Increased nitric oxide availability worsens the cardiac performance during early re-perfusion period in adult rats

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Faten M.A. Diab ◽  
Mahmoud H. Ayobe ◽  
Mohamed F. Abdel-Salam ◽  
Mohammed F.S. Otman ◽  
Enas A. Abdel-Hady
Keyword(s):  
Nitric Oxide ◽  
Flow Rate ◽  
Cardiac Performance ◽  
Control Group ◽  
Adult Rats ◽  
Significant Deterioration ◽  
No Donor ◽  
Langendorff Preparation ◽  
Perfusion Period ◽  
Myocardial Flow

Abstract Objectives Re-perfusion is the standard therapy for acute myocardial infarction, despite the associated pathologies that may contribute to irreversible myocardial injury. The present study aims to clarify the alterations in cardiac activities in response to experimental cardiac ischemic arrest followed by re-perfusion in isolated hearts perfused with nitric oxide (NO) donor, l-arginine, or NO inhibitor, Nω-Nitro-l-arginine methyl ester hydrochloride (l-NAME), to shed light on the possible role of NO in the re-perfusion process. Methods Hearts isolated from adult Wistar rats were studied on Langendorff preparation under basal conditions and during 30 min re-perfusion following 30 min of total global ischemia. Rats were randomly divided into three groups; control and l-arginine or l-NAME infused heart groups. Cardiac tissue content of malondialdhyde, catalase and nitrite was also measured. Results Compared to the control group, both l-arginine and l-NAME infused hearts showed increased basal chronotropy and myocardial flow rate. Following ischemia and during the whole period of re-perfusion, the three groups demonstrated significant deterioration in the inotropic activity and compromised myocardial flow rate. l-arginine infused hearts revealed depressed inotropy and chronotropy, weak systolic and diastolic functions with compromised myocardial flow at early 5 min of re-perfusion, yet with significantly higher myocardial flow rate by the end of re-perfusion. Conclusions Reducing NO availability by l-NAME revealed mild impact on the ischemia re-perfusion induced contractile dysfunction, whereas excess NO worsens cardiac performance at the early re-perfusion period.

Chronic Nitric Oxide Deficiency is Associated with Altered Leutinizing Hormone and Follicle-Stimulating Hormone Release in Ovariectomized Rats1

2002 ◽  
Vol 227 (9) ◽  
pp. 817-822 ◽  
Author(s):  
Maria J. Barnes ◽  
Karen Lapanowski ◽  
Jose A. Rafols ◽  
David M. Lawson ◽  
Joseph C. Dunbar
Keyword(s):  
Nitric Oxide ◽  
Follicle Stimulating Hormone ◽  
Independent Effect ◽  
Control Group ◽  
Gonadotropin Secretion ◽  
No Donor ◽  
Ovx Rats ◽  
Nos Inhibitor ◽  
Stimulating Hormone

Nitric oxide (NO) synthase (NOS) has been found in the gonadotrophs and folliculo-stellate cells of the anterior pituitary. Previous observations from our laboratory suggest that NO may play a role in regulating gonadotropin secretion. Because estrogen secretion by the ovary can influence gonadotropin secretion, we investigated the hypothesis that chronic in vivo NO deficiency has a direct estrogen-independent effect on luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion. Chronic NO deficiency was induced by adding an NOS inhibitor, N-nitro-L-arginine (L-NNA, 0.6 g/l) to the drinking water of ovariectomized (OVX) rats. The control OVX rats were untreated. After 6–8 weeks, the animals were sacrificed, and the pituitaries were removed and perfused continuously for 4 hr in the presence of pulsatile gonadotropin-releasing hormone (GnRH, 500 ng/pulse) every 30 min. S-Nitroso-l-acetyl penicillamine (SNAP, an NO donor, 0.1 mM) or l-nitro-arginine methyl ester (L-NAME, an NOS inhibitor, 0.1 mM) was added to the media and perfusate samples were collected at 10-min intervals. GnRH-stimulated LH and FSH levels were significantly lower in pituitaries from OVX/NO-deficient pituitaries compared with pituitaries from the OVX control group. The addition of SNAP significantly decreased LH and FSH secretion by pituitaries from OVX control animals, but significantly increased their secretion by pituitaries from the OVX/NO-deficient animals. L-NAME also suppressed LH and FSH secretion by pituitaries from the OVX control animals and stimulated their release by pituitaries from the NO-deficient/OVX animals. Immunohisto-chemistry of frontal sections through the hypothalamus demonstrated that OVX/NO deficiency is associated with increased GnRH in the median eminence. We conclude that NO has a chronic stimulatory effect on LH and FSH release and the subsequent altered secretory responsiveness to NO agonist or antagonist is the result of chronic NO suppression.

Effect of chronic lithium administration on endothelium-dependent relaxation of rat mesenteric bed: role of nitric oxide

2007 ◽  
Vol 85 (10) ◽  
pp. 1038-1046 ◽  
Author(s):  
Banafsheh Afsharimani ◽  
Leila Moezi ◽  
Hamed Sadeghipour ◽  
Bahareh Rahimzadeh-Rofouyi ◽  
Maliheh Nobakht ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nadph Diaphorase ◽  
Control Group ◽  
No Donor ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed ◽  
Vascular Beds ◽  
Oxide Synthase ◽  
And Control

The mechanism of action of lithium, an effective treatment for bipolar disease, is still unknown. In this study, the mesenteric vascular beds of control rats and rats that were chronically treated with lithium were prepared by the McGregor method, and the mesenteric vascular bed vasorelaxation responses were examined. NADPH-diaphorase histochemistry was used to determine the activity of NOS (nitric oxide synthase) in mesenteric vascular beds. We demonstrated that ACh-induced vasorelaxation increased in the mesenteric vascular bed of rats treated with lithium. Acute Nο-nitro-l-arginine methyl ester (l-NAME) administration in the medium blocked ACh-induced vasorelaxation in the control group more effectively than in lithium-treated rats, while the vasorelaxant response to sodium nitroprusside, a NO donor, was not different between lithium-treated and control groups. Acute aminoguanidine administration blocked ACh-induced vasorelaxation of lithium-treated rats, but had no effect in the control rats. Furthermore, NOS activity, determined by NADPH-diaphorase staining, was significantly greater in the mesenteric vascular beds from chronic lithium-treated rats than in those from control rats. These data suggest that the enhanced ACh-induced endothelium-derived vasorelaxation in rat mesenteric bed from chronic lithium-treated rats might be associated with increased NOS activity, likely via iNOS. Simultaneous acute l-NAME and indomethacin administration suggests the possible upregulation of EDHF (endothelium-derived hyperpolarizing factor) in lithium-treated rats.

Abstract 16791: Oral Administration of Synthetic Prostacyclin Agonist Ono-1301 Prevents Deterioration of Cardiac Performance by Preserving Cardiac Structural Proteins in the Delta-sarcoglycan-deficient Hamster: Promising Treatment for Patients With DCM

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Shigeru Miyagawa ◽  
Yoshiki Sakai ◽  
Satsuki Fukushima ◽  
Shigeo Masuda ◽  
Atsuhiro Saito ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Oral Administration ◽  
Systolic Function ◽  
Cardiac Performance ◽  
Structural Proteins ◽  
Control Group ◽  
Dependent Manner ◽  
Significant Deterioration

Background: Although drugs such as beta blockers are reported to be effective for dilated cardiomyopathy (DCM), they are only effective in selected patients, and new therapeutics based on different mechanisms are still needed. We hypothesized that synthetic prostacyclin agonist (ONO-1301) would preserve the structural proteins in distressed cardiomyocytes, thus attenuating the deterioration of cardiac performance in the delta sarcoglycan-deficient hamster. Methods and Results: In an in vitro study, ONO-1301 was added to the culture medium of non-myocyte cells and the expression of several cytokines including VEGF was examined by ELISA. For the in vivo study, ONO-1301 (A: 3, n=5, B: 1, n=6, C: 0.3, n=7, D: 0.1 mg/kg/dose, n=7) was orally administered to delta-sarcoglycan-deficient hamsters every day from 8 to 20 weeks after birth. The control group (n=6) was untreated. Functional performance was evaluated by US before, 2, 4, 6, and 8 weeks after administration of ONO-1301. A histological analysis focusing on basement-membrane structural proteins, such as α-sarcoglycan, β-sarcoglycan, and α-dystroglycan, fibrosis, and hypertrophy was performed. In vitro, ONO-1301 enhanced the cytokine expressions dose dependently. In vivo, systolic function (EF) was gradually increased in the ONO-1301-treated groups, while it showed significant deterioration in the control group (45.7±2.9, 42.0±2.6, 32.3±1.0, 30.3±2.5, 26.3±2.7%, in groups A, B, C, D, and control, respectively, P<0.05). ONO-1301 also significantly attenuated the LV dilatation in a dose-dependent manner. Immunostaining revealed that all the cardiac structural proteins were preserved in the basement membrane of cardiomyocytes in the 3.0 mg/kg ONO-1301 treatment group, while they disappeared in the control. The % fibrosis and cell hypertrophy were significantly attenuated in the ONO-1301-treated group compared with the control. Conclusions: Oral administration of synthetic prostacyclin agonists, which can enhance cytokine expressions in non-myocyte cells, may preserve cardiac structural proteins in the delta sarcoglycan-deficient hamster, to maintain cardiac performance. This promising drug may inhibit the progression of the disease pathology in DCM, prolonging their life.

Effect of aging on nitric oxide-mediated penile erection in rats

1995 ◽  
Vol 268 (1) ◽  
pp. H467-H475 ◽  
Author(s):  
H. Garban ◽  
D. Vernet ◽  
A. Freedman ◽  
J. Rajfer ◽  
N. Gonzalez-Cadavid
Keyword(s):  
Nitric Oxide ◽  
Muscle Relaxation ◽  
Phosphodiesterase Inhibitor ◽  
Smooth Muscle Relaxation ◽  
Adult Rats ◽  
No Donor ◽  
Tissue Sections ◽  
Old Rats ◽  
Nos Inhibitor ◽  
Erectile Response

Aging is an important risk factor for impotence in men. Because nitric oxide (NO) appears to be the mediator of corpora cavernosal smooth muscle relaxation, we have examined in 5-, 20-, and 30-mo-old rats, designated “adult,” “old,” and “senescent,” respectively, whether aging causes a decrease of erectile response that may correlate with lower NO synthase (NOS) in the penis. Electric field stimulation (EFS) of the cavernosal nerve showed that the maximum intracavernosal pressure (MIP) declined in the old and senescent rats to 80 and 51% of the adult value, respectively. A low systemic dose of the NOS inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME; 2 mg/kg), reduced the MIP by only 38% in the adult rats but decreased it in the old and senescent rats by 72 and 80%, respectively. In the absence of EFS, intracavernosal papaverine (phosphodiesterase inhibitor), or nitroglycerin (NO donor), caused a lower erectile response in the old and senescent rats compared with the adult animals (MIP: 41 and 14%, respectively; duration of the erection 46 and 21%, respectively). Tissue sections from old and senescent penises showed increasing degrees of sclerotic degeneration. In comparison with the adult rats, the penile soluble NOS activity per gram of tissue that is sensitive to L-NAME decreased significantly by 63% in the senescent rats but was elevated in the old rats. These results indicate that aging causes an erectile failure due to factors initially independent from an impairment of penile NO synthesis but which are compounded in the very old rats by the decrease of penile NOS activity.

scholarly journals Involvement of N-methyl-D-aspartate receptors and nitric oxide in the anticonvulsant effects of dantrolene against pentylenetetrazole-induced seizures in mice

2017 ◽  
Vol 04 (02) ◽  
pp. 112-118
Author(s):  
Akbarzadeh Samad ◽  
Heidary Fatemeh ◽  
Keshavarz Mojtaba
Keyword(s):  
Nitric Oxide ◽  
Nmda Receptors ◽  
Clonic Seizure ◽  
Negative Control ◽  
No Synthase ◽  
Tonic Clonic Seizure ◽  
Control Group ◽  
No Donor ◽  
Clonic Seizures ◽  
Anticonvulsant Effects

Abstract Objective N-methyl-d-aspartate (NMDA) receptors and nitric oxide (NO) have important roles in the pathology and treatment of pentylenetetrazole (PTZ)-induced seizures. We aimed to show the involvement of these two systems in the anticonvulsant effects of dantrolene against PTZ-induced seizures. Methods The male albino Swiss strain of mice (N = 56) randomly allocated to the seven separate groups and treated with dantrolene (40 mg/kg), dantrolene (40 mg/kg) + L-arginine (100 mg/kg, a NO donor), dantrolene (40 mg/kg) + N-Nitroarginine methyl ester (L-NAME) (100 mg/kg, a NO synthase inhibitor), dantrolene (40 mg/kg) + NMDA (50 mg/kg), dantrolene (40 mg/kg) + MK801 (1 mg/kg, a selective NMDA antagonist), Diazepam (5 mg/kg, the positive control) and saline (the negative control). Seizures were induced by intraperitonial injection of PTZ (90 mg/kg). The onsets of clonic and tonic-clonic seizures, as well as the death of animals, were recorded. Results Dantrolene significantly increased the onset of clonic, tonic-clonic seizures and death of animals challenged with PTZ. The onset of tonic-clonic seizure in animals treated with dantrolene alone and dantrolene + L-NAME was higher than the control group. In contrast, the onset of tonic-clonic seizure in the animals treated with dantrolene + L-arginine was significantly lower than the dantrolene-treated group. The onset of clonic and tonic-clonic seizures in animals treated with dantrolene + MK801 were significantly higher than the control and dantrolene + NMDA groups. Conclusion Dantrolene protected animals against PTZ-induced seizures and mortality. The inhibition of NO synthase and NMDA receptors may contribute to the dantrolene anticonvulsant effects on the PTZ-induced seizure.

Nitric oxide and cGMP do not affect fluid flux in isolated rat lungs

1996 ◽  
Vol 80 (1) ◽  
pp. 69-76 ◽  
Author(s):  
M. R. Eichinger ◽  
B. R. Walker
Keyword(s):  
Nitric Oxide ◽  
Whole Blood ◽  
Second Messengers ◽  
Venous Pressure ◽  
Weight Ratio ◽  
Control Group ◽  
Sprague Dawley ◽  
Fluid Flux ◽  
No Donor ◽  
Isolated Rat

We sought to examine the influence of nitric oxide (NO) and the second messengers guanosine 3′,5′-cyclic monophosphate (cGMP) and intracellular Ca2+ on fluid flux in lungs isolated from male Sprague-Dawley rats and perfused with saline (containing 4% albumin) or with whole blood. Lungs were allowed to equilibrate for a period of 30 min without treatment (control group) or with one of the following agents: the exogenous NO donor spermine NONOate, the nitric oxide synthase inhibitor N omega-nitro-L-arginine (L-NNA), 8-BrcGMP, the Ca2- ionophore ionomycin, or the endothelial injurious agent protamine. After equilibration, perfusate reservoir height was increased to five incremental settings to increase pulmonary venous pressure and enhance fluid flux. Perfusate reservoir weight was monitored continuously as an index of fluid flux. The lung wet-to-dry weight ratio was determined on completion of the experiments. Increasing reservoir height was associated with an increase in pulmonary arterial, pulmonary capillary, and pulmonary venous pressures and an increase in fluid flux. However, treatment with exogenous NO or inhibition of endogenous NO was without effect on fluid flux in saline lungs at two different flow rates or in whole blood-perfused lungs. Similarly, treatment with cGMP and ionomycin did not alter fluid flux. Protamine pretreatment resulted in a significant increase in fluid flux at the highest reservoir setting, although exogenous NO and L-NNA pretreatments were without further effect on the protamine-treated lungs. Thus a role for NO and the second messengers cGMP and Ca2+ in modulating fluid flux could not be demonstrated in the isolated rat lung.

Effect of nitric oxide on spinal evoked potentials and survival rate in rats with decompression sickness

2015 ◽  
Vol 118 (1) ◽  
pp. 20-28
Author(s):  
T. Randsoe ◽  
C. F. Meehan ◽  
H. Broholm ◽  
O. Hyldegaard
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Survival Rate ◽  
Evoked Potentials ◽  
Decompression Sickness ◽  
Bubble Formation ◽  
Control Group ◽  
Protective Effects ◽  
No Donor ◽  
Long Acting

Nitric oxide (NO) releasing agents have, in experimental settings, been shown to decrease intravascular nitrogen bubble formation and to increase the survival rate during decompression sickness (DCS) from diving. The effect has been ascribed to a possible removal of preexisting micronuclei or an increased nitrogen washout on decompression through augmented blood flow rate. The present experiments were conducted to investigate whether a short- or long-acting NO donor [glycerol trinitrate (GTN) or isosorbide-5-mononitrate (ISMN), respectively] would offer the same protection against spinal cord DCS evaluated by means of spinal evoked potentials (SEPs). Anesthetized rats were decompressed from a 1-h hyperbaric air dive at 506.6 kPa (40 m of seawater) for 3 min and 17 s, and spinal cord conduction was studied by measurements of SEPs. Histological samples of the spinal cord were analyzed for lesions of DCS. In total, 58 rats were divided into 6 different treatment groups. The first three received either saline ( group 1), 300 mg/kg iv ISMN ( group 2), or 10 mg/kg ip GTN ( group 3) before compression. The last three received either 300 mg/kg iv ISMN ( group 4), 1 mg/kg iv GTN ( group 5), or 75 μg/kg iv GTN ( group 6) during the dive, before decompression. In all groups, decompression caused considerable intravascular bubble formation. The ISMN groups showed no difference compared with the control group, whereas the GTN groups showed a tendency toward faster SEP disappearance and shorter survival times. In conclusion, neither a short- nor long-acting NO donor had any protective effect against fatal DCS by intravenous bubble formation. This effect is most likely due to a fast ascent rate overriding the protective effects of NO, rather than the total inert tissue gas load.

scholarly journals Cardiac Inotropic Effect of Long-Term Administration of Oral Thymoquinone

2019 ◽  
Vol 2019 ◽  
pp. 1-6
Author(s):  
Lubna Ibrahim Al Asoom ◽  
Mohammad Taha Al-Hariri
Keyword(s):  
Relaxation Time ◽  
Cardiac Hypertrophy ◽  
Flow Rate ◽  
Nigella Sativa ◽  
Control Group ◽  
Peak Tension ◽  
Time To Peak ◽  
Term Administration ◽  
Myocardial Flow

Back Ground. Long-term administration of Nigella sativa showed cardiac hypertrophic and positive inotropic effects. Thymoquinone (TQ) is an active ingredient in Nigella sativa. Therefore, we aimed to test the cardiac effects of long-term TQ administration. Materials and Methods. Twenty adult Wistar rats weighing (150-250 g) were divided into two groups: control and TQ. A TQ-olive oil solution was administered orally to the TQ group (dose 10 mg/kg) for two months. An equivalent volume of olive oil was given to the control group. Langendorff isolated hearts were studied. Peak tension, time to peak tension, half relaxation time, and myocardial flow rate were determined. Heart and left ventricle weights and ratios were recorded. Results. The TQ group exhibited significantly higher peak tension than the control group. There were no significant differences between the two groups in time to peak tension, half relaxation time, and myocardial flow rate. Likewise, there were no signs of cardiac hypertrophy. Conclusions. Long-term administration of oral TQ induced a positive inotropic effect in the form of an increase in peak tension. TQ administration did not result in cardiac hypertrophy or an increased cardiac metabolic demand at the studied dose. TQ may be a promising inotropic agent.

Effect of nitric oxide synthase inhibitors on ovum transport and oviductal smooth muscle activity in the rat oviduct

Reproduction ◽  
2000 ◽  
pp. 111-117 ◽  
Author(s):  
S Perez Martinez ◽  
M Viggiano ◽  
AM Franchi ◽  
MB Herrero ◽  
ME Ortiz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Fold Increase ◽  
Control Group ◽  
Pregnant Rats ◽  
No Donor ◽  
Nos Inhibitors ◽  
Ovum Transport ◽  
Egg Transport ◽  
Oxide Synthase

The effect of the inhibition of nitric oxide synthase (NOS) on ovum transport and oviductal motility in rats was investigated. Three different NOS inhibitors were injected into the ovarian bursa at oestrus or day 3 of pregnancy. Oviducts and uteri were flushed 24 h later and the presence of ova was recorded. In oestrous and pregnant rats, treatment resulted in accelerated egg transport, as shown by a decrease in the number of ova present in the oviducts. In cyclic rats, intrabursal injection of 1 mg kg-1 of either N-monomethyl-L-arginine (L-NMMA) or N omega nitro-L-arginine methyl ester (L-NAME) elicited a 30% reduction in the number of ova present in the oviducts, whereas in pregnant animals, the same dose of L-NMMA produced a reduction of 40%. Simultaneous administration of the NO donor spermine NONOate (5 mg kg-1) completely reversed the effect of L-NMMA. Tubal motility was assessed by microsphere displacement analysis within the oviduct. Surrogate ova were transferred to the oviductal lumen at oestrus and 24 h later the effect of intraoviductal injection of 1 microgram L-NMMA or vehicle was assessed. The microspheres in the isthmus showed an oscillating motion, and periods in which movement was not detectable. However, L-NMMA treatment produced a 3.6-fold increase in the maximum instant velocities and a significant reduction in the resting periods of the microspheres compared with the control group (P < 0.001). These results provide evidence that NO inhibition increases tubal motility that results in accelerated ovum transport, and indicate that NO could act as a paracrine signal between different layers of the oviductal wall, providing a role for endogenous NO in regulation of tubal function.

scholarly journals P1052ASUPPRESSION OF BLOOD COAGULATION ON THE SURFACE OF A DIALYSIS MEMBRANE USING A DIALYSATE CONTAINING 800 PPM OF NITRIC OXIDE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Kozue Kobayashi ◽  
Maho Sato ◽  
Yuhei Yoshida ◽  
Kokubo Kenichi ◽  
Hirosuke Kobayashi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Adverse Effects ◽  
Blood Coagulation ◽  
Flow Rate ◽  
Blood Clotting ◽  
Control Group ◽  
Dialysis Membrane ◽  
Hemodialysis Session ◽  
Ldh Activity ◽  
Dialysate Flow Rate

Abstract Background and Aims Activation of platelets and leukocytes when blood comes in contact with a dialysis membrane surface leads to increased oxidative stress and release of proinflammatory cytokines, which may result in complications in dialysis patients. Within the blood vessels, nitric oxide (NO) generated by nitric oxide synthase on the endothelial cells suppresses both aggregation/activation of platelets and migration/adhesion of leukocytes. We previously showed in a rat hemodialysis model that NO (800 ppm) gas added to the dialysate can suppress blood coagulation on the surface of a dialysis membrane. The aim of the present study was to determine, using a rat hemodialysis model, the appropriate concentration of NO that would most effectively prevent blood coagulation without causing any adverse effects. Method Male Sprague Dawley rats weighing 300 to 400 g were used for the experiments. After the rats were anesthetized (isoflurane, 1.5%-3.0%), extracorporeal circulation was established by removal of blood from the carotid artery and returning it to the tail vein. During the experiment, the blood flow rate was kept at 1.0 mL/min, and the dialysate flow rate at 3 mL/min. Heparin was administered by bolus injection (0.7 unit/g-mouse) at the start of the hemodialysis, and no further heparin was added during the 4-hour hemodialysis session. A cellulose triacetate membrane and polymethylpentene membrane were used for making the small dialyzer and gas exchanger, respectively (the prototype module was manufactured by NIPRO, Co., Japan). NO (200 ppm, 400 ppm, or 800 ppm) was added to the dialysate via the gas exchanger in the NO groups, and N2 gas was added to the dialysate in the control group. During the experiment, the arterial pressure, dialyzer inlet pressure, venous pressure, activated whole blood clotting time (ACT) and methemoglobin (met-Hb) concentration were measured. After circulation, the amount of coagulated blood was measured by the hemoglobin (Hb) content and lactate dehydrogenase (LDH) activity in the eluate from the residual blood clotting in the dialyzer. Results The 4-hour hemodialysis session achievement rate was highest in the NO-800 ppm group (control, 54%; NO-200 ppm, 66%; NO-400 ppm, 77%; NO-800 ppm, 85%). The blood met-Hb content was below 10% in all the NO groups. The Hb content and LDH activity in the eluate were significantly lower in the NO groups than in the control group. These results indicate that addition of higher concentrations of NO was associated with a lower likelihood of coagulation on the dialyzer and in the dialysis circuit and a higher likelihood of smooth and successful 4-hour dialysis sessions. Addition of NO was associated with little risk of adverse effects such as met-Hb accumulation and reduction of blood pressure. Therefore, 800 ppm is considered as the most appropriate concentration of NO to be added to the dialysate for effectively inhibiting blood coagulation without causing any adverse effects. Conclusion Our experiment in a rat hemodialysis model showed that 800 ppm was the most appropriate concentration of NO to be added to the dialysate to suppress blood coagulation on the surface of the dialysis membrane without causing any adverse effects.

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