Clopidogrel reduces the inflammatory response of lung in a rat model of decompression sickness

Bao, Xiao-Chen; Chen, Hong; Fang, Yiqun; Yuan, Huijun; Peng, You; Ma, Jing; Wang, Fangfang

doi:10.1016/j.resp.2015.02.003

Cited by 12 publications

(9 citation statements)

References 36 publications

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“…Bubbles can cause vasoconstriction, leading to the presence of ischemia, edema, and hemorrhages in target organs such as the lung ( 3 ). Severe pulmonary hemorrhages were present in the rabbits that died from compression–decompression than those that survived decompression after 1 h. Pulmonary hemorrhages have also been described in rats ( 19 , 29 ), rabbits ( 4 ), and stranded cetaceans with pathological signs of DCS ( 7 , 12 ).…”

Section: Discussionmentioning

confidence: 89%

Decompressive Pathology in Cetaceans Based on an Experimental Pathological Model

et al. 2021

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Decompression sickness (DCS) is a widely known clinical syndrome in human medicine, mainly in divers, related to the formation of intravascular and extravascular gas bubbles. Gas embolism and decompression-like sickness have also been described in wild animals, such as cetaceans. It was hypothesized that adaptations to the marine environment protected them from DCS, but in 2003, decompression-like sickness was described for the first time in beaked whales, challenging this dogma. Since then, several episodes of mass strandings of beaked whales coincidental in time and space with naval maneuvers have been recorded and diagnosed with DCS. The diagnosis of human DCS is based on the presence of clinical symptoms and the detection of gas embolism by ultrasound, but in cetaceans, the diagnosis is limited to forensic investigations. For this reason, it is necessary to resort to experimental animal models to support the pathological diagnosis of DCS in cetaceans. The objective of this study is to validate the pathological results of cetaceans through an experimental rabbit model wherein a complete and detailed histopathological analysis was performed. Gross and histopathological results were very similar in the experimental animal model compared to stranded cetaceans with DCS, with the presence of gas embolism systemically distributed as well as emphysema and hemorrhages as primary lesions in different organs. The experimental data reinforces the pathological findings found in cetaceans with DCS as well as the hypothesis that individuality plays an essential role in DCS, as it has previously been proposed in animal models and human diving medicine.

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Section: Discussionmentioning

confidence: 89%

Decompressive Pathology in Cetaceans Based on an Experimental Pathological Model

et al. 2021

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“…Because inflammation has been repeatedly reported after diving, we also assessed whether enalapril treatment could act through its anti-inflammatory action. Previous studies showed that IL-6 is increased with DCS (Ersson et al, 1998 ; Blatteau et al, 2012 ; Bao et al, 2015 ) but not asymptomatic individuals (Chen et al, 2011 ; Blatteau et al, 2012 ). In our study rats treated with enalapril did not have modified levels of this biomarker.…”

Section: Discussionmentioning

confidence: 93%

Angiotensin Converting Enzyme Inhibitor Has a Protective Effect on Decompression Sickness in Rats

et al. 2018

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Introduction: Commercial divers, high altitude pilots, and astronauts are exposed to some inherent risk of decompression sickness (DCS), though the mechanisms that trigger are still unclear. It has been previously showed that diving may induce increased levels of serum angiotensin converting enzyme. The renin angiotensin aldosterone system (RAAS) is one of the most important regulators of blood pressure and fluid volume. The purpose of the present study was to control the influence of angiotensin II on the appearance of DCS.Methods: Sprague Dawley rats have been pre-treated with inhibitor of angiotensin II receptor type 1 (losartan; 10 mg/kg), angiotensin-converting enzyme (ACE) inhibitor (enalapril; 10 mg/kg), and calcium-entry blocker (nifedipine; 20 mg/kg). The experimental groups were treated for 4 weeks before exposure to hyperbaric pressure while controls were not treated. Seventy-five rats were subjected to a simulated dive at 1000 kPa absolute pressure for 45 min before starting decompression. Clinical assessment took place over a period of 60 min after surfacing. Blood samples were collected for measurements of TBARS, interleukin 6 (IL-6), angiotensin II (ANG II) and ACE.Results: The diving protocol induced 60% DCS in non-treated animals. This ratio was significantly decreased after treatment with enalapril, but not other vasoactive drugs. Enalapril did not change ANG II or ACE concentration, while losartant decreased post dive level of ACE but not ANG II. None of the treatment modified the effect of diving on TBARS and IL-6 values.Conclusion: Results suggests that the rennin angiotensin system is involved in a process of triggering DCS but this has to be further investigated. However, a vasorelaxation mediated process, which potentially could increase the load of inert gas during hyperbaric exposure, and antioxidant properties were excluded by our results.

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“…Anti-inflammatory properties of clopidogrel can be an explanation for its protective effect. 19 However, further studies with more patients are needed to prove its efficacy.…”

Section: Discussionmentioning

confidence: 99%

Mortality and morbidity in patients with spontaneous intracerebral hemorrhage: A single-center experience

Faghih-Jouybari

Raof

Abdollahzade

et al. 2021

CJN

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Background: Intracerebral hemorrhage (ICH) is the most common cause of non-ischemic strokes. Considering high mortality and poor functional status following ICH, we investigated factors that can predict short-term outcome and affect recovery of these patients. Methods: In this prospective descriptive study, 100 patients with non-traumatic ICH were included. Clinical and radiographic data were collected and extent of disability was measured by modified Rankin Scale (mRS) at discharge, 1 week, 1 month, and 3 months after discharge. Results: 32 of 100 cases died at hospital and 6 more expired during 3-month follow-up. Risk factors of in-hospital mortality were warfarin use, surgical intervention, and high ICH score. Functional status of patients significantly improved 3 months after discharge. Factors associated with poor recovery were age older than 70, history of coronary artery disease (CAD), low Glasgow Coma Scale (GCS) at admission, elevated mean arterial pressure (MAP), longer hospitalization, and high ICH score. Conclusion: ICH was associated with high rate of mortality (36%). Warfarin use, surgical intervention, and high ICH score were predictive of mortality during hospitalization and 3-month follow-up. Improvement of functional status began after 1 month and significantly improved 3 months after discharge.

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Clopidogrel reduces the inflammatory response of lung in a rat model of decompression sickness

Cited by 12 publications

References 36 publications

Decompressive Pathology in Cetaceans Based on an Experimental Pathological Model

Decompressive Pathology in Cetaceans Based on an Experimental Pathological Model

Angiotensin Converting Enzyme Inhibitor Has a Protective Effect on Decompression Sickness in Rats

Mortality and morbidity in patients with spontaneous intracerebral hemorrhage: A single-center experience

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