Clinical observation of ulinastatin combined with CRRT in the treatment of early cardiopulmonary resuscitation

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Abstract

The clinical efficacy of ulinastatin (UTI) combined with continuous renal replacement therapy (CRRT) in the treatment after early cardiopulmonary resuscitation (CPR) was evaluated. A total of 70 patients who were successfully treated with CPR in Ganzhou People's Hospital from October 2016 to March 2017 were selected as the subjects. The patients were randomly divided into control group (35 cases, conventional treatment) and UTI combined with CRRT group (35 cases, UTI + CRRT). The whole blood of patients was collected at 0, 3, 6 and 12 h after CPR. Reverse transcription-polymerase chain reaction assay was used to detect the changes of toll-like receptor 4 (TLR4) gene in mRNA levels between the two groups, i-STAT system 300 was used to analyze pH level, SO ₂, HCO ₃ ⁻ and lactic acid (LAC) concentration; Abbott AXSYM system was used to detect the expression of cardiac troponin I (cTnI) in serum; the concentration of plasma malondialdehyde (MDA) was examined by a special kit; interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in patients was determined by enzyme-linked immunosorbent assay. The effect of UTI combined with CRRT in the early stage of CPR was analyzed. The levels of TLR4, cTnI, TNF-α, IL-6 and MDA in the plasma of patients in both groups were significantly increased (P<0.05), but the expression level in UTI + CRRT group was lower than that in control group (P<0.05). Compared with the control group, the HCO ₃ ⁻ decreased significantly (P<0.05) in the UTI + CRRT group at 3 h, while the pH and SO ₂ did not change significantly. UTI + CRRT could significantly shorten the average recovery time of consciousness and the average recovery time of consciousness and spontaneous respiration in patients treated with CPR (P<0.05). Moreover, the score of APACHE II was significantly lower than that of control group (P<0.05). UTI combined with CRRT treatment can significantly improve the patient's condition after early CPR.

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Pathophysiology of ischaemia-reperfusion injury.

Donna Carden, D. Granger (2000)

Reperfusion of ischaemic tissues is often associated with microvascular dysfunction that is manifested as impaired endothelium-dependent dilation in arterioles, enhanced fluid filtration and leukocyte plugging in capillaries, and the trafficking of leukocytes and plasma protein extravasation in postcapillary venules. Activated endothelial cells in all segments of the microcirculation produce more oxygen radicals, but less nitric oxide, in the initial period following reperfusion. The resulting imbalance between superoxide and nitric oxide in endothelial cells leads to the production and release of inflammatory mediators (e.g. platelet-activating factor, tumour necrosis factor) and enhances the biosynthesis of adhesion molecules that mediate leukocyte-endothelial cell adhesion. Some of the known risk factors for cardiovascular disease (hypercholesterolaemia, hypertension, and diabetes) appear to exaggerate many of the microvascular alterations elicited by ischaemia and reperfusion (I/R). The inflammatory mediators released as a consequence of reperfusion also appear to activate endothelial cells in remote organs that are not exposed to the initial ischaemic insult. This distant response to I/R can result in leukocyte-dependent microvascular injury that is characteristic of the multiple organ dysfunction syndrome. Adaptational responses to I/R injury have been demonstrated that allow for protection of briefly ischaemic tissues against the harmful effects of subsequent, prolonged ischaemia, a phenomenon called ischaemic preconditioning. There are two temporally and mechanistically distinct types of protection afforded by this adaptational response, i.e. acute and delayed preconditioning. The factors (e.g. protein kinase C activation) that initiate the acute and delayed preconditioning responses appear to be similar; however the protective effects of acute preconditioning are protein synthesis-independent, while the effects of delayed preconditioning require protein synthesis. The published literature in this field of investigation suggests that there are several potential targets for therapeutic intervention against I/R-induced microvascular injury. Copyright 2000 John Wiley & Sons, Ltd.

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Out-of-hospital cardiac arrest in the 1990's: a population-based study in the Maastricht area on incidence, characteristics and survival.

Jacqueline J.M. de Vreede-Swagemakers, Anton Gorgels, Willy Dubois-Arbouw … (1997)

We sought to describe the incidence, characteristics and survival of out-of-hospital sudden cardiac arrest (SCA) in the Maastricht area of The Netherlands. Incidence and survival rates of out-of-hospital SCA in different communities are often based on the number of victims resuscitated by the emergency medical services. Our population-based study in the Maastricht area allows information on all victims of witnessed and unwitnessed SCA occurring outside the hospital. Incidence, patient characteristics and survival rates were determined by prospectively collecting information on all cases of SCA occurring in the age group 20 to 75 years between January 1, 1991 and December 31, 1994. Survival rates were related to the site of the event (at home vs. outside the home) and the presence or absence of a witness and rhythm at the time of the resuscitation attempt in out-of-hospital SCA. Five hundred fifteen patients were included (72% men, 28% women). In 44% of men and 53% of women, SCA was most likely the first manifestation of heart disease. In patients known to have had a previous myocardial infarction (MI), the mean interval between the MI and SCA was 6.5 years, with >50% having a left ventricular ejection fraction >30%. The mean yearly incidence of SCA was 1 in 1,000 inhabitants. Of all deaths in the age groups studied, 18.5% were sudden. Nearly 80% of SCAs occurred at home. In 60% of all cases of SCA a witness was present. Cardiac resuscitation, which was attempted in 51% of all subjects, resulted overall in 32 (6%) of 515 patients being discharged alive from the hospital. Survival rates for witnessed SCA were 8% (16 of 208 subjects) at home and 18% (15 of 85 subjects) outside the home (95% confidence interval 1% to 18.8%). The majority of victims of SCA cannot be identified before the event. Sudden cardiac arrest usually occurs at home, and the survival of those with a witnessed SCA at home was low compared with that outside the home, indicating the necessity of optimizing out-of-hospital resuscitation, especially in the at-home situation.

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Involvement of TLR4/type I IL-1 receptor signaling in the induction of inflammatory mediators and cell death induced by ethanol in cultured astrocytes.

Maria Pascual-Lucas, C Guerri, Ana Martinez … (2005)

Activated astroglial cells are implicated in neuropathogenesis of many infectious and inflammatory diseases of the brain. A number of inflammatory mediators and cytokines have been proposed to play a key role in glial cell-related brain damage. Cytokine production seems to be initiated by signaling through TLR4/type I IL-1R (IL-1RI) in response to their ligands, LPS and IL-1beta, playing vital roles in innate host defense against infections, inflammation, injury, and stress. We have shown that glial cells are stimulated by ethanol, up-regulating cytokines and inflammatory mediators associated with TLR4 and IL-1RI signaling pathways in brain, suggesting that ethanol may contribute to brain damage via inflammation. We explore the possibility that ethanol, in the absence of LPS or IL-1beta, triggers signaling pathways and inflammatory mediators through TLR4 and/or IL-1RI activation in astrocytes. We show in this study that ethanol, at physiologically relevant concentrations, is capable of inducing rapid phosphorylation within 10 min of IL-1R-associated kinase, ERK1/2, stress-activated protein kinase/JNK, and p38 MAPK in astrocytes. Then an activation of NF-kappaB and AP-1 occurs after 30 min of ethanol treatment along with an up-regulation of inducible NO synthase and cyclooxygenase-2 expression. Finally, we note an increase in cell death after 3 h of treatment. Furthermore, by using either anti-TLR4- or anti-IL-1RI-neutralizing Abs, before and during ethanol treatment, we inhibit ethanol-induced signaling events, including NF-kappaB and AP-1 activation, inducible NO synthase, and cyclooxygenase-2 up-regulation and astrocyte death. In summary, these findings indicate that both TLR4 and IL-1RI activation occur upon ethanol treatment, and suggest that signaling through these receptors mediates ethanol-induced inflammatory events in astrocytes and brain.

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Author and article information

Journal

Journal ID (nlm-ta): Exp Ther Med

Journal ID (iso-abbrev): Exp Ther Med

Journal ID (publisher-id): ETM

Title: Experimental and Therapeutic Medicine

Publisher: D.A. Spandidos

ISSN (Print): 1792-0981

ISSN (Electronic): 1792-1015

Publication date (Print): December 2017

Publication date (Electronic): 17 October 2017

Publication date PMC-release: 17 October 2017

Volume: 14

Issue: 6

Pages: 6064-6068

Affiliations

Department of Emergency, Ganzhou People's Hospital, Ganzhou, Jiangxi 341000, P.R. China

Author notes

Correspondence to: Dr Xianghong Liu, Department of Emergency, Ganzhou People's Hospital, 17 Hongqi Avenue, Ganzhou, Jiangxi 341000, P.R. China, E-mail: liuqinghongdr@ 123456163.com

Article

Publisher ID: ETM-0-0-5325

DOI: 10.3892/etm.2017.5325

PMC ID: 5740734

SO-VID: bb5dc55b-3159-4d76-89a0-7c97745f0f55

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This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

Clinical observation of ulinastatin combined with CRRT in the treatment of early cardiopulmonary resuscitation

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Most cited references 15

Pathophysiology of ischaemia-reperfusion injury.

Out-of-hospital cardiac arrest in the 1990's: a population-based study in the Maastricht area on incidence, characteristics and survival.

Involvement of TLR4/type I IL-1 receptor signaling in the induction of inflammatory mediators and cell death induced by ethanol in cultured astrocytes.

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