scholarly journals Beneficial effects of inhaled nitric oxide with intravenous steroid in an ischemia–reperfusion model involving aortic clamping

2018 ◽  
Vol 31 ◽  
pp. 039463201775148 ◽  
Author(s):  
Waldemar Gozdzik ◽  
Stanisław Zielinski ◽  
Marzena Zielinska ◽  
Kornel Ratajczak ◽  
Piotr Skrzypczak ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Response ◽  
Mrna Expression ◽  
Oxygen Delivery ◽  
Ischemia Reperfusion ◽  
Systemic Inflammatory Response ◽  
Inhaled Nitric Oxide ◽  
Tlr4 Expression ◽  
Sham Surgery ◽  
Tlr4 Mrna

This study evaluated the effects of inhaled nitric oxide (iNO) therapy combined with intravenous (IV) corticosteroids on hemodynamics, selected cytokines, and kidney messenger RNA toll-like receptor 4 (mRNA TLR4) expression in ischemia–reperfusion injury animal model. The primary endpoint was the evaluation of circulatory, respiratory, and renal function over time. We also investigated the profile of selected cytokines and high-mobility group box 1 (HMGB1) protein, as well as renal mRNA TLR4 activation determined by quantitative real-time polymerase chain reaction analysis. Pigs (n = 19) under sevoflurane AnaConDa anesthesia/sedation were randomized and subjected to abdominal laparotomy and alternatively suprarenal aortic cross-clamping (SRACC) for 90 min or sham surgery: Group 1 (n = 8) iNO (80 ppm) + IV corticosteroids (25 mg ×3) started 30 min before SRACC and continued 2 h after SRACC release, followed with decreased iNO (30 ppm) until the end of observation, Group 2 (n = 8) 90 min SRACC, Group 3 (n = 3)—sham surgery. Renal biopsies were sampled 1 hr before SRACC and at 3 and 20 h after SRACC release. Aortic clamping increased TLR4 mRNA expression in ischemic kidneys, but significant changes were recorded only in the control group ( P = 0.016). Treatment with iNO and hydrocortisone reduced TLR4 mRNA expression to pre-ischemic conditions, and the difference observed in mRNA expression was significant between control and treatment group after 3 h ( P = 0.042). Moreover, animals subjected to treatment with iNO and hydrocortisone displayed an attenuated systemic inflammatory response and lowered pulmonary vascular resistance plus increased oxygen delivery. The results indicated that iNO therapy combined with IV corticosteroids improved central and systemic hemodynamics, oxygen delivery, and diminished the systemic inflammatory response and renal mRNA TLR4 expression.

scholarly journals No Signs of Inflammation during Knee Surgery with Ischemia: A Study Involving Inhaled Nitric Oxide

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Lars Hållström ◽  
Claes Frostell ◽  
Anders Herrlin ◽  
Eva Lindroos ◽  
Ingrid Lundberg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Response ◽  
Reperfusion Injury ◽  
Cell Activation ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide ◽  
Endothelial Cell Activation ◽  
Soluble Adhesion Molecules ◽  
Group 2

Nitric oxide donors and inhaled nitric oxide (iNO) may decrease ischemia/reperfusion injury as reported in animal and human models. We investigated whether the attenuation of reperfusion injury, seen by others, in patients undergoing knee arthroplasty could be reproduced when patients had spinal anesthesia. 45 consecutive patients were randomized into three groups (n=15). Groups 1 and 3 were receiving iNO 80 ppm or placebo (nitrogen, N2) throughout the entire operation, and group 2 only received iNO in the beginning and at the end of the operation. Blood samples were collected before surgery, at the end of the surgery, and 2 hours postoperatively. Muscle biopsies were taken from quadriceps femoris muscle before and after ischemia. There were no increases in plasma levels of soluble adhesion molecules: ICAM, VCAM, P-selectin, E-selectin, or of HMGB1, in any of the groups. There were low numbers of CD68+ macrophages and of endothelial cells expression of ICAM, VCAM, and P-selectin in the muscle analyzed by immunohistochemistry, prior to and after ischemia. No signs of endothelial cell activation or inflammatory response neither systemically nor locally could be detected. The absence of inflammatory response questions this model of ischemia/reperfusion, but may also be related to the choice of anesthetic method EudraCTnr.

Inhaled Nitric Oxide Attenuates Reperfusion Inflammatory Responses in Humans

2007 ◽  
Vol 106 (2) ◽  
pp. 275-282 ◽  
Author(s):  
Mali Mathru ◽  
Ruksana Huda ◽  
Daneshvari R. Solanki ◽  
Stephen Hays ◽  
John D. Lang
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Response ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide ◽  
Human Model ◽  
Pulmonary Vasculature ◽  
Nuclear Factor Kappab ◽  
Control Group ◽  
Nuclear Factor ◽  
Nitrate And Nitrite

Background Reduced bioavailability of endothelium-derived nitric oxide associated with reperfusion could potentially exacerbate the inflammatory response during reperfusion. Evidence suggests the pharmacologic effects of inhaled nitric oxide may extend beyond the pulmonary vasculature, and this is attributed to nitric oxide-derived complexes in blood that ultimately orchestrate antiinflammatory effects. In this study, the authors evaluated the potential for inhaled nitric oxide (80 ppm) to attenuate inflammation instigated by ischemia-reperfusion in a human model using patients undergoing knee surgery where a tourniquet was used to produce a bloodless surgical field. Methods Inhaled nitric oxide (80 ppm) was administered before tourniquet application and continued throughout reperfusion until the completion of surgery. Venous blood samples were collected before and after reperfusion, for the measurements of nitrate and nitrite, CD11b/CD18, soluble P-selectin, and lipid hydroperoxide. Muscle biopsies were obtained from the quadriceps muscle before skin closure and analyzed for myeloperoxide, conjugated dienes, and nuclear factor-kappaB translocation. Results Administration of inhaled nitric oxide (80 ppm) significantly attenuated the inflammatory response characterized by reduced expression of CD11b/CD18, P-selectin, and nuclear factor kappaB compared with the control group. This was accompanied by increased plasma levels of nitrate and nitrite and reduced oxidative stress. Conclusions Administration of inhaled nitric oxide at 80 ppm significantly reduces inflammation in lower extremity ischemia-reperfusion in humans. This observation supports the concept that during diseases characterized by dysfunction in nitric oxide metabolism, inhaled nitric oxide may be an effective therapy to replenish systemic nitric oxide, thus retarding inflammatory-mediated injury.

Abstract 11053: The Association Between the Systemic Immune-Inflammation Index with the Duration of Cardiopulmonary Bypass in Cardiac Surgery: A Retrospective, Single-Center Study

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Yanan Hu ◽  
Yi Liu ◽  
Yongzhe Liu ◽  
Hui Chen ◽  
Wei Jiang ◽  
...  
Keyword(s):  
Cardiac Surgery ◽  
Inflammatory Response ◽  
Hospital Stay ◽  
Time Course ◽  
Ischemia Reperfusion ◽  
Systemic Inflammatory Response ◽  
Surgical Trauma ◽  
Neutrophil Lymphocyte Ratio ◽  
Lymphocyte Ratio ◽  
Immune Inflammation

Introduction: Systemic inflammatory response evoked by cardiac surgery involving a cardio-pulmonary bypass (CPB) in combination of surgical trauma, ischemia/reperfusion injury, hypothermia, and endotoxin release contributed to the postoperative morbidity and mortality. This study aimed to explore the potential of neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII) as novel markers to evaluate and predict the adverse clinical outcomes after longer CPB time in cardiac surgery. Methods: Patients who underwent cardiac surgery with or without CPB were allocated into two groups, CPB group (n=11) and N-CPB group (n=21). The time course of NLR, PLR, SII, and C-reactive protein (CPR) were analyzed at preoperative day 1 and postoperative day 1, 3, and 7. The baseline and postoperative parameters, the ICU and hospital stay were recorded. Results: There were no differences of baseline parameters between groups. The level of NLR, PLR, SII, and CPR at postoperative day 1 was higher than that in the preoperative day 1 in both groups (p < 0.01). The level of NLR, SII and CPR at postoperative day 3 was higher than that in the preoperative day 1 in both groups (p < 0.05). The NLR and SII at postoperative day 3 were higher in CPB group than that in N-CPB group (p < 0.05). The ICU and hospital stay was longer in CPB group than N-CPB group (p < 0.05). Conclusions: The longer duration of CPB time induced higher systemic inflammatory response characterized by higher level of NLR, PLR and SII. The SII predicted the poor outcome after longer CPB. The peak of systemic inflammatory response occurred on the third day after cardiac surgery.

Preventive influence of inhaled nitric oxide on lung ischemia-reperfusion injury

Surgery Today ◽  
1999 ◽  
Vol 29 (9) ◽  
pp. 897-901 ◽  
Author(s):  
Hiroyuki Yamagishi ◽  
Chojiro Yamashita ◽  
Masayoshi Okada
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Inhaled Nitric Oxide

Microcirculatory perfusion deficits are not essential for remote parenchymal injury within the liver

1999 ◽  
Vol 277 (1) ◽  
pp. G55-G60 ◽  
Author(s):  
Robert W. Brock ◽  
Michael W. Carson ◽  
Kenneth A. Harris ◽  
Richard F. Potter
Keyword(s):  
Inflammatory Response ◽  
Ischemia Reperfusion ◽  
Systemic Inflammatory Response ◽  
Microvascular Perfusion ◽  
Hepatocellular Injury ◽  
Indirect Measures ◽  
In Vivo Labeling ◽  
Parenchymal Injury ◽  
Perfusion Deficits

A normotensive model of hindlimb ischemia-reperfusion in Wistar rats was used to test the hypothesis that microvascular perfusion deficits contribute to the initiation of remote hepatic injury during a systemic inflammatory response. Animals were randomly assigned to one of three groups: 4 h of ischemia with 6 h of reperfusion (I/R-6; n = 4), 4 h of ischemia with 3 h of reperfusion (I/R-3; n = 5), or no ischemia (naive; n = 5). With intravital fluorescence microscopy, propidium iodide (PI; 0.05 mg/100 g body wt) was injected for the in vivo labeling of lethally injured hepatocytes (number/10−1mm3). PI-positive hepatocytes increased progressively over the 6-h period (naive 32.9 ± 7.8 vs. I/R-3 92.8 ± 11.5 vs. I/R-6 232 ± 39.2), with no difference between periportal and pericentral regions of the lobule. Additionally, a significant decrease in continuously perfused sinusoids (naive 70.0 ± 1.5 vs. I/R-3 65.0 ± 1.0 vs. I/R-6 48.8 ± 0.9%) was measured. Regional sinusoidal perfusion differences were only observed after 3 h of limb reperfusion. Indirect measures of hepatocellular injury using alanine transaminase levels support the progressive nature of hepatic parenchymal injury (0 h 57.8 ± 6.5 vs. 3 h 115.3 ± 20.7 vs. 6 h 125.6 ± 19.5 U/l). Evidence from this study suggests that remote hepatic parenchymal injury occurs early and progresses after the induction of a systemic inflammatory response and that microvascular perfusion deficits are not essential for the initiation of such injury.

Sign in / Sign up

Export Citation Format

Share Document