Ketamine and Midazolam Differentially Inhibit Nonadrenergic Noncholinergic Lower Esophageal Sphincter Relaxation in Rabbits

Kohjitani, Atsushi; Miyawaki, Takuya; Funahashi, Makoto; Higuchi, Hitoshi; Matsuo, Ryuji; Shimada, Masahiko

doi:10.1097/00000542-200302000-00026

Cited by 18 publications

(8 citation statements)

References 55 publications

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“…Gastric dilatation and severe refl ux esophagitis caused by chronic ketamine abuse has not been described in the medical literature previously. Ketamine has been shown to reduce the lower esophageal sphincter tone in nonhuman models (13). Smooth muscle relaxation in the upper gastrointestinal tract might have caused dysmotility, dilatation, and stasis of food in the stomach and chronic esophageal refl ux in this patient.…”

Section: Discussionmentioning

confidence: 82%

Multiorgan Dysfunction Related to Chronic Ketamine Abuse

Pappachan

Raj

Thomas

et al. 2014

Baylor University Medical Center Proceedings

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Section: Discussionmentioning

confidence: 82%

Multiorgan Dysfunction Related to Chronic Ketamine Abuse

Pappachan

Raj

Thomas

et al. 2014

Baylor University Medical Center Proceedings

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“…Our observations also indicate that the vagally stimulated LES relaxation is mediated through axial stretch on the LES exerted by the longitudinal muscle contraction of the esophagus. (6), rabbit (19,22), and opossum (12,17)] to study the LES. For several reasons, opossum has been used most extensively because the LES and distal esophagus in the opossums, similar to humans, consist of smooth muscle.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of stretch-activated excitatory and inhibitory responses in the lower esophageal sphincter

Jiang¹,

Bhargava²,

Mittal³

2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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We recently found that an orally directed stretch of the esophagus activates a neurally mediated relaxation of the lower esophageal sphincter (LES). Goals of our study were to characterize the neural mechanisms responsible for axial and transverse stretch-activated responses in the LES. LES pressure was monitored in anesthetized and artificially ventilated mice. Sutures were placed in the esophagus to exert graded stretch in the longitudinal and transverse directions. Effects of bilateral vagotomy and pharmacological agents on the stretch-activated LES responses were investigated. The relationship between vagally stimulated axial stretch and LES relaxation was also studied. Stretch in the longitudinal and transverse directions caused a dose-dependent LES relaxation and contraction, respectively, that were not affected by bilateral vagotomy and sympathectomy but were blocked by tetrodotoxin. In bilateral vagotomized animals, hexamethonium, atropine, pyridoxalphosphate-6-azophenyl-2',4' disulfonic acid (PPADS), and ondansetron did not block the stretch-activated LES relaxation and contraction. Axial stretch-activated LES relaxation was blocked by nitric oxide inhibitor and transverse stretch-activated LES contraction was blocked by a combination of atropine and substance P antagonist. Electrical stimulation of the vagus nerve induced LES relaxation and axial stretch on the LES, both of which were blocked by rocuronium. Axial and transverse stretch-activated LES relaxation and contraction were present in the W/W(v) mice that lack interstitial cells of Cajal (ICC). Stretch-activated LES relaxation and contraction are mediated through mechanosensitive neurons located in the myenteric plexus, which involves neither synaptic transmission nor ICC.

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“…Several pre-anesthetic and anesthetic drugs, such as atropine, diazepam, acepromazine, diazepam, xylazine, morphine, halothane, and isoflurane can lead to GER by decreasing the tone of the LES (Kim et al ., 1977;Strombeck and Harrold, 1985;Cox et al ., 1988;Hashim and Waterman, 1993;Tournadre et al ., 1998;Kohjitani et al ., 2003;Epstein and Swirsky, 2009; Tables 1 and 2). …”

Section: Influence Of Different Drugs On Ger In Anesthetized Dogsmentioning

confidence: 99%

Gastroesophageal reflux in anesthetized dogs: a review

Rodríguez-Alarcón

Rivera-Barreno

Díaz

et al. 2015

Rev Colomb Cienc Pecu

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SummaryGastroesophageal reflux can be a catastrophic illness in small animals during anesthesia since its complications can cause serious pathologies, such as esophagitis, esophageal stenosis and aspiration pneumonia. With an incidence from 12 to 78.5% in anesthetized dogs, gastroesophageal reflux is normally silent during anesthesia and will be notices only if regurgitation occurs and stomach acid is present in the nasal or oral cavities. In humans, gastroesophageal reflux disease (GERD) is a well-defined pathology where the lower esophageal sphincter has a sustained weakness. However, in dogs, gastroesophageal reflux disease as such is not well established, if at all; it has only been described as gastroesophagic reflux, occurring principally in anesthetized animals. There are several factors influencing the presentation of reflux in anesthetized dogs, which may be inherent to the patient (e.g. age, sex, breed, weight, or body condition), medications used prior to and during anesthesia, type of surgery or position of the animal during surgery. The objective of this review is to discuss a series of conditions that could predispose dogs to gastroesophageal reflux during anesthesia and to assist in the prevention and diagnosis of this condition.

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Ketamine and Midazolam Differentially Inhibit Nonadrenergic Noncholinergic Lower Esophageal Sphincter Relaxation in Rabbits

Abstract: These findings suggest that ketamine inhibits NANC LES relaxation by the extracellular production of superoxide anion, and that midazolam inhibits it by the inhibition of nitric oxide synthase activity.

Cited by 18 publications

References 55 publications

Multiorgan Dysfunction Related to Chronic Ketamine Abuse

Multiorgan Dysfunction Related to Chronic Ketamine Abuse

Mechanism of stretch-activated excitatory and inhibitory responses in the lower esophageal sphincter

Gastroesophageal reflux in anesthetized dogs: a review

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