• Journal of Veterinary Clinics
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• v.18 no.1
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• pp.61-64
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• 2001

A 1.2 kg, five-month-old, female domestic short-hair cat was referred to Seoul National University Veterinary Medical Teaching Hospital with a history of vomiting immediatley after eating. Clinical signs were depression, anorexia, severe dehydration and vomiting since weaning. According to history taking, physical examination, complete blood count, serum chemical profile and contrast radiographic study, it was diagnosed as congenital sliding esophageal hiatal hernia. Diaphragmatic plication, esophagopexy and left-sided belt-loop gastropexy were performed. Ranitidine (2 mg/kg, IV, q12h) and sucralfate suspension (20 mg/kg, PO, q6h) were administered with low-fat liquified diet to treat reflux esophagitis. Clinical signs related to esophageal hiatal hernia disappeared immediately after surgical treatment and did not recur for 4 months.

• Journal of Veterinary Clinics
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• v.20 no.2
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• pp.248-251
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• 2003

Esophageal obstruction as a result of persistence of the right aortic arch was diagnosed in a 3-month-old male Persian cat. Regurgitation right after weaning and retardation were noted in this cat. Survey radiographic signs on the lateral view include ventral deviation of the thoracic trachea caused by draping of the dilated esophagus over the dorsum of the trachea and a distinct interface of the dorsal wall of the esophagus silhouetting with the cranial thoracic hypaxial muscles. On the ventrodorsal view, the cranial mediastinum was widened with soft tissue density. The trachea was deviated to the right. In an esophagram, the segmental dilation of the esophagus with constriction of the lumen just cranial to the heart base was apparent. Thoracotomy was performed and corrective surgery was carried out. At surgery, it was confirmed that the esophagus was constricted at the cranial to the base of the heart.

• Korean Journal of Veterinary Research
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• v.58 no.2
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• pp.111-114
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• 2018

A 6-year-old female domestic short hair cat presented with acute onset of vomiting, anorexia, lethargy, and tachypnea. The cat was apparently healthy prior to presentation without history of trauma. On diagnostic imagings, the entire stomach and spleen were detected in the thoracic cavity. An emergent celiotomy was performed, and a type-4 hiatal hernia was confirmed; the stomach, spleen, pancreas, and duodenum were herniated through the esophageal hiatus. It was corrected using phrenicoplasty, esophagopexy, and left-sided gastropexy and there was no recurrence 16 months after surgery. This is the first case report of an idiopathic type-4 hiatal hernia in a cat.

• Biomolecules & Therapeutics
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• v.26 no.6
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• pp.546-552
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• 2018

A comprehensive collection of proteins senses local changes in intracellular $Ca^{2+}$ concentrations ($[Ca^{2+}]_i$) and transduces these signals into responses to agonists. In the present study, we examined the effect of sphingosine-1-phosphate (S1P) on modulation of intracellular $Ca^{2+}$ concentrations in cat esophageal smooth muscle cells. To measure $[Ca^{2+}]_i$ levels in cat esophageal smooth muscle cells, we used a fluorescence microscopy with the Fura-2 loading method. S1P produced a concentration-dependent increase in $[Ca^{2+}]_i$ in the cells. Pretreatment with EGTA, an extracellular $Ca^{2+}$ chelator, decreased the S1P-induced increase in $[Ca^{2+}]_i$, and an L-type $Ca^{2+}$-channel blocker, nimodipine, decreased the effect of S1P. This indicates that $Ca^{2+}$ influx may be required for muscle contraction by S1P. When stimulated with thapsigargin, an intracellular calcium chelator, or 2-Aminoethoxydiphenyl borate (2-APB), an $InsP_3$ receptor blocker, the S1P-evoked increase in $[Ca^{2+}]_i$ was significantly decreased. Treatment with pertussis toxin (PTX), an inhibitor of $G_i$-protein, suppressed the increase in $[Ca^{2+}]_i$ evoked by S1P. These results suggest that the S1P-induced increase in $[Ca^{2+}]_i$ in cat esophageal smooth muscle cells occurs upon the activation of phospholipase C and subsequent release of $Ca^{2+}$ from the $InsP_3$-sensitive $Ca^{2+}$ pool in the sarcoplasmic reticulum. These results suggest that S1P utilized extracellular $Ca^{2+}$ via the L type $Ca^{2+}$ channel, which was dependent on activation of the $S1P_4$ receptor coupled to PTX-sensitive $G_i$ protein, via phospholipase C-mediated $Ca^{2+}$ release from the $InsP_3$-sensitive $Ca^{2+}$ pool in cat esophageal smooth muscle cells.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.5
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• pp.393-400
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• 2009

NO released by myenteric neurons controls the off contraction induced by electrical field stimulation (EFS) in distal esophageal smooth muscle, but in the presence of nitric oxide synthase (NOS) inhibitor, L-NAME, contraction by EFS occurs at the same time. The authors investigated the intracellular signaling pathways related with G protein and ionic channel EFS-induced contraction using cat esophageal muscles. EFS-induced contractions were significantly suppressed by tetrodotoxin ($1\;{\mu}M$) and atropine ($1\;{\mu}M$). Furthermore, nimodipine inhibited both on and off contractions by EFS in a concentration dependent meaner. The characteristics of 'on' and 'off contraction and the effects of G-proteins, phospholipase, and $K^+$ channel on EFS-induced contraction in smooth muscle were also investigated. Pertussis toxin (PTX, a $G_i$ inactivator) attenuated both EFS-induced contractions. Cholera toxin (CTX, $G_s$ inactivator) also decreased the amplitudes of EFS-induced off and on contractions. However, phospholipase inhibitors did not affect these contractions. Pinacidil (a $K^+$ channel opener) decreased these contractions, and tetraethylammonium (TEA, ${K^+}_{Ca}$ channel blocker) increased them. These results suggest that EFS-induced on and off contractions can be mediated by the activations Gi or Gs proteins, and that L-type $Ca^{2+}$ channel may be activated by G-protein ${\alpha}$ subunits. Furthermore, ${K^+}_{Ca^-}$ channel involve in the depolarization of esophageal smooth muscle. Further studies are required to characterize the physiological regulation of $Ca^{2+}$ channel and to investigate the effects of other $K^+$ channels on EFS-induced on and off contractions.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.248.1-248.1
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• 2002

It has been shown that C2-ceramide (C2), short chain ceramide, plays a role in mediating contraction of cat esophageal smooth muscle cells. We examined the effect of newly synthesized ceramide analogues on the C2-ceramide induced contraction in esophageal smooth muscle cells isolated with collagenase. C2-ceramide produced contraction of smooth muscle cells in a dose dependent manner. (omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.77.3-78
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• 2003

We previously shown that sphingosylphosphorylcholine, a lysophosphatidic acid, produced contraction in isolated single cells of cat ilium. We investigated the mechanism of sphingosine-1-phosphate (S1P)-induced contraction of circular smooth muscle cells in cat esophagus. S1P produced esophageal contraction in a dose dependent manner. The maximal contraction (l0$\^$-7/ M) induced at 1min. Pertusis toxin (PTX) inhibited contraction induced by S1P, suggesting that the contraction is mediated to a PTX-sensitive G-protein. (omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.75.1-75.1
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• 2003

Low-frequency electrical field stimulation of transmural nerves of cat esophageal circular smooth muscle produces an “off contraction”, which occurs after electirical field stimulation (EFS) of transmural nerves is stopped. We previously examined signal transduction pathways mediating ACh-induced contraction of circular smooth muscle of esophagus. The extracellular Ca$\^$2+/ is needed for the contraction, results in the activation PKC. EFS-induced contraction was abolished by the pretreatments of tetrodotoxin(1 ${\mu}$M) and atropine (1 ${\mu}$M). (omitted)

• Archives of Pharmacal Research
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• v.29 no.5
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• pp.400-404
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• 2006

This study examined the effect of Gamma-Amino butyric acid (GABA) and selective GABA receptor related drugs on the electrically stimulated relaxation in the lower esophageal sphincter muscle (LES) of a cat. Tetrodotoxin $(10^{-6}\;M)$ suppressed the electrically stimulated (0.5-5 Hz) relaxation of the LES. However, guanethidine $(10^{-6}\;M)$ and atropine $(10^{-6}\;M)$ had no effect indicating that the relaxations were neurally mediated via the nonadrenergic and noncholinergic (NANC) pathways. NG-nitro-L-arginine methyl ester ($10^{-4}M$, L-NAME) also inhibited the relaxant response but did not completely abolish the electrically stimulated relaxation with 60% inhibition, which suggests the involvement of nitric oxide as an inhibitory transmitter. This study examined the role of GABA, an inhibitory neurotransmitter, on neurally mediated LES relaxation. GABA ($10^{-3}-10^{-5}M$, non selective receptor agonist), muscimol ($10^{-3}-10^{-5}M$, GABA-A agonist), and baclofen ($10^{-3}-10^{-5}M$, GABA-B agonist) had no significant effect on the electrically stimulated relaxation. Moreover, bicuculline ($10^{-5}M$, GABA-A antagonist) and phaclofen ($10^{-5}M$, GABA-B antagonist) had no inhibitory effect on the electrically stimulated relaxation. This suggests that GABA and the GABA receptor are not involved in the electrically stimulated NANC relaxation in the cat LES.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.4
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• pp.137-142
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• 2008

Ceramide has emerged as a novel second messenger for intracellular signalling. It is produced from sphingomyelin and is involved in the control of cell differntiation, proliferation, and apoptosis. $C_2$-ceramide, short chain ceramide, plays a role in mediating contraction of cat esophageal smooth muscle cells. We examined the effect of synthesized ceramide analogues on the $C_2$-ceramide and ACh-induced contraction in esophageal smooth muscle cells isolated with collagenase. CY3523, CY3525, or CY3723 inhibited $C_2$-ceramide induced contraction, in a time dependent manne. Each analogue also inhibited the contraction in concentration dependent manners. CY 3523, CY 3525, and CY 3723 had no effect to the contraction induced by PMA. The inhibition with CY3523, CY3525 and CY3723 on the $C_2$-ceramide induced contraction was recovered by PMA. These analogues decreased the density of MAPK bands (p44/42 or p38) in the western blot. These results suggest that ceramide analogues can inhibit $C_2$-ceramide induced contraction via PKC and MAPK dependent pathway.