Decompressive Pathology in Cetaceans Based on an Experimental Pathological Model

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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Decompression sickness responsive to delayed treatment with hyperbaric oxygen: a case report of two divers

Undersea and Hyperbaric Medicine ◽

10.22462/10.12.2020.3 ◽

2020 ◽

pp. 551-554

Author(s):

Amy L. Inman ◽

◽

Lana P. Sorrell ◽

Anthony T. Lagina ◽

◽

...

Keyword(s):

Hyperbaric Oxygen ◽

Standard Treatment ◽

Clinical Symptoms ◽

Decompression Sickness ◽

Scuba Diving ◽

Gas Embolism ◽

Delayed Treatment ◽

Cardiopulmonary Complications ◽

Recreational Scuba ◽

Hbo2 Therapy

With the increasing popularity of recreational scuba diving, rare complications are becoming more commonly encountered. Although diving is generally safe, novice divers may be unfamiliar with the potential hazards of scuba diving and the resulting sequelae. Dive-related injuries are commonly due to barotrauma or from breathing gas at increased pressures, resulting in decompression illness (DCI), a term that includes both decompression sickness (DCS) and arterial gas embolism (AGE). Symptoms can range from minor aches and pains to neurologic or cardiopulmonary complications resulting in death. Clinical symptoms and diagnosis may initially go unrecognized and can present in a delayed manner, often remote to the diving location. When DCI is suspected standard treatment with hyperbaric oxygen (HBO2) therapy should be considered immediately. Current literature questions the efficacy of delayed HBO2 therapy longer than 24-48 hours after symptom onset. Here we present a case of two divers who simultaneously experienced DCS and were both successfully treated after receiving delayed HBO2 therapy nearly eight days after initiation of symptoms.

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Antidiarrheal activity of methanolic extract of Moringa oleifera lam roots in experimental animal models

International Journal of Pharmaceutical Research ◽

10.31838/ijpr/2018.10.03.100 ◽

2018 ◽

Keyword(s):

Animal Models ◽

Experimental Animal ◽

Moringa Oleifera ◽

Methanolic Extract ◽

Experimental Animal Models ◽

Antidiarrheal Activity ◽

Moringa Oleifera Lam

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Hyperbaric treatment of air or gas embolism: current recommendations

Undersea and Hyperbaric Medicine ◽

10.22462/10.12.2019.13 ◽

2019 ◽

pp. 673-683

Author(s):

Richard E. Moon ◽

Keyword(s):

Animal Studies ◽

Decompression Sickness ◽

Bubble Formation ◽

Endothelial Damage ◽

Neurological Deficits ◽

Breath Hold ◽

Gas Embolism ◽

Hyperbaric Treatment ◽

Pulmonary Capillaries ◽

Venous Gas Embolism

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac “vapor lock” and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence-based review of adjunctive therapies is presented.

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Evogliptin Suppresses Calcific Aortic Valve Disease by Attenuating Inflammation, Fibrosis, and Calcification

Cells ◽

10.3390/cells10010057 ◽

2021 ◽

Vol 10 (1) ◽

pp. 57

Author(s):

Bongkun Choi ◽

Eun-Young Kim ◽

Ji-Eun Kim ◽

Soyoon Oh ◽

Si-On Park ◽

...

Keyword(s):

Animal Models ◽

Aortic Valve ◽

Aortic Valve Disease ◽

Rabbit Model ◽

Cytokine Expression ◽

Rate Of Change ◽

Valve Disease ◽

High Cholesterol Diet ◽

Calcific Aortic Valve Disease ◽

Valvular Calcification

Calcific aortic valve disease (CAVD) accompanies inflammatory cell infiltration, fibrosis, and ultimately calcification of the valve leaflets. We previously demonstrated that dipeptidyl peptidase-4 (DPP-4) is responsible for the progression of aortic valvular calcification in CAVD animal models. As evogliptin, one of the DPP-4 inhibitors displays high specific accumulation in cardiac tissue, we here evaluated its therapeutic potency for attenuating valvular calcification in CAVD animal models. Evogliptin administration markedly reduced calcific deposition accompanied by a reduction in proinflammatory cytokine expression in endothelial nitric oxide synthase-deficient mice in vivo, and significantly ameliorated the mineralization of the primary human valvular interstitial cells (VICs), with a reduction in the mRNA expression of bone-associated and fibrosis-related genes in vitro. In addition, evogliptin ameliorated the rate of change in the transaortic peak velocity and mean pressure gradients in our rabbit model as assessed by echocardiography. Importantly, evogliptin administration in a rabbit model was found to suppress the effects of a high-cholesterol diet and of vitamin D2-driven fibrosis in association with a reduction in macrophage infiltration and calcific deposition in aortic valves. These results have indicated that evogliptin prohibits inflammatory cytokine expression, fibrosis, and calcification in a CAVD animal model, suggesting its potential as a selective therapeutic agent for the inhibition of valvular calcification during CAVD progression.

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