The Experts below are selected from a list of 168 Experts worldwide ranked by ideXlab platform

Tong J. Gan - One of the best experts on this subject based on the ideXlab platform.

  • Selective Serotonin 5-HT3 Receptor Antagonists for Postoperative Nausea and Vomiting
    CNS Drugs, 2005
    Co-Authors: Tong J. Gan
    Abstract:

    Selective serotonin 5-HT_3 receptor antagonists have proven safe and effective for the management of postoperative nausea and vomiting. Dolasetron, granisetron, ondansetron and tropisetron selectively and competitively bind to 5-HT_3 receptors, blocking serotonin binding at vagal afferents in the gut and in the regions of the CNS involved in emesis, including the Chemoreceptor Trigger Zone and the nucleus tractus solitarii. Despite their shared mechanism of action, 5-HT_3 receptor antagonists have different chemical structures and exhibit differences in receptor binding affinity, dose response and duration of effect. Furthermore, although dolasetron, granisetron, ondansetron and tropisetron are all extensively metabolised by the cytochrome P450 (CYP) system, different components of this system predominate in the metabolism of each of these agents. Hence, although these agents are considered equally effective in the overall population, their pharmacokinetic and pharmacodynamic differences may explain the variability in individual responses to these drugs. This review discusses the pharmacological profiles of dolasetron, granisetron, ondansetron and tropisetron, and the clinical implications of differences in their profiles.

  • Selective serotonin 5-HT3 receptor antagonists for postoperative nausea and vomiting: Are they all the same?
    CNS drugs, 2005
    Co-Authors: Tong J. Gan
    Abstract:

    Selective serotonin 5-HT3 receptor antagonists have proven safe and effective for the management of postoperative nausea and vomiting. Dolasetron, granisetron, ondansetron and tropisetron selectively and competitively bind to 5-HT3 receptors, blocking serotonin binding at vagal afferents in the gut and in the regions of the CNS involved in emesis, including the Chemoreceptor Trigger Zone and the nucleus tractus solitarii. Despite their shared mechanism of action, 5-HT3 receptor antagonists have different chemical structures and exhibit differences in receptor binding affinity, dose response and duration of effect. Furthermore, although dolasetron, granisetron, ondansetron and tropisetron are all extensively metabolised by the cytochrome P450 (CYP) system, different components of this system predominate in the metabolism of each of these agents. Hence, although these agents are considered equally effective in the overall population, their pharmacokinetic and pharmacodynamic differences may explain the variability in individual responses to these drugs. This review discusses the pharmacological profiles of dolasetron, granisetron, ondansetron and tropisetron, and the clinical implications of differences in their profiles.

Toru Matsunaga - One of the best experts on this subject based on the ideXlab platform.

  • Neuropharmacological mechanisms of emesis. I. Effects of antiemetic drugs on motion- and apomorphine-induced pica in rats.
    Methods and findings in experimental and clinical pharmacology, 1995
    Co-Authors: Noriaki Takeda, Satoshi Hasegawa, Arata Horii, Morita M, Uno A, Atsushi Yamatodani, Toru Matsunaga
    Abstract:

    The effects of diphenhydramine, domperidone, ondansetron, and diphenidol on motion- and apomorphine-induced pica (i.e., kaolin ingestion) in rats as the measure analogous to emesis in other species were examined. Diphenhydramine (10 and 20 mg/kg) and diphenidol (30 mg/kg) inhibited kaolin intake induced by 60-min double rotation, while domperidone and ondansetron did not. Kaolin intake induced by apomorphine (10 mg/kg) was inhibited by domperidone (2 mg/kg and diphenidol (30 mg/kg), but not by diphenhydramine or ondansetron. These findings suggest that the emetic pathways through the inner ear (double rotation) and the Chemoreceptor Trigger Zone (apomorphine) are pharmacolagically independent and are mediated by histamine H 1 receptors and dopamine D 2 receptors, respectively. Diphenidol may inhibit a common locus of emesis.

  • Neuropharmacological mechanisms of emesis. II. Effects of antiemetic drugs on cisplatin-induced pica in rats.
    Methods and findings in experimental and clinical pharmacology, 1995
    Co-Authors: Noriaki Takeda, Satoshi Hasegawa, Arata Horii, Morita M, Uno A, Atsushi Yamatodani, Toru Matsunaga
    Abstract:

    The effects of diphenhydramine, domperidone, ondansetron, and diphenidol on cisplatin-induced pica (i.e., kaolin ingestion) in rats as the measure analogous to emesis in other species were examined. Ondansetron (2 mg/kg) and diphenidol (30 mg/kg) inhibited kaolin intake induced by cisplatin (10 mg/kg), but diphenhydramine and domperidone did not. Diphenhydramine and diphenidol have been shown to inhibit kaolin intake induced by double rotation, while domperidone and ondansetron did not, and kaolin intake induced by apomorphine was inhibited by domperidone and diphenidol, but not by diphenhydramine or ondansetron. These observations, together with the present findings, suggest that the emetic pathways through the inner ear (double rotation), Chemoreceptor Trigger Zone (apomorphine) and visceral afferent (cisplatin), are pharmacologically independent and are mediated by histamine H 1 receptors, dopamine D 2 receptors and serotonin 5-HT 3 receptors, respectively. It is conceivable that diphenidol may inhibit the emetic center itself although the receptor on which it acts is not known.

  • Neuropharmacology of motion sickness and emesis
    Acta Oto-laryngologica, 1993
    Co-Authors: Noriaki Takeda, Masahiro Morita, Satoshi Hasegawa, Arata Horii, Takeshi Kubo, Toru Matsunaga
    Abstract:

    Histamine H 1 -receptors are involved in the development of the symptoms and signs of motion sickness, including emesis. On provocative motion stimulus, a signal for sensory conflict activates the histaminergic neuron system, and the histaminergic descending impulse stimulates H 1 -receptors in the emetic center of the brain stem. The histaminergic input to the emetic center through H 1 -receptors is independent of dopamine D 2 -receptors in the Chemoreceptor Trigger Zone and serotonin 5HT 3 -receptors in the visceral afferent, which are -also involved in the emetic reflex

  • Neuropharmacology of Motion Sickness and Emesis: A review
    Acta oto-laryngologica. Supplementum, 1993
    Co-Authors: Noriaki Takeda, Masahiro Morita, Satoshi Hasegawa, Arata Horii, Takeshi Kubo, Toru Matsunaga
    Abstract:

    Histamine H1-receptors are involved in the development of the symptoms and signs of motion sickness, including emesis. On provocative motion stimulus, a signal for sensory conflict activates the histaminergic neuron system, and the histaminergic descending impulse stimulates H1-receptors in the emetic center of the brain stem. The histaminergic input to the emetic center through H1-receptors is independent of dopamine D2-receptors in the Chemoreceptor Trigger Zone and serotonin 5HT3-receptors in the visceral afferent, which are also involved in the emetic reflex. Antihistamines block emetic H1-receptors to prevent motion sickness. Acetylcholine muscarinic receptors are involved in the generation of signals for sensory conflict. Anti-cholinergic drugs prevent motion sickness by modifying the neural store to facilitate the acquisition of habituation to provocative motion.

  • Pica in rats is analogous to emesis: an animal model in emesis research.
    Pharmacology biochemistry and behavior, 1993
    Co-Authors: Noriaki Takeda, Masahiro Morita, Satoshi Hasegawa, Toru Matsunaga
    Abstract:

    Abstract Mitchell et al. (1976, 1977) suggested that pica, eating of nonnutritive substances such as kaolin, is an illness-response behavior in rats. In the present study, we first confirmed their suggestion and then examined the effects of antiemetics on emetic-induced pica in rats. Intraperitoneal injection of apomorphine induced dose-dependent kaolin consumption. Pretreatment with domperidone inhibited apomorphine-induced kaolin intake. Oral administration of copper sulfate and intraperitoneal injection of cisplatin also induced dose-dependent kaolin consumption. Pretreatment with ondansetron inhibited cisplatin-induced kaolin intake. These findings suggest that pica in rats was induced through 1) dopamine D2 receptors in the Chemoreceptor Trigger Zone, and 2) the stomach, partly via 5-HT3 receptors in the visceral afferents in the stomach wall. The present findings support the conclusion that pica i rats is analogous to vomiting in other species and suggest that pica in rats is mediated by the same mechanisms as vomiting in humans. Accordingly, we extended the utility of the animal model to pharmacological research of emesis with pica as an analogue to emesis.

F. C. Inall - One of the best experts on this subject based on the ideXlab platform.

  • The physiology and pharmacology of postoperative nausea and vomiting
    Anaesthesia, 1994
    Co-Authors: R. J. Naylor, F. C. Inall
    Abstract:

    he main function of emesis is to remove toxins from the body. The emetic response will also be Triggered by cancer chemotherapy and radiotherapy or surgery under general anaesthesia. The mechanism of activation of the vomiting system is dependent on stimulation of gastrointestinal (mechanoreceptors and Chemoreceptors) and/or central pathways which activate the Chemoreceptor Trigger Zone in the area postrema. Postoperative emesis is activated by a range of factors before, during and after anaesthesia. The precise mechanism of action of any one of the influencing factors can only be speculated as there has been very little basic research into this area, due largely to the lack of an appropriate model for postoperative nausea and vomiting

  • The physiology and pharmacology of postoperative nausea and vomiting.
    Anaesthesia, 1994
    Co-Authors: R. J. Naylor, F. C. Inall
    Abstract:

    The main function of emesis is to remove toxins from the body. The emetic response will also be Triggered by cancer chemotherapy and radiotherapy or surgery under general anaesthesia. The mechanism of activation of the vomiting system is dependent on stimulation of gastrointestinal (mechanoreceptors and Chemoreceptors) and/or central pathways which activate the Chemoreceptor Trigger Zone in the area postrema. Postoperative emesis is activated by a range of factors before, during and after anaesthesia. The precise mechanism of action of any one of the influencing factors can only be speculated as there has been very little basic research into this area, due largely to the lack of an appropriate model for postoperative nausea and vomiting. The range of agents used in the prevention and treatment of emesis are effective to varying degrees, but some are associated with poor side effect profiles making them particularly unsuitable for prophylactic use. Newer antiemetics, which selectively antagonise 5-HT3 receptors, have proved effective and well tolerated in the treatment of chemotherapy-induced emesis and postoperative nausea and vomiting.

Noriaki Takeda - One of the best experts on this subject based on the ideXlab platform.

  • Neural mechanisms of motion sickness.
    The journal of medical investigation : JMI, 2001
    Co-Authors: Noriaki Takeda, Masahiro Morita, Arata Horii, S Nishiike, T Kitahara, A Uno
    Abstract:

    Three kinds of neurotransmitters: histamine, acetylcholine and noradrenaline, play important roles in the neural processes of motion sickness, because antihistamines, scopolamine and amphetamine are effective in preventing motion sickness. Histamine H1-receptors are involved in the development of the symptoms and signs of motion sickness, including emesis. On provocative motion stimuli, a neural mismatch signal activates the histaminergic neuron system in the hypothalamus, and the histaminergic descending impulse stimulates H1-receptors in the emetic center of the brainstem. The histaminergic input to the emetic center through H1-receptors is independent of dopamine D2-receptors in the Chemoreceptor Trigger Zone in the area postrema and serotonin 5HT3-receptors in the visceral afferent, which are also involved in the emetic reflex. Antihistamines block emetic H1-receptors to prevent motion sickness. Scopolamine prevents motion sickness by modifying the neural store to reduce the neural mismatch signal and by facilitating the adaptation/habituation processes. The noradrenergic neuron system in the locus coeruleus is suppressed by the neural mismatch signal. Amphetamine antagonizes mismatch-induced suppression of noradrenergic neural transmission, resulting in preventing motion sickness.

  • Neuropharmacological mechanisms of emesis. I. Effects of antiemetic drugs on motion- and apomorphine-induced pica in rats.
    Methods and findings in experimental and clinical pharmacology, 1995
    Co-Authors: Noriaki Takeda, Satoshi Hasegawa, Arata Horii, Morita M, Uno A, Atsushi Yamatodani, Toru Matsunaga
    Abstract:

    The effects of diphenhydramine, domperidone, ondansetron, and diphenidol on motion- and apomorphine-induced pica (i.e., kaolin ingestion) in rats as the measure analogous to emesis in other species were examined. Diphenhydramine (10 and 20 mg/kg) and diphenidol (30 mg/kg) inhibited kaolin intake induced by 60-min double rotation, while domperidone and ondansetron did not. Kaolin intake induced by apomorphine (10 mg/kg) was inhibited by domperidone (2 mg/kg and diphenidol (30 mg/kg), but not by diphenhydramine or ondansetron. These findings suggest that the emetic pathways through the inner ear (double rotation) and the Chemoreceptor Trigger Zone (apomorphine) are pharmacolagically independent and are mediated by histamine H 1 receptors and dopamine D 2 receptors, respectively. Diphenidol may inhibit a common locus of emesis.

  • Neuropharmacological mechanisms of emesis. II. Effects of antiemetic drugs on cisplatin-induced pica in rats.
    Methods and findings in experimental and clinical pharmacology, 1995
    Co-Authors: Noriaki Takeda, Satoshi Hasegawa, Arata Horii, Morita M, Uno A, Atsushi Yamatodani, Toru Matsunaga
    Abstract:

    The effects of diphenhydramine, domperidone, ondansetron, and diphenidol on cisplatin-induced pica (i.e., kaolin ingestion) in rats as the measure analogous to emesis in other species were examined. Ondansetron (2 mg/kg) and diphenidol (30 mg/kg) inhibited kaolin intake induced by cisplatin (10 mg/kg), but diphenhydramine and domperidone did not. Diphenhydramine and diphenidol have been shown to inhibit kaolin intake induced by double rotation, while domperidone and ondansetron did not, and kaolin intake induced by apomorphine was inhibited by domperidone and diphenidol, but not by diphenhydramine or ondansetron. These observations, together with the present findings, suggest that the emetic pathways through the inner ear (double rotation), Chemoreceptor Trigger Zone (apomorphine) and visceral afferent (cisplatin), are pharmacologically independent and are mediated by histamine H 1 receptors, dopamine D 2 receptors and serotonin 5-HT 3 receptors, respectively. It is conceivable that diphenidol may inhibit the emetic center itself although the receptor on which it acts is not known.

  • Neuropharmacology of motion sickness and emesis
    Acta Oto-laryngologica, 1993
    Co-Authors: Noriaki Takeda, Masahiro Morita, Satoshi Hasegawa, Arata Horii, Takeshi Kubo, Toru Matsunaga
    Abstract:

    Histamine H 1 -receptors are involved in the development of the symptoms and signs of motion sickness, including emesis. On provocative motion stimulus, a signal for sensory conflict activates the histaminergic neuron system, and the histaminergic descending impulse stimulates H 1 -receptors in the emetic center of the brain stem. The histaminergic input to the emetic center through H 1 -receptors is independent of dopamine D 2 -receptors in the Chemoreceptor Trigger Zone and serotonin 5HT 3 -receptors in the visceral afferent, which are -also involved in the emetic reflex

  • Neuropharmacology of Motion Sickness and Emesis: A review
    Acta oto-laryngologica. Supplementum, 1993
    Co-Authors: Noriaki Takeda, Masahiro Morita, Satoshi Hasegawa, Arata Horii, Takeshi Kubo, Toru Matsunaga
    Abstract:

    Histamine H1-receptors are involved in the development of the symptoms and signs of motion sickness, including emesis. On provocative motion stimulus, a signal for sensory conflict activates the histaminergic neuron system, and the histaminergic descending impulse stimulates H1-receptors in the emetic center of the brain stem. The histaminergic input to the emetic center through H1-receptors is independent of dopamine D2-receptors in the Chemoreceptor Trigger Zone and serotonin 5HT3-receptors in the visceral afferent, which are also involved in the emetic reflex. Antihistamines block emetic H1-receptors to prevent motion sickness. Acetylcholine muscarinic receptors are involved in the generation of signals for sensory conflict. Anti-cholinergic drugs prevent motion sickness by modifying the neural store to facilitate the acquisition of habituation to provocative motion.

R. J. Naylor - One of the best experts on this subject based on the ideXlab platform.

  • The physiology and pharmacology of postoperative nausea and vomiting
    Anaesthesia, 1994
    Co-Authors: R. J. Naylor, F. C. Inall
    Abstract:

    he main function of emesis is to remove toxins from the body. The emetic response will also be Triggered by cancer chemotherapy and radiotherapy or surgery under general anaesthesia. The mechanism of activation of the vomiting system is dependent on stimulation of gastrointestinal (mechanoreceptors and Chemoreceptors) and/or central pathways which activate the Chemoreceptor Trigger Zone in the area postrema. Postoperative emesis is activated by a range of factors before, during and after anaesthesia. The precise mechanism of action of any one of the influencing factors can only be speculated as there has been very little basic research into this area, due largely to the lack of an appropriate model for postoperative nausea and vomiting

  • The physiology and pharmacology of postoperative nausea and vomiting.
    Anaesthesia, 1994
    Co-Authors: R. J. Naylor, F. C. Inall
    Abstract:

    The main function of emesis is to remove toxins from the body. The emetic response will also be Triggered by cancer chemotherapy and radiotherapy or surgery under general anaesthesia. The mechanism of activation of the vomiting system is dependent on stimulation of gastrointestinal (mechanoreceptors and Chemoreceptors) and/or central pathways which activate the Chemoreceptor Trigger Zone in the area postrema. Postoperative emesis is activated by a range of factors before, during and after anaesthesia. The precise mechanism of action of any one of the influencing factors can only be speculated as there has been very little basic research into this area, due largely to the lack of an appropriate model for postoperative nausea and vomiting. The range of agents used in the prevention and treatment of emesis are effective to varying degrees, but some are associated with poor side effect profiles making them particularly unsuitable for prophylactic use. Newer antiemetics, which selectively antagonise 5-HT3 receptors, have proved effective and well tolerated in the treatment of chemotherapy-induced emesis and postoperative nausea and vomiting.