Evaluation of low back pain frequency and related factors among people over 18 years of age.

AIMS: The present study aimed to evaluate the incidence of LBP and related factors in over 18-year-olds. MATERIALS AND METHODS: This research was a cross-sectional study involving individuals over 18 years of age with any complaints in the period from May 2015-June 2016 at different hospitals. The research data were evaluated by the SPSS 15.0 statistical package program. Descriptive statistics were presented as mean (±) standard deviation, median (min, max), frequency distribution, and percentage. Pearson's Chi-square test, Yates corrected Chi-square test, and Fisher's test were used as statistical methods. Statistical significance was accepted as P < 0.05. RESULTS: A total of 5,989 people admitted during that period and 50% unknown frequency were taken to reach 1715 subject persons with 2% deviation and 95% confidence interval which reached 1720. The sociodemographic status, occupational conditions, the frequency of low back pain, and risk factors have been evaluated. Around 92.9% of individuals of 65 years of age and older have lifelong LPB while 57.1% have present LBP. The difference was statistically significant for "the satisfaction of working people" and "individuals working more than 41 h a week." (P < 0.001). CONCLUSION: Low back pain is still a serious problem that can be avoided by ensuring optimal working conditions and a healthier life.

Surgical outcomes of sleeve resections performed for non-small cell lung cancer; A single center experience.

BACKGROUND: Although bronchial sleeve resections were performed instead of pneumonectomy in patients with insufficient pulmonary function initially, it is currently available as an alternative to pneumonectomy even in patients with adequate pulmonary reserve. AIMS: In this study, we aimed to evaluate the sleeve resections performed for lung cancer in terms of technical, postoperative complication mortality, survival rates and survival factors, complication and to compare them with the literature. METHODS: Patients who underwent sleeve lung resection with diagnosis of non-small cell lung cancer at our department between January 2012 and December 2017 were included in the study. Patients' data were analyzed according to tumor size, tumor histopathology, hilar/mediastinal lymph nodes invasion status, postoperative complications, operative mortality, resection type, overall survival and diseases-free survival, tumor location, and length of stay in intensive care unit. RESULTS: A total of 71 patients included the study. Right upper sleeve lobectomy was applied to 40 (56.3%) patients and left upper sleeve lobectomy was performed to 19 (26.8%) patients. The most common histopathological diagnosis was squamous cell carcinoma. The mean tumor diameter was 3.39 (SD: 2.25) cm. There was no nodal invasion in 41 (57.7%) patients and N1 nodal positivity was detected in 18 (25.4%) patients and N2 positivity in 12 (16.9%) patients. Median survival time was 43.6 months (35.4-51.8 months), the 3- and 5-year overall survival were 65.7% and 40.6%, respectively. There was a statistically significant correlation relationship between nodal invasion and recurrence, but this relation was not found in overall survival. CONCLUSION: In our study, no significant correlation was found between mediastinal lymph node invasion and overall survival. Supporting this result with multi-centered and prospective studies may encourage surgeons for sleeve resection in indicated patients had lung cancer with nodal invasion.

Prognostic significance of standardised uptake value (SUVmax ) measured on 18F-fluorodeoxyglucose positron emission tomography/computed tomography in patients with small cell lung cancer.

Certain prognostic factors for small cell lung cancer (SCLC) have been validated, but the prognostic role of 18F-FDG PET/CT still remains unclear. The aim of this study was to evaluate the prognostic significance of 18F-FDG PET/CT in patients with SCLC. We reviewed 142 patients with pathologically proven SCLC who underwent pre-treatment 18F-FDG PET/CT. Standardised uptake value (SUVmax ) and other potential prognostic variables were chosen for analysis. The mean age of the study population was 58.2 ± 10.1 years (range, 25-84), and 124 (87.3%) patients were men. The median SUVmax value was 11.6 (4.0-29.3). Among the variables included in the univariate analysis, performance status (P = 0.001), disease stage (P < 0.001), administration of thoracic radiotherapy (TRT; P < 0.001), albumin level (P = 0.030) and LDH level (P < 0.001) showed prognostic significance. Further, multivariate analysis showed that performance status (P = 0.007), albumin level (P = 0.002), LDH level (P < 0.001) and administration of TRT (P = 0.001) were independent prognostic factors for survival. In conclusion, performance status, TRT, LDH level and albumin level were identified as important prognostic factors, while 18F-FDG PET/CT uptake of the primary lesions did not have any prognostic significance for survival in patients with SCLC.

Giant Cornu Cutaneum Superimposed on Basal Cell Carcinoma.

Cornu cutaneum (CC) is a clinical term that describes the horn-like keratotic lesions extending vertically from the skin. Benign, premalignant or malignant lesions may be present at the base of CC. Seborrhoeic keratosis and squamous cell carcinoma (SCC) are the most commonly reported benign and malignant forms, respectively. Basal cell carcinoma (BCC) at the base is rare. Here, we report on an 85-year old female patient having multiple CC lesions, one being giant on her face and two of the lesions diagnosed with BCC at the base. This case is of significance due to the presence of giant and multiple CC and detection of BCC at the base of more than one lesion. This present case indicates the need for the treatment of possible malignant lesions underlying CC in the elderly by total surgical excision.

Candesartan mediates microcirculation in acute necrotizing pancreatitis.

AIM: In the present study we aimed to determine the effect of an AT-II antagonist candesartan on pancreatic microcirculation in an experimental model of acute necrotizing pancreatitis. MATERIALS AND METHODS: There were five study groups with 10 animals in each. Pancreatitis was induced by intravenous infusion of cerulein and coadministration of glycodeoxycholate into biliopancreatic canal. Candesartan is given at 6th and 18th hour to the 24th and 48th hour groups, respectively. At 24th and 48th hours; following anaesthesia laparotomy was performed and laser Doppler flowmetry was performed in the pancreatic tissue of the animals. Following scarification blood samples were obtained for amylase, myeloperoxidase, IL-6 and tumour necrosis factor alpha. Tissue samples from the pancreas were obtained for histopathological analysis, endothelial cell apoptosis (TUNEL assay) and matrix metalloproteinase-9 immunohistochemistry. RESULTS: Pancreatic microcirculation was higher in the candesartan treated groups (p < 0.05). Myeloperoxidase, IL-6 and tumour necrosis factor alpha was found to be lower in the candesartan treated groups (p < 0.05). The pancreatic edema and inflammation were found to be reduced in the candesartan treated groups (p < 0.05). Endothelial apoptosis was found to be reduced by cadesartan treatment but it did not reach statistical significance (p > 0.05). Tissue matrix metalloproteinase -9 levels were found to be reduced with candesartan treatment (p < 0.05). CONCLUSION: Treatment with candesartan in the early phases of acute necrotizing pancreatitis effective on microcirculation of pancreatic tissue (Tab. 3, Fig. 6, Ref. 28).

Memantine induces apoptosis and inhibits cell cycle progression in LNCaP prostate cancer cells.

Deregulated cancer cell metabolism plays an important role in cancer progression. Cancer cell metabolism has been in the centre of attention in therapeutical cancer cell targeting. Repurposed chemical agents, such as metformin and aspirin, have been studied extensively as preventive and therapeutic agents. Metformin is Food and Drug administration (FDA)-approved antidiabetic drug cheaper than other chemotherapeutic agents that were shown to have anticancer effects. Memantine is an FDA-approved Alzheimer's drug. Drug repositioning studies offer wide range of benefits, such as reduced time, cost and risk over de novo drug discovery. Therefore, we aimed to target glucose and glutamine metabolism in androgen-dependent LNCaP cells by using metformin and memantine and investigate these agents' effects on prostate cancer cell proliferation in vitro. We evaluated the effects of metformin and memantine on the protein expression levels of genes that play significant roles in apoptosis and cell cycle progression (Casp3, Casp9, Bcl-2, Survivin, Bax, c-Myc, HIF1A, CCND1, CDK4 and GAPDH) by Western blotting. Alzheimer's drug memantine exerted cytotoxic effects at 0.25 mM and metformin at 2.5 mM. We identified for the first time that memantine exerts antineoplastic activity (0.25 mM) by triggering Bax-dependent pathway of apoptosis. In addition to that both molecules have shown similar patterns on pro- and anti-apoptotic protein expression levels, such as Bcl-2, Casp3, Survivin and Bax. Our preclinic results indicate that memantine might be used as a new repositioned drug in cancer treatment. Beyond targeting glucose metabolism, glutamine metabolism also holds great promise for a potential treatment option.

The influence of nitric oxide donors on the responses to nitrergic nerve stimulation in the mouse duodenum.

We investigated whether exogenous nitric oxide (NO) donors have a prejunctional and/or postjunctional inhibitory effect on the nitrergic responses and whether this inhibitory effect was mediated by NO itself and in part, by cyclic GMP in mouse duodenal strips. N(omega)-nitro-L-arginine inhibited relaxations induced by electrical field stimulation of nitrergic nerves, but not those with acidified NaNO2. Furthermore, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) inhibited both types of relaxations while 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT) and N-ethylmaleimide were ineffective. NO donors, nitroglycerin and sodium nitroprusside, inhibited relaxations induced by nitrergic nerve stimulation, but not those with acidified NaNO2. Hemoglobin, exogenous Cu(2+)/Zn(2+) superoxide dismutase, diethyldithiocarbamic acid and pyrogallol did not influence the relaxation with nitrergic nerve stimulation. However, hemoglobin, diethyldithiocarbamic acid, pyrogallol and diethyldithiocarbamic acid plus pyrogallol attenuated the inhibitory effect of NO donors on relaxation with nitrergic nerve stimulation, and exogenous superoxide dismutase potentiated this inhibitory effect. Moreover, nitrergic nerve-mediated relaxations were inhibited by 8-bromo-cyclic GMP, but not by 8-bromo-cyclic AMP. These results suggest that exogenous NO donors have a prejunctional inhibitory effect on the nerve-mediated nitrergic relaxation and that the inhibitory effects of nitroglycerin and sodium nitroprusside are NO-dependent, but not related to NO metabolites such as peroxynitrite or a nitrosothiol intermediate. However, a contribution of S-nitrosothiol formed intracellularly cannot be entirely ruled out. Also, this prejunctional inhibition is mediated, at least in part, by the cyclic GMP, but not the cyclic AMP, pathway.

A possible role of S-nitrosothiols at the nitrergic relaxations in the mouse corpus cavernosum.

Relaxations induced by electrical field stimulation and acetylcholine were compared with those induced by acidified sodium nitrite, sodium nitroprusside, S-nitrosoglutathione and S-nitroso-N-acetyl-D,L-penicillamine in the mouse corpus cavernosum precontracted with phenylephrine. NG-nitro-L-arginine inhibited electrical field stimulation- or acetylcholine-induced relaxation, but was ineffective on relaxations caused by the other stimuli. Hydroquinone and pyrogallol had no inhibitory action on the relaxations caused by any stimulus except acidified sodium nitrite. Incubation of the tissue with diethyldithiocarbamic acid significantly inhibited the relaxations induced by all stimuli except papaverine. In the tissues pre-treated with diethyldithiocarbamic acid, superoxide dismutase, hydroquinone and pyrogallol failed to yield restore or further inhibit the relaxations in response to electrical field stimulation or acetylcholine. LY 83583 (6-anilino-5,8-quinolinedione) and hydroxocobalamin clearly inhibited the relaxant responses to electrical field stimulation, acetylcholine, S-nitrosoglutathione and acidified sodium nitrite whereas there was significant enhancement of the relaxation produced by S-nitroso-N-acetyl-D,L-penicillamine. These findings suggest that the relaxant factor released from non-adrenergic non-cholinergic nerves or endothelial cells in mouse cavernosal tissue may be a superoxide anion-resistant nitric oxide-containing molecule and that S-nitrosoglutathione rather than S-nitroso-N-acetyl-D,L-penicillamine could be a suitable candidate for this.

Effects of vitamin E and sodium selenate on neurogenic and endothelial relaxation of corpus cavernosum in the diabetic mouse.

We studied the effect of vitamin E and sodium selenate treatment on the neurogenic and endothelium-dependent relaxation of isolated corpus cavernosum obtained from streptozotocin-induced diabetic mice. Relaxant responses of corpus cavernosum precontracted by phenylephrine to electrical field stimulation and to acetylcholine were significantly decreased in diabetic mice. There was no significant difference between diabetic and non-diabetic groups for the relaxant response of corpus cavernosum to sodium nitroprusside and papaverine. Treatment with sodium selenate, but not vitamin E, partially prevented the impairment of the neurogenic relaxation, whereas both had a significant, partial restorative action on endothelial dysfunction in corpus cavernosum obtained from diabetic groups. Neither agent exhibited a significant action on the relaxant responses of corpus cavernosum obtained from non-diabetic mice. A decrease in the sensitivity of the neurogenic impairment to antioxidant action may develop more rapidly than that of endothelial dysfunction in streptozotocin-induced diabetic mice.

Effect of neocuproine, a selective Cu(I) chelator, on nitrergic relaxations in the mouse corpus cavernosum.

The effects of neocuproine and bathocuproine, Cu(I) and Cu(II) chelators, respectively, were studied on relaxations in response to electrical field stimulation, acetylcholine, S-nitrosoglutathione, acidified sodium nitrite and sodium nitroprusside in the mouse corpus cavernosum precontracted with phenylephrine. Neocuproine significantly inhibited relaxations induced by electrical field stimulation, acetylcholine and S-nitrosoglutathione, but not by acidified sodium nitrite and sodium nitroprusside. The pre-prepared neocuproine-Cu(I) complex was ineffective on the responses. The discrepancy between the shape of relaxations in response to electrical field stimulation or to acetylcholine and S-nitrosoglutathione was abolished by adding CuCl(2) into the bathing medium. The copper action was blocked by neocuproine but not by bathocuproine. However, the pre-prepared bathocuproine-Cu(II) complex did not accelerate the relaxations affected by CuCl(2). These findings suggest that a Cu(I)-dependent mechanism may play a role in the relaxation induced by the endogenous relaxant factor as well as by S-nitrosoglutathione in mouse cavernosal tissue.

Effects of some divalent cations on nitrergic relaxations in the mouse corpus cavernosum.

Acute effects of some divalent cations (Cd2+, Ni2+, Co2+, Zn2+, Mn2+ and Sn2+) were investigated on neurogenic and endothelium-dependent relaxations in the isolated mouse corpus cavernosum. Neither neurogenic nor endothelium-dependent relaxation was affected by cations at the concentrations used (up to 100 microM), except Cd2+. Although Cd2+ (20 and 40 microM) did not cause any significant alteration in the acetylcholine- (ACh) or sodium nitroprusside- (SNP) induced relaxation, it inhibited electrical field stimulation- (EFS) produced relaxation significantly. Zn2+ and selenium could not reverse this inhibitory action. Cd2+ did block the EFS-evoked guanethidine-sensitive contraction in the presence of N(G)-nitro-L-arginine. Elevation of external Ca2+ content significantly reduced the inhibitions due to Cd2+ on the EFS-induced relaxation and on the EFS-evoked guanethidine-sensitive contraction. In the Ca2+-omitted medium, EFS-induced relaxation disappeared, while acetylcholine-elicited relaxation resisted. Verapamil was ineffective on the relaxation produced by EFS or acetylcholine. However, it significantly diminished phenylephrine-induced contractions. These findings suggest that unlike other cations at the concentrations used in the present study, Cd2+ may have an effect on an external Ca2+-dependent mechanism at the neuronal level, and this effect may be responsible for its acute inhibitory action on the neurogenic relaxation in the mouse corpus cavernosum.

Restorative effects of zinc and selenium on nitrergic relaxations impaired by cadmium in the mouse corpus cavernosum.

We investigated whether Cd2+ intake (in drinking water, 15 ppm) for 30 days can affect the nitrergic relaxations of the mouse corpus cavernosum (CC) and whether Zn2+ (25 mg kg(-1) via a stomach tube at 48-h intervals) or sodium selenate (8 microg kg(-1) day(-1) intraperitoneally) has a restorative action on the impairment in the response. Relaxant responses of the CC obtained from Cd2+-treated mice to electrical field stimulation (neurogenic) or acetylcholine (endothelium dependent) were significantly inhibited. A partial restoration was observed in the nitrergic relaxation of the CC obtained from Zn2+- or sodium selenate-co-treated animals. Neither agent exhibited any significant action on the responses of the tissue from control mice. There was no significant difference between Cd2+-treated and control mice in respect of the relaxation amplitude induced by sodium nitroprusside or papaverine. These results suggest that Cd2+ intake may impair the nitrergic relaxation of the mouse CC, and, co-treatment with Zn2+ or sodium selenate may partially improve the nitrergic mechanisms in the tissue.

Possible roles of nitric oxide and vasoactive intestinal polypeptide on relaxation induced by isoprenaline in isolated muscle strips of the mouse gastric fundus.

The possible role of nitric oxide (NO) and vasoactive intestinal polypeptide on isoprenaline-induced relaxation of the mouse longitudinal gastric fundal strips precontracted with 5.4 x 10(-7) M carbachol was investigated. Isoprenaline (5 x 10(-7) M, 10(-6) M and 5 x 10(-6) M) produced a concentration-dependent relaxations. NG-nitro L-arginine (10(-4) M) partly inhibited isoprenaline-induced relaxation. The inhibitory action of NG-nitro L-arginine was reversed by 4 x 10(-4) M L-arginine but not by 4 x 10(-4) M D-arginine. NG-nitro L-arginine (10(-4) M) did not affect the relaxation caused by sodium nitroprusside (10(-6) M). Vasoactive intestinal polypeptide antibody 7913 (1:160 dilution) partly inhibited isoprenaline-induced relaxation. This inhibition was greater on the response to the higher isoprenaline concentration (5 x 10(-6) M) than to the lower concentration (10(-6) M). The combination of vasoactive intestinal polypeptide antibody and NG-nitro L-arginine significantly enhanced the inhibition on 10(-6) M isoprenaline action. These results suggest that nitric oxide and vasoactive intestinal polypeptide may partly contribute to the relaxation induced by isoprenaline in the mouse gastric fundus precontracted with carbachol.

The role of Na+ channels in twitch generation during exposure of the frog rectus abdominis to Ca-free Ringer solution with Na2EDTA.

The aim of the study was to investigate whether Na+ channels play a role in the twitch component of the response of the isolated frog rectus abdominis to Ca(2+)-free Ringer solution with 0.2 mM Na2EDTA by using tetrodotoxin and some other well known drugs that exhibit a blocking action on Na+ channels. In the presence of 5 x 10(-7) M tetrodotoxin, the twitch component, measured isotonically, disappeared. Although 10(-7) M d-tubocurarine was found to be ineffective, a complete blockage of twitch amplitude was observed at 5 x 10(-6) M concentration of the drug. The inhibitory action of d-tubocurarine on twitch response was not antagonized by 10(-6) and 10(-5) M carbachol. Propranolol (10(-6) - 10(-5) M), lidocaine (2 x 10(-6) - 10(-5) M), quinine (10(-6) - 2 x 10(-5) M) and quinidine (10(-6) - 2 x 10(-5) M) inhibited maximal twitch amplitude in a concentration dependent manner. These findings strongly suggest that activation of tetrodotoxin sensitive Na+ channel may play a primary role at twitch generation during exposure of the frog rectus abdominis to Ca(2+)-free Ringer solution with Na2 EDTA.

Possible postsynaptic action of aminoglycosides in the frog rectus abdominis.

The present study was undertaken to investigate the postsynaptic effects of aminoglycosides on contractions evoked by acetylcholine (ACh), KCl, electrical field stimulation (EFS) and Na(+)- and Ca(2+)-free Ringer solution with 0.2 mM Na2 EDTA (NaFCaFR) in the isolated frog rectus abdominis. Neomycin inhibited contraction elicited by ACh, NaFCaFR, and EFS at the higher frequencies (8 and 10 Hz) but not those elicited by KCl and EFS at the lower frequencies (2, 3 and 5 Hz). D-tubocurarine inhibited ACh-induced contractions in a concentration-dependent manner. In addition, drug reduced EFS-evoked contractions to a limited extent. Lower concentrations (10(-5), 5 x 10(-5), 10(-4), 2 x 10(-4) and 3 x 10(-4) M) but not higher concentrations (4 x 10(-4) and 5 x 10(-4) M) of methoxyverapamil exhibited a concentration-dependent inhibitory action on NaFCaFR-induced contractions. Similar inhibitions of the same type of contraction were displayed by aminoglycosides (neomycin, streptomycin, netilmycin, gentamycin and amikacin). These results suggest that in addition to their antagonistic action on nicotinic receptors in the frog rectus abdominis, aminoglycosides may exert stabilizing effects on some functional components contributing to contractions at the membrane.

Inhibitory actions of hydroxocobalamin, cyanocobalamin, and folic acid on the ultraviolet light-induced relaxation of the frog upper oesophageal strip.

The applications of ultraviolet (UV) light (336 nm) on the upper oesophageal strips of frog elicited relaxant responses in the presence of NaNO2 (50 microM). The tissues were mounted under the tension 0.5 g in an organ bath containing Ringer solution, maintained at 25 degrees C and gassed with 100% O2. The responses were recorded on a kymograph via an isotonic lever. Antimegaloblastic agents, including hydroxocobalamin (1, 10, and 100 microM), cyanocobalamin (1, 10, 25, and 100 microM), and folic acid (1, 10, 50, 100, and 200 microM), significantly attenuated the relaxation response to UV light. Folinic acid (1, 10, 25, and 100 microM), however, enhanced the relaxation. Pyrogallol (50 microM), hydroquinone (50 microM), and diethyldithiocarbamic acid (8 mM) were found ineffective for attenuation, though FeSO4 (200, 400, and 500 microM) and hemoglobin (50 microM), respectively, exerted significant inhibition. L-arginine methylester (500 microM) did not impair UV-induced relaxation. Based on these results, we concluded that a mechanism involving undefined action(s) of antimegaloblastic drugs may cause alterations in the UV light-induced relaxation of the tissue used.

Papaverine-induced and endothelium-dependent relaxation in the isolated rat aortic strip.

In the present study, we aimed to obtain further evidence in favour of the hypothesis that nitric oxide (NO) is a major mediator of endothelium-dependent vasorelaxation and to clarify whether NO plays a role in papaverine-induced vasorelaxation. The relaxant effects of acetylcholine (Ach), acidified NaNO2 or papaverine were investigated on isolated helical strips of the rat thoracic aorta precontracted with phenylephrine in an organ bath containing Krebs solution aerated with 95% O2 and 5% CO2. The relaxation was quantified as % peak reduction of phenylephrine contracture. Saponin abolished the relaxant effects of Ach completely whereas it had no effect on the responses to acidified NaNO2 or papaverine. NG-nitro-L-arginine (L-NOARG) reduced the effects of Ach significantly, but it was ineffective on the relaxation induced by acidified NaNO2. The inhibitory action of L-NOARG was partly restored by L-arginine, but not by D-arginine. Hemoglobin, hydroxocobalamin and hydroquinone exhibited significant inhibition on the relaxation evoked by Ach and acidified NaNO2. L-NOARG, hydroxocobalamin and hydroquinone caused only limited but significant decrease in the relaxation due to papaverine. This phenomenon was also observed by increasing phenylephrine concentration leading to an enhancement in the contraction. Our findings strongly support the view that Ach-induced relaxation of rat aorta strips is mediated by free NO released from the endothelium and the results suggest that NO may indirectly contribute to papaverine-induced relaxation.

Involvement of nitric oxide in non-adrenergic non-cholinergic relaxation and action of vasoactive intestinal polypeptide in circular muscle strips of the rat gastric fundus.

We examined the characteristics of the non-adrenergic non-cholinergic (NANC) nerve induced relaxation and the possible interaction between nitric oxide (NO) and vasoactive intestinal polypeptide (VIP) on the basal tone of the circular muscle of the rat gastric fundus. Electrically induced NANC relaxations were partly inhibited by N(omega)-nitro-L-arginine (100 microM), whereas sodium nitroprusside (SNP; 10 microM) and VIP (5 nM) induced relaxations were not affected. 2-Amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT; 5 microM) also inhibited the responses to electrical stimuli to a similar extent as N(omega)-nitro-L-arginine but not VIP. However, AMT plus N(omega)-nitro-L-arginine did not give an additional inhibition above that of each drug alone on NANC relaxations, and dexamethasone (10 microM) had no effect on NANC nerve induced relaxations. 1H-[1,2,4,]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 10 microM), a selective inhibitor of guanylate cyclase, abolished the responses to NANC nerve stimulation and SNP, while VIP responses were not influenced. N-ethylmaleimide (100 microM), an adenylate cyclase inhibitor, attenuated relaxations to NANC nerve stimulation, VIP and isoproterenol (1 nM), while having no effect on those to SNP, but in combination with N(omega)-nitro-L-arginine, there was no additional inhibition on the responses to nerve stimulation. Alpha-chymotrypsin (10 u ml(-1)) severely diminished VIP induced relaxations, but did not reduce electrical responses. In conclusion, these results suggest that NO is involved in the relaxations induced by short-term electrical stimulation. However, another possible unidentified transmitter that can trigger the accumulation of cyclic GMP is not entirely ruled out and there is no interaction between NO and VIP in the circular muscle strip of the rat gastric fundus, even in the basal state of the tissue.

An in vitro study of nonadrenergic-noncholinergic activity on the cavernous tissue of mouse.

The relaxant effects of electrical field stimulation (EFS) and exogenously applied acetylcholine (ACh) or acidified NaNO2 (a-NaNO2) were investigated in the isolated mouse corpus cavernosum precontracted with phenylephrine hydrochloride (PE). Tetrodotoxin (TTX) blocked the relaxant effects of EFS completely, whereas it had no effect on the responses to ACh or a-NaNO2. Guanethidine and indomethacin failed to affect the electrically or ACh-induced relaxations. Atropine completely blocked the effect of ACh; however, it caused a slight reduction in the relaxation evoked by EFS. NG-Nitro-L-arginine (L-NOARG) reduced the effects of EFS and ACh significantly, but it was ineffective on the relaxations induced by a-NaNO2. The inhibitory action of L-NOARG was partly restored by L-arginine, but not by D-arginine. Methylene blue (MB) and hydroxocobalamin (HC) exhibited significant inhibition on the relaxations evoked by EFS, ACh and a-NaNO2. Hydroquinone (HQ) reduced relaxation due to a-NaNO2, but did not affect that of EFS and ACh. Our findings suggest that EFS-induced relaxations of mouse cavernosal tissue are mediated by a transmitter which probably resembles an organic nitrate.

The effect of Ba2+ on the nitrergic mechanism in the isolated frog lung preparation.

1. The present study was undertaken to investigate effects of Ba2+ on the isolated frog lung strips depolarized by 20 mM K+ in Ca2+ free Ringer solution. 2. Ba2+ produced monophasic relaxant response, whereas Ca2+ induced biphasic response consisting of a transient relaxation and a marked contraction. Both kinds of relaxation were inhibited completely by L-NOARG. L-arginine reversed the action of L-NOARG. 3. Ferrous sulfate, pyrogallol, hydroquinone, and vanadate reduced the Ba(2+)-induced relaxation in a concentration-dependent manner. 4. These findings suggest that Ba(+)-induced relaxation may fully be mediated by the nitrergic mechanism and the effect of Ba2+ on the nitric oxide synthase may be more selective than Ca2+.