Different effects of endotoxic shock on the respiratory function of liver and heart mitochondria in rats

Kozlov, Andrey V.; Staniek, Katrin; Haindl, Susanne; Piskernik, Christina; Öhlinger, W.; Gille, Lars; Nohl, Hans; Bahrami, Soheyl; Redl, Heinz

doi:10.1152/ajpgi.00331.2005

Cited by 53 publications

(42 citation statements)

References 33 publications

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“…24,40,41 However at 4 and particularly at 8 h, RC was significantly decreased, recovering at 12 h. This is in line with reports showing impaired mitochondrial function at 4 h after LPS challenge in feline, 20 and improved mitochondrial function at 16 h in rats. 17,40 We show that both a decrease in RC at 4 h and an increase later on is also valid for rats. However, the impairment of mitochondrial function at 4 h is only temporary.…”

Section: Discussionsupporting

confidence: 90%

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A novel endotoxin-induced pathway: upregulation of heme oxygenase 1, accumulation of free iron, and free iron-mediated mitochondrial dysfunction

Duvigneau

Piskernik

Haindl

et al. 2008

Laboratory Investigation

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100

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Mitochondria are involved in the development of organ failure in critical care diseases. However, the mechanisms underlying mitochondrial dysfunction are not clear yet. Inducible hemoxygenase (HO-1), a member of the heat shock protein family, is upregulated in critical care diseases and considered to confer cytoprotection against oxidative stress. However, one of the products of HO-1 is Fe 2 þ which multiplies the damaging potential of reactive oxygen species catalyzing Fenton reaction. The aim of this study was to clarify the relevance of free iron metabolism to the oxidative damage of the liver in endotoxic shock and its impact on mitochondrial function. Endotoxic shock in rats was induced by injection of lipopolysaccharide (LPS) at a dose of 8 mg/kg (i.v.). We observed that the pro-inflammatory cytokine TNF-a and the liver necrosis marker aspartate aminotransferase were increased in blood, confirming inflammatory response to LPS and damage to liver tissue, respectively. The levels of free iron in the liver were significantly increased at 4 and 8 h after onset of endotoxic shock, which did not coincide with the decrease of transferrin iron levels in the blood, but rather with expression of the inducible form of heme oxygenase (HO-1). The proteins important for sequestering free iron (ferritin) and the export of iron out of the cells (ferroportin) were downregulated facilitating the accumulation of free iron in cells. The temporarily increased concentration of free iron in the liver correlated with the temporary impairment of both mitochondrial function and tissue ATP levels. Addition of exogenous iron ions to mitochondria isolated from control animals resulted in an impairment of mitochondrial respiration similar to that observed in endotoxic shock in vivo. Our data suggest that free iron released by HO-1 causes mitochondrial dysfunction in pathological situations accompanied by endotoxic shock.

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Section: Discussionsupporting

confidence: 90%

“…These data provide a mechanistic rationale for previously published articles [40][41][42][43] reporting beneficial effects of the iron chelator desferioxamine in sepsis models. Notably, the increase in hepatic intracellular iron levels was not due to decreased levels of transferrin-bound iron in blood.…”

Section: Discussionsupporting

confidence: 60%

A novel endotoxin-induced pathway: upregulation of heme oxygenase 1, accumulation of free iron, and free iron-mediated mitochondrial dysfunction

Duvigneau

Piskernik

Haindl

et al. 2008

Laboratory Investigation

Self Cite

100

View full text Add to dashboard Cite

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“…This is because of the multiple mechanisms of mitochondrial dysfunction, like substrate deficit, enzymatic blockage and cellular membrane damage [41], independent of the hemodynamic and microcirculatory state [42].…”

Section: Treating the Hypoperfusionmentioning

confidence: 99%

Perfusion Measurement of the Septic Patient in the Emergency Department

Devia-Jaramillo¹

2014

Emergency Medicine

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Sepsis is a deadly disease, more complex and frequent every day, that requires management from different specialists. The emergency physician is the first and one of the most important physicians that has to deal with the septic critically ill patients, because an appropriate initial management is key to a favorable outcome.In the emergency department it can be hard to predict which patients will become sicker just with information from the vital signs, and it's even harder to predict which patients will require a more intensive medical treatment. That is the reason why there must be more resources to measure tissue perfusion in an early and simple way in the emergency room, so that the emergency physician can manage to establish which patients requires earlier intervention to improve their perfusion state, despite not showing any clinically evident signs that help in the diagnosis of their current state.The goal of this paper is to propose a diagnostic and therapeutic algorithm for the hypoperfused patient with septic shock in the emergency department.venous oxygen saturation, arterial and venous lactate, microcirculatory study in different anatomical sites and oxygenation indexes.The emergency department, a place of rapid transit, with time constraints, progressive overcrowding and limited physical space, requires efficient indicators of early appearance and simple implementation in the system. That is why this article aims to show a proposal of early detection of hypoperfusion in the septic patient in the emergency room.

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“…Использовали стандартную модель получения эндотоксического шока [5][6][7]. Для этого крысам вводили липополисахарид В из расчёта 25 мг/кг.…”

Section: методикаunclassified

Effects of low power laser radiation of blue, green and red ranges on free radical processes in rat blood in endotoxic shock

IuA

et al. 2013

BIOMED KHIM

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Целью данной работы было исследование влияния низкоинтенсивного лазерного излучения синего (441,2 нм), зелёного (532,5 нм) и красного (632,8 нм) диапазонов на свободнорадикальные процессы в крови крыс при экспериментальном эндотоксическом шоке. В работе использовали модель эндотоксического шока, получаемую интраперитонеальным введением липополисахарида В (25 мг/кг). Были проведены измерения функциональной активности лейкоцитов крови (методом люминол-зависимой хемилюминесценции), супероксиддисмутазной активности плазмы крови (методом с нитросиним тетразолием) и окисления липидов мембран эритроцитов (по измерению флуоресценции цис-паринариевой кислоты). Обнаружено, что низкоинтенсивное лазерное излучение оказывает сильное влияние на все исследуемые процессы как в группах животных, которым вводили липополисахарид В, так и в контрольных группах. Наиболее выраженное действие излучения наблюдали в группах животных, которым вводили липополисахарид. В этих группах лазерное излучение вызывало возрастание всех исследуемых показателей. При дозе облучения (0,75 Дж/см 2 ) наиболее эффективным оказалось излучение в зеленом диапазоне спектра. При дозе 1,5 Дж/см 2 сильное влияние оказывало излучение, как в зелёной, так и в красной областях спектра. Обсуждаются возможные механизмы наблюдаемых процессов.Ключевые слова: эндотоксический шок, низкоинтенсивное лазерное излучение, хемилюминесценция, активные формы кислорода, лейкоциты, супероксиддисмутазная активность, свободнорадикальное окисление липидов.ВВЕДЕНИЕ. Сепсис (эндотоксический шок, синдром системного воспаления (ССВ)) и последующий синдром полиорганной недостаточности (СПН) являются наиболее серьезными проявлениями внедрения бактериальной инфекции. Сегодня СПН -одна из частых причин смерти и довольно распространенный патофизиологический процесс. Около 1% всех больных и до 20-30% больных в реанимационных палатах так или иначе имеют 411 * -адресат для переписки

show abstract

Different effects of endotoxic shock on the respiratory function of liver and heart mitochondria in rats

Cited by 53 publications

References 33 publications

A novel endotoxin-induced pathway: upregulation of heme oxygenase 1, accumulation of free iron, and free iron-mediated mitochondrial dysfunction

A novel endotoxin-induced pathway: upregulation of heme oxygenase 1, accumulation of free iron, and free iron-mediated mitochondrial dysfunction

Perfusion Measurement of the Septic Patient in the Emergency Department

Effects of low power laser radiation of blue, green and red ranges on free radical processes in rat blood in endotoxic shock

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