receptors and alpha 1-adrenoceptors in the rat CNS. In vitro binding and autoradiographic studies.
European Journal of Pharmacology, 1991Co-Authors: Anne Marie Laporte, Lee E Schechter, Francisco Javier Bolanos Jimenez, Daniel Vergé, Michel Hamon, Henry GozlanAbstract:The tritiated derivative of the potent antihypertensive agent, 5-methyl-Urapidil, was used as a radioligand in binding studies with rat brain membranes and tissue sections. Serotonin and prazosin inhibited [3H]5-methyl-Urapidil binding to membranes from the rat hippocampus, cerebral cortex and brainstem biphasically, leading to the definition of serotonin high-affinity and prazosin high-affinity [3H]5-methyl-Urapidil binding sites. Comparison of these serotonin-sensitive [3H]5-methyl-Urapidil binding sites with the 5-HT1A sites labelled by [3H]8-hydroxy-2-(di-n-propylamino)tetralin ([3H]8-OH-DPAT) revealed striking similarities regarding pharmacological properties, respective densities and regional distribution. On the other hand, the prazosin-sensitive [3H]5-methyl-Urapidil binding sites should correspond to the alpha 1A-subtype of adrenoceptors which has recently been defined. Detailed autoradiographic investigations allowed the detection of 5-HT1A sites labelled by both [3H]5-methyl-Urapidil and [3H]8-OH-DPAT in the posterior raphe nuclei (pallidus and obscurus) which are possibly involved in the hypotensive action of 5-methyl-Urapidil. These data demonstrate that [3H]5-methyl-Urapidil is a useful radioligand for the visualization and quantification of both 5-HT1A serotonin receptors and alpha 1A-adrenoceptors in the central nervous system.
Konrad R. G. Schwarzkopf - One of the best experts on this subject based on the ideXlab platform.
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The Effects of Urapidil on Thermoregulatory Thresholds in Volunteers
2013Co-Authors: Harald G. Fritz, Hansjoerg Hoff, Michael Hartmann, Waheedullah Karzai, Konrad R. G. SchwarzkopfAbstract:In a previous study we have shown that the antihypertensive drug, Urapidil, stops postanesthetic shivering. One possible mechanism in the inhibition of postanesthetic shivering by Urapidil may be alterations in thermoregulatory thresholds. We therefore studied the effects of Urapidil on vasoconstriction and shivering thresholds during cold-induced shivering in volunteers. Seven healthy male volunteers were cooled by an infusion of saline at 4°C on two study days separated by 48 h. Thermoregulatory vasoconstriction was estimated using forearm minus fingertip skin-temperature gradients, and values exceeding 0°C were considered to represent significant vasoconstriction. The rectal core temperatures at the beginning of shivering and at vasoconstriction were considered the thermoregulatory thresholds. Before cooling, either 25 mg of urapidi
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The effects of Urapidil on thermoregulatory thresholds in volunteers.
Anesthesia & Analgesia, 2002Co-Authors: H. Fritz, Hansjoerg Hoff, Michael Hartmann, Waheedullah Karzai, Konrad R. G. SchwarzkopfAbstract:UNLABELLED In a previous study we have shown that the antihypertensive drug, Urapidil, stops postanesthetic shivering. One possible mechanism in the inhibition of postanesthetic shivering by Urapidil may be alterations in thermoregulatory thresholds. We therefore studied the effects of Urapidil on vasoconstriction and shivering thresholds during cold-induced shivering in volunteers. Seven healthy male volunteers were cooled by an infusion of saline at 4 degrees C on two study days separated by 48 h. Thermoregulatory vasoconstriction was estimated using forearm minus fingertip skin-temperature gradients, and values exceeding 0 degrees C were considered to represent significant vasoconstriction. The rectal core temperatures at the beginning of shivering and at vasoconstriction were considered the thermoregulatory thresholds. Before cooling, either 25 mg of Urapidil or placebo was administered randomly and blindly to each volunteer. When shivering occurred continuously for 10 min, another 25 mg of Urapidil was administered IV to completely stop shivering. Urapidil led to a decrease in core temperature at vasoconstriction and shivering threshold by 0.4 degrees C plus/minus 0.2 degrees C (P < 0.001) and 0.5 degrees C plus/minus 0.3 degrees C (P < 0.01), respectively. Oxygen consumption increased during shivering by 70% plus/minus 30% (P < 0.01) in comparison with baseline and decreased levels after shivering stopped, despite the continued low core temperature. Our investigation shows that Urapidil stops postanesthetic shivering by decreasing important thermoregulatory thresholds. This means that shivering, not hypothermia, is treated, and hypothermia will need more attention in the postanesthesia care unit. IMPLICATIONS In this study we show that the antihypertensive drug Urapidil stops cold-induced shivering and decreases normal thermoregulatory responses, i.e., the thresholds for vasoconstriction and shivering, in awake volunteers.
