Purpose: : This study investigated coronavirus disease-19 (COVID-19) related stress, resilience, and organizational commitment, and determined the factors influencing nurses’ organizational commitment at an infectious disease hospital of COVID-19. Methods: : A cross-sectional descriptive survey was conducted with 138 nurses. Data analysis, including descriptive statistics, independent t-tests, one-way ANOVA, Pearson’s correlations, and multiple regression analysis, were performed using SPSS 26.0 program. Results: : Factors influencing organizational commitment included resilience (β=0.31, p<.001), position (β=0.31, p<.001), COVID-19 related stress (β=-0.26, p<.001), and COVID-19 nursing period (β=-0.19, p=.012). These variables explained 29.6% of the organizational commitment. Conclusion : In order to enhance the organizational commitment of nurses in infectious disease hospitals of COVID-19, active program development and intervention are required at the organizational level to improve nurses’ resilience and relieve stress related to nursing infectious disease patients.

Purinergic receptors play an important role in regulating gastrointestinal (GI) motility. Interstitial cells of Cajal (ICCs) are pacemaker cells that regulate GI smooth muscle activity. We studied the functional roles of external adenosine 5′-triphosphate (ATP) on pacemaker activity in cultured ICCs from mouse small intestines by using the whole-cell patch clamp technique and intracellular Ca²⁺ ([Ca²⁺]ᵢ) imaging. External ATP dose-dependently depolarized the resting membrane and produced tonic inward pacemaker currents, and these effects were antagonized by suramin, a purinergic P2 receptor antagonist. ATP-induced effects on pacemaker currents were suppressed by an external Na⁺-free solution and inhibited by the nonselective cation channel blockers, flufenamic acid and niflumic acid. The removal of external Ca²⁺ or treatment with thapsigargin (inhibitor of Ca²⁺ uptake into endoplasmic reticulum) inhibited the ATP-induced effects on pacemaker currents. Spontaneous [Ca²⁺]ᵢ oscillations were enhanced by external ATP. These results suggest that external ATP modulates pacemaker activity by activating nonselective cation channels via external Ca²⁺ influx and [Ca²⁺]ᵢ release from the endoplasmic reticulum. Thus, it seems that activating the purinergic P2 receptor may modulate GI motility by acting on ICCs in the small intestine.
Adenosine ; Adenosine Triphosphate ; Animals ; Endoplasmic Reticulum ; Flufenamic Acid ; Interstitial Cells of Cajal ; Intestine, Small ; Membranes ; Mice ; Muscle, Smooth ; Niflumic Acid ; Pacemaker, Artificial ; Receptors, Purinergic ; Receptors, Purinergic P2 ; Suramin ; Thapsigargin

The inhibitory effects of Asparagus cochinchinensis against inflammatory response induced by lipopolysaccharide (LPS), substance P and phthalic anhydride (PA) treatment were recently reported for some cell lines and animal models. To evaluate the hepatotoxicity and nephrotoxicity of A. cochinchinensis toward the livers and kidneys of ICR mice, alterations in related markers including body weight, organ weight, urine composition, liver pathology and kidney pathology were analyzed in male and female ICR mice after oral administration of 150, 300 and 600 mg/kg body weight/day saponin-enriched extract of A. cochinchinensis (SEAC) for 14 days. The saponin, total flavonoid and total phenol levels were found to be 57.2, 88.5 and 102.1 mg/g in SEAC, respectively, and the scavenging activity of SEAC gradually increased in a dose-dependent manner. Moreover, body and organ weight, clinical phenotypes, urine parameters and mice mortality did not differ between the vehicle and SEAC treated group. Furthermore, no significant alterations were measured in alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), blood urea nitrogen (BUN) and the serum creatinine (Cr) in the SEAC treated group relative to the vehicle treated group. Moreover, the specific pathological features induced by most toxic compounds were not observed upon liver and kidney histological analysis. Overall, the results of the present study suggest that SEAC does not induce any specific toxicity in the livers and kidneys of male and female ICR mice at doses of 600 mg/kg body weight/day.
Administration, Oral ; Alanine Transaminase ; Alkaline Phosphatase ; Animals ; Aspartate Aminotransferases ; Blood Urea Nitrogen ; Body Weight ; Cell Line ; Creatinine ; Female ; Humans ; Kidney ; L-Lactate Dehydrogenase ; Liver ; Male ; Mice ; Mice, Inbred ICR* ; Models, Animal ; Mortality ; Organ Size ; Pathology ; Phenol ; Phenotype ; Saponins ; Substance P

This study aimed to investigate the effect of pituitary adenylate cyclase-activating peptide (PACAP) on the pacemaker activity of interstitial cells of Cajal (ICC) in mouse colon and to identify the underlying mechanisms of PACAP action. Spontaneous pacemaker activity of colonic ICC and the effects of PACAP were studied using electrophysiological recordings. Exogenously applied PACAP induced hyperpolarization of the cell membrane and inhibited pacemaker frequency in a dose-dependent manner (from 0.1 nM to 100 nM). To investigate cyclic AMP (cAMP) involvement in the effects of PACAP on ICC, SQ-22536 (an inhibitor of adenylate cyclase) and cell-permeable 8-bromo-cAMP were used. SQ-22536 decreased the frequency of pacemaker potentials, and cell-permeable 8-bromo-cAMP increased the frequency of pacemaker potentials. The effects of SQ-22536 on pacemaker potential frequency and membrane hyperpolarization were rescued by co-treatment with glibenclamide (an ATP-sensitive K+ channel blocker). However, neither N(G)-nitro-L-arginine methyl ester (L-NAME, a competitive inhibitor of NO synthase) nor 1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one (ODQ, an inhibitor of guanylate cyclase) had any effect on PACAP-induced activity. In conclusion, this study describes the effects of PACAP on ICC in the mouse colon. PACAP inhibited the pacemaker activity of ICC by acting through ATP-sensitive K+ channels. These results provide evidence of a physiological role for PACAP in regulating gastrointestinal (GI) motility through the modulation of ICC activity.
8-Bromo Cyclic Adenosine Monophosphate ; Animals ; Cell Membrane ; Colon* ; Cyclic AMP ; Glyburide ; Interstitial Cells of Cajal* ; Membranes ; Mice ; NG-Nitroarginine Methyl Ester ; Pituitary Adenylate Cyclase-Activating Polypeptide*

Interstitial cells of Cajal (ICCs) from the urinary bladder regulate detrusor smooth muscle activities. We cultured ICCs from the urinary bladder of mice and performed patch clamp and intracellular Ca2+ ([Ca2+]i) imaging to investigate whether cultured ICCs can be a valuable tool for cellular functional studies. The cultured ICCs displayed two types of spontaneous electrical activities which are similar to those recorded in intact bladder tissues. Spontaneous electrical activities of cultured ICCs were nifedipine-sensitive. Carbachol and ATP, both excitatory neurotransmitters in the urinary bladder, depolarized the membrane and increased the frequency of spike potentials. Carbachol increased [Ca2+]i oscillations and basal Ca2+ levels, which were blocked by atropine. These results suggest that cultured ICCs from the urinary bladder retain rhythmic phenotypes similar to the spontaneous electrical activities recorded from the intact urinary bladder. Therefore, we suggest that cultured ICCs from the urinary bladder may be useful for cellular and molecular studies of ICCs.
Action Potentials ; Adenosine Triphosphate ; Animals ; Atropine ; Carbachol ; Interstitial Cells of Cajal* ; Membranes ; Mice* ; Muscle, Smooth ; Neurotransmitter Agents ; Phenotype ; Urinary Bladder*

In this study we determined whether or not 5-hydroxytryptamine (5-HT) has an effect on the pacemaker activities of interstitial cells of Cajal (ICC) from the mouse small intestine. The actions of 5-HT on pacemaker activities were investigated using a whole-cell patch-clamp technique, intracellular Ca2+ ([Ca2+]i) analysis, and RT-PCR in ICC. Exogenously-treated 5-HT showed tonic inward currents on pacemaker currents in ICC under the voltage-clamp mode in a dose-dependent manner. Based on RT-PCR results, we found the existence of 5-HT2B, 3, 4, and 7 receptors in ICC. However, SDZ 205557 (a 5-HT4 receptor antagonist), SB 269970 (a 5-HT7 receptor antagonist), 3-tropanylindole - 3 - carboxylate methiodide (3-TCM; a 5-HT3 antagonist) blocked the 5-HT-induced action on pacemaker activity, but not SB 204741 (a 5-HT2B receptor antagonist). Based on [Ca2+]i analysis, we found that 5-HT increased the intensity of [Ca2+]i. The treatment of PD 98059 or JNK II inhibitor blocked the 5-HT-induced action on pacemaker activity of ICC, but not SB 203580. In summary, these results suggest that 5-HT can modulate pacemaker activity through 5-HT3, 4, and 7 receptors via [Ca2+]i mobilization and regulation of mitogen-activated protein kinases.
Animals ; Flavonoids ; Gastrointestinal Motility ; Imidazoles ; Interstitial Cells of Cajal ; Intestine, Small ; Mice ; Mitogen-Activated Protein Kinases ; para-Aminobenzoates ; Patch-Clamp Techniques ; Phenols ; Pyridines ; Receptor, Serotonin, 5-HT2B ; Receptors, Serotonin ; Receptors, Serotonin, 5-HT4 ; Serotonin ; Sulfonamides

PURPOSE: Baroreceptor reflex regulation has been shown to reset towards a higher blood pressure level. This study was designed to assess alterations of chronotropic baroreflexes in two-kidney, one clip (2K1C) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. METHODS: Arterial pressure and heart rate (HR) were monitored continuously during intravenous infusions of phenylephrine or sodium nitroprusside. Ensuing reflex HR responses during each drug infusion were determined in two ways: (a) at 10 s intervals (time analysis), and (b) with every 10 mmHg change in pressure (pressure analysis). RESULTS: Both pressor and depressor responses produced by phenylephrine or sodium nitroprusside were comparable between normotensive and hypertensive rats. Both reflex tachycardia and bradycardia were attenuated in 2K1C hypertensive rats as compared with normotensive rats, whereas no significant differences were shown in DOCA-salt hypertensive rats. CONCLUSION: These results indicate that chronotropic baroreflexes are impaired in 2K1C hypertensive rats, but not in DOCA-salt hypertensive rats.
Animals ; Arterial Pressure ; Baroreflex ; Blood Pressure ; Bradycardia ; Desoxycorticosterone ; Dihydrotachysterol ; Heart Rate ; Hypertension ; Infusions, Intravenous ; Nitroprusside ; Phenylephrine ; Rats ; Reflex ; Tachycardia

PURPOSE: Hypertension may be involved an alteration of intrinsic basal tone in vascular smooth muscle. The purpose of this study was to investigate the vasorelaxant effect of atrial natriuretic peptide (ANP) on isolated non-contracted aorta from two-kidney, one clip (2K1C) renovascular hypertensive rats. METHODS: 2K1C hypertension was induced by clipping the left renal artery and were used 6 weeks later. Age-matched rats receiving a sham treatment, which served as controls. The thoracic aortae were mounted in tissue baths to measure the isometric tension. RESULTS: ANP diminished basal tone in previously unstimulated thoracic aortic rings from 2K1C hypertensive rats, while it had no effect in the control rats. Endothelial destruction potentiated the vasorelaxant effect of ANP on basal tone in 2K1C rats. A similar potentiation of the ANP response was observed by pre-treatment with N omega-nitro-L-arginine methyl ester (L-NAME) or methylene blue in aortic rings with endothelium. Treatment with calcium-free Krebs decreased basal tone and abolished ANPresponse. These effects were observed only in aortic rings from 2K1C rats. Similarly, staurosporine and calphostin C, inhibitors of protein kinase C (PKC), lowered basal tone and abolished ANP-response in hypertensive rats. CONCLUSION: These results demonstrate that ANP has a vasorelaxant effect on basal tone in 2K1C renovascular hypertension. Inhibition of ANP effects on basal tone by calcium-free Krebs and PKC antagonists suggests that altered Ca2+ -active tone is involved in hypertension, that modifies the response of vascular smooth muscle to the ANP.
Animals ; Aorta ; Aorta, Thoracic ; Atrial Natriuretic Factor ; Baths ; Endothelium ; Hypertension ; Hypertension, Renovascular ; Methylene Blue ; Muscle, Smooth, Vascular ; Naphthalenes ; NG-Nitroarginine Methyl Ester ; Placebos ; Protein Kinase C ; Rats ; Renal Artery ; Salicylamides ; Staurosporine

Although many studies show that thromboxane A2 (TXA2) has the action of gastrointestinal (GI) motility using GI muscle cells and tissue, there are no reports on the effects of TXA2 on interstitial cells of Cajal (ICC) that function as pacemaker cells in GI tract. So, we studied the modulation of pacemaker activities by TXA2 in ICC with whole cell patch-clamp technique. Externally applied TXA2 (5 micrometer) produced membrane depolarization in current-clamp mode and increased tonic inward pacemaker currents in voltage-clamp mode. The tonic inward currents by TXA2 were inhibited by intracellular application of GDP-beta-S. The pretreatment of ICC with Ca2+ free solution and thapsigargin, a Ca2+-ATPase inhibitor in endoplasmic reticulum, abolished the generation of pacemaker currents and suppressed the TXA2-induced tonic inward currents. However, chelerythrine or calphostin C, protein kinase C inhibitors, did not block the TXA2-induced effects on pacemaker currents. These results suggest that TXA2 can regulate intestinal motility through the modulation of ICC pacemaker activities. This modulation of pacemaker activities by TXA2 may occur by the activation of G protein and PKC independent pathway via extra and intracellular Ca2+ modulation.
Animals ; Benzophenanthridines ; Endoplasmic Reticulum ; Gastrointestinal Motility ; Gastrointestinal Tract ; GTP-Binding Proteins ; Guanosine Diphosphate ; Interstitial Cells of Cajal ; Intestines ; Membranes ; Mice ; Muscle Cells ; Naphthalenes ; Patch-Clamp Techniques ; Protein Kinase C ; Thapsigargin ; Thionucleotides ; Thromboxane A2

The effects of (-)-epigallocatechin gallate (EGCG) on pacemaker activities of cultured interstitial cells of Cajal (ICC) from murine small intestine were investigated using whole-cell patch-clamp technique at 30degrees C and Ca2+ image analysis. ICC generated spontaneous pacemaker currents at a holding potential of -70 mV. The treatment of ICC with EGCG resulted in a dose-dependent decrease in the frequency and amplitude of pacemaker currents. SQ-22536, an adenylate cyclase inhibitor, and ODQ, a guanylate cyclase inhibitor, did not inhibit the effects of EGCG. EGCG-induced effects on pacemaker currents were not inhibited by glibenclamide, an ATP-sensitive K+ channel blocker and TEA, a Ca2+-activated K+ channel blocker. Also, we found that EGCG inhibited the spontaneous [Ca2+]i oscillations in cultured ICC. In conclusion, EGCG inhibited the pacemaker activity of ICC and reduced [Ca2+]i oscillations by cAMP-, cGMP-, ATP-sensitive K+channel-independent manner.
Adenine ; Adenylyl Cyclases ; Animals ; Gastrointestinal Motility ; Glyburide ; Guanylate Cyclase ; Interstitial Cells of Cajal ; Intestine, Small ; Mice ; Patch-Clamp Techniques ; Tea