In vivo visualization of nitric oxide and interactions among platelets, leukocytes, and endothelium following hemorrhagic shock and reperfusion

Hiratsuka, Mie; Katayama, Tohru; Uematsu, Kazuhiko; Kiyomura, Masaki; M, Ito

doi:10.1007/s00011-009-0011-0

Cited by 20 publications

(14 citation statements)

References 32 publications

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“…A DAF study of hemorrhagic shock (blood pressure reduced to 40 mm Hg for 20 min) in rat mesentery reports that venular endothelial NO production is reduced significantly within 30 min after restoring blood volume, with no difference from controls after 24 hr of recovery. 120 An increase in NO production in mast cells was observed after 24 hr, which could be attributed to NO production from iNOS. However, it is not possible to determine absolute NO levels in the microcirculation from any of these in vivo DAF studies.…”

Section: Soluble Guanylate Cyclase As Primary Target Of Nitric Omentioning

confidence: 94%

Nitric Oxide Signaling in the Microcirculation

Buerk

Barbee

Jaron

2011

Crit Rev Biomed Eng

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Several apparent paradoxes are evident when one compares mathematical predictions from models of nitric oxide (NO) diffusion and convection in vasculature structures with experimental measurements of NO (or related metabolites) in animal and human studies. Values for NO predicted from mathematical models are generally much lower than in vivo NO values reported in the literature for experiments, specifically with NO microelectrodes positioned at perivascular locations next to different sizes of blood vessels in the microcirculation and NO electrodes inserted into a wide range of tissues supplied by the microcirculation of each specific organ system under investigation. There continues to be uncertainty about the roles of NO scavenging by hemoglobin versus a storage function that may conserve NO, and other signaling targets for NO need to be considered. This review describes model predictions and relevant experimental data with respect to several signaling pathways in the microcirculation that involve NO.

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Section: Soluble Guanylate Cyclase As Primary Target Of Nitric Omentioning

confidence: 94%

Nitric Oxide Signaling in the Microcirculation

Buerk

Barbee

Jaron

2011

Crit Rev Biomed Eng

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“…It has been shown that low NO bioavailability or NO inhibition can induce the expression of eCAMs [19-21], platelet activation and adhesion to endothelial cells [22,23] and increase baseline leukocyte rolling and adherence [24,25], and administration of NO donors inhibits endothelial activation [26]. Low NO bioavailability is a major player in vascular inflammation commonly observed in hemolytic syndromes such as sickle cell crisis, in which acellular hemoglobin acts as a strong NO scavenger [27].…”

Section: Introductionmentioning

confidence: 99%

Exogenous nitric oxide decreases brain vascular inflammation, leakage and venular resistance during Plasmodium berghei ANKA infection in mice

Zaniní

Cabrales

Barkho

et al. 2011

J Neuroinflammation

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BackgroundCerebral malaria (CM) is a lethal complication of Plasmodium falciparum infections. In the Plasmodium berghei ANKA (PbA) murine model, CM is associated with marked brain inflammation, increased expression of endothelial cell adhesion molecules and leukocyte and platelet accumulation in brain vessels, causing vascular occlusion and decreased blood flow, damaging the endothelium and leading to blood-brain barrier breakdown, leakage and hemorrhages. Exogenous nitric oxide (NO) administration largely prevents the syndrome. Here we evaluated whether the mechanism of action of NO in preventing murine CM is related to its anti-inflammatory properties and to protection of the endothelium.MethodsC57Bl/6 mice infected with PbA were treated twice a day with saline or dipropylenetriamineNONOate (DPTA-NO). Endothelial cell adhesion molecule (ICAM-1, VCAM, E- and P-selectin) expression in brain tissue on day 6 of infection was assessed in both groups by western blot. For intravital microscopy studies, DPTA-NO-treated and saline-treated mice with a previously implanted closed cranial window were injected with albumin-FITC, anti-CD45-TxR and anti-CD41-FITC antibodies on day 6 of infection for quantification of albumin leakage, leukocyte and platelet adherence in pial vessels.ResultsPbA-infected mice treated with the NO-donor DPTA-NO showed decreased expression of ICAM-1 and P-selectin, but not VCAM-1, in the brain, compared to saline-treated mice. DPTA-NO treatment also decreased the number of adherent leukocytes and platelets in pial vessels, particularly in venules 30-50 μm in diameter, decreased inflammatory vascular resistance and prevented the occurrence of arteriolar and venular albumin leakage observed in saline-treated PbA-infected mice, as assessed by intravital microscopy.ConclusionsThese results indicate that the protective effect of exogenous NO on murine CM is associated with decreased brain vascular expression of inflammatory markers resulting in attenuated endothelial junction damage and facilitating blood flow.

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“…[3] Certain studies have provided evidence that cell barrier dysfunction and vascular hyperpermeability can be caused by an I/R injury via a local inflammatory response, resulting in vascular protein leakage. Glomerular barrier dysfunction and proteinuria have also been observed in the kidneys of patients with systemic I/R injuries [13]–[18], [23]. Hiratsuka et al reported that these responses could be observed via microscopy within 30 min of an I/R injury in rats.…”

Section: Discussionmentioning

confidence: 99%

“…Hiratsuka et al reported that these responses could be observed via microscopy within 30 min of an I/R injury in rats. [18] We therefore suspected that proteinuria may be the initial clinical presentation of a post-resuscitative I/R injury. Proteinuria would present much earlier than myocardial dysfunction, which has been reported to occur at a median time of 6.8 h following OHCA.…”

Section: Discussionmentioning

confidence: 99%

“…[10] In addition, serum bicarbonate and pH levels may be influenced by various conditions (i.e., apnea-related CO 2 retention, chronic lung diseases, and metabolic diseases). Previous studies have demonstrated that vascular protein leakage due to cell barrier dysfunction presents as soon as 30 min following shock and an I/R injury, [13]–[18] which is much earlier than myocardial dysfunction, which has been reported to occur at a median time of 6.8 h after OHCA. [6] Most importantly, in the kidney, glomerular barrier dysfunction and proteinuria were also demonstrated in patients with systemic I/R injuries.…”

Section: Introductionmentioning

confidence: 99%

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The Post-Resuscitative Urinalysis Associate the Survival of Patients with Non-Traumatic Out-of-Hospital Cardiac Arrest

Chang

et al. 2013

PLoS ONE

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ObjectiveTo analyze whether urine output and urinalysis results are predictive of survival and neurologic outcomes in patients with non-traumatic out-of-hospital cardiac arrest (OHCA).MethodsInformation was obtained from 1,340 patients with non-traumatic OHCA who had achieved a sustained return of spontaneous circulation (ROSC). Factors that were associated with survival in the post-resuscitative period were evaluated. The association between urine output and fluid challenge in the early resuscitative period was analyzed and compared between the survivors and the non-survivors. The results of the initial urinalysis, including the presence of proteinuria and other findings, were used to evaluate the severity of vascular protein leakage and survival. The association between proteinuria and the neurologic outcomes of the survivors was also analyzed. The clinical features of capillary leakage were examined during the post-resuscitative period.ResultsOf the 1,340 patients, 312 survived. A greater urine output was associated with a higher chance of survival. The initial urine output increased in proportion to the amount of fluid that was administered during early resuscitation in the emergency department for the survivors but not for the non-survivors (p<0.05). In the initial urinalysis, proteinuria was strongly associated with survival, and severe proteinuria indicated significantly poorer neurologic outcomes (p<0.05 for both comparisons). Proteinuria was associated with a risk of developing signs of capillary leakage, including body mass index gain and pitting edema (both p<0.001).ConclusionThe severity of proteinuria during the early post-resuscitative period was predictive of survival.

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In vivo visualization of nitric oxide and interactions among platelets, leukocytes, and endothelium following hemorrhagic shock and reperfusion

Abstract: Mesenteric endothelial cell dysfunction after H/R 0.5 h is associated with reduced NO, whereas after H/R 24 h is related to increase NO in mast cells.

Cited by 20 publications

References 32 publications

Nitric Oxide Signaling in the Microcirculation

Nitric Oxide Signaling in the Microcirculation

Exogenous nitric oxide decreases brain vascular inflammation, leakage and venular resistance during Plasmodium berghei ANKA infection in mice

The Post-Resuscitative Urinalysis Associate the Survival of Patients with Non-Traumatic Out-of-Hospital Cardiac Arrest

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