Inter-individual differences in cytokine release in patients undergoing cardiac surgery with cardiopulmonary bypass

Roth-Isigkeit, Angela; Hasselbach, Lisa; Ocklitz, Evelyn; Brückner, Stefan; A, Ros; Gehring, Hartmut; Schmucker, P.; Rink, Lothar; Seyfarth, M

doi:10.1046/j.1365-2249.2001.01521.x

Cited by 52 publications

(45 citation statements)

References 51 publications

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“…Both values are in the range of individual serum levels found in patients with sepsis, acute respiratory distress syndrome, and pneumonia. 2,4 Also, in patients suffering from left ventricular dysfunction 1 or after reperfusion of the ischemic heart in cardiopulmonary bypass, 37 IL-6 serum levels are known to be elevated. This may consequently lead to further deterioration of cardiac function, because IL-6 is known to be an independent predictor for worsening of heart failure in patients with end-stage heart failure.…”

Section: · Dmentioning

confidence: 99%

Interleukin-6 Causes Myocardial Failure and Skeletal Muscle Atrophy in Rats

et al. 2005

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Background-The impact of interleukin (IL)-6 on skeletal muscle function remains the subject of controversy. Methods and Results-The effects of 7-day subcutaneous administration of recombinant human IL-6 were examined at 3 doses, 50, 100, or 250 g · kg Ϫ1 · d Ϫ1 , in rats. Skeletal muscle mass decreased dose-dependently (with increasing dose: in the diaphragm, Ϫ10%, PϭNS; Ϫ15%, Pϭ0.0561; and Ϫ15% PϽ0.05; and in the gastrocnemius, Ϫ9%, PϭNS; Ϫ9%, PϭNS; and Ϫ18%, PϽ0.005) because of decreases in cross-sectional area of all fiber types without alterations in diaphragm contractile properties. Cardiovascular variables showed a dose-dependent heart dilatation (for end-diastolic volume: control, 78 L; moderate dose, 123 L; and high dose, 137 L, PϽ0.001), reduced end-systolic pressure (control, 113 mm Hg; moderate dose, 87 mm Hg; and high dose, 90 mm Hg; Pϭ0.037), and decreased myocardial contractility (for preload recruitable stroke work: control, 79 mm Hg; moderate dose, 67 mm Hg; and high dose, 48 mm Hg; PϽ0.001). Lung edema was confirmed by an increased wet-to-dry ratio (control, 4.2; moderate dose, 4.6; and high dose, 4.5; PϽ0.001) and microscopy findings. These cardiovascular alterations led to decreases in organ blood flow, particularly in the diaphragm (control, 0.56 mL · min Ϫ1 · g

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Section: · Dmentioning

confidence: 99%

Interleukin-6 Causes Myocardial Failure and Skeletal Muscle Atrophy in Rats

et al. 2005

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“…Oral arginine also improved endothelial dysfunction in patients with essential hypertension (11). Plasma and intracellular levels of arginine are altered in certain disease states, hypertension, hypercholesterolemia, and diabetes (12)(13)(14). As part of the treatment regimen, L-arginine may serve as a safer and more easily administered alternative to inhaled NO gas or NO donors.…”

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confidence: 99%

Receptor-mediated activation of nitric oxide synthesis by arginine in endothelial cells

Joshi¹,

Ferguson²,

Johnson

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Arginine contains the guanidinium group and thus has structural similarity to ligands of imidazoline and ␣-2 adrenoceptors (␣-2 AR). Therefore, we investigated the possibility that exogenous arginine may act as a ligand for these receptors in human umbilical vein endothelial cells and activate intracellular nitric oxide (NO) synthesis. Idazoxan, a mixed antagonist of imidazoline and ␣-2 adrenoceptors, partly inhibited L-arginine-initiated NO formation as measured by a Griess reaction. Rauwolscine, a highly specific antagonist of ␣-2 AR, at very low concentrations completely inhibited NO formation. Like L-arginine, agmatine (decarboxylated arginine) also activated NO synthesis, however, at much lower concentrations. We found that dexmedetomidine, a specific agonist of ␣-2 AR was very potent in activating cellular NO, thus indicating a possible role for ␣-2 AR in L-arginine-mediated NO synthesis. D-arginine also activated NO production and could be inhibited by imidazoline and ␣-2 AR antagonists, thus indicating nonsubstrate actions of arginine. Pertussis toxin, an inhibitor of G proteins, attenuated L-arginine-mediated NO synthesis, thus indicating mediation via G proteins. L-type Ca 2؉ channel blocker nifedipine and phospholipase C inhibitor U73122 inhibited NO formation and thus implicated participation of a second messenger pathway. Finally, in isolated rat gracilis vessels, rauwolscine completely inhibited the L-arginine-initiated vessel relaxation. Taken together, these data provide evidence for binding of arginine to membrane receptor(s), leading to the activation of endothelial NO synthase (eNOS) NO production through a second messenger pathway. These findings provide a previously unrecognized mechanistic explanation for the beneficial effects of L-arginine in the cardiovascular system and thus provide new potential avenues for therapeutic development. agmatine ͉ rauwolscine ͉ calcium A rginine is critical to normal growth and multiple physiological processes. It serves as a precursor for the synthesis not only of proteins but also of NO, urea, polyamines, and agmatine. The unequivocal demonstration that NO is the product of NO synthase (NOS)-catalyzed oxidation of L-arginine led to widespread interest in the actions of L-arginine. The K m of L-arginine for endothelial NOS (eNOS) is determined to be 2.9 M (1), and the intracellular L-arginine concentrations are in the range of 0.8-2.0 mM. In other words, cells maintain saturating levels of L-arginine as a substrate for NO synthases. However, an external supply of L-arginine is still required for the cellular production of NO (2). This requirement of exogenous arginine for the cellular NO production is termed ''arginine paradox.'' A number of mechanisms have been proposed to address this phenomenon, including endogenous NOS inhibitors and compartmentalization of intracellular L-arginine. Some have proposed that endogenous NOS inhibitors [e.g., asymmetric dimethylarginine (ADMA)] modulate NO levels by antagonizing intracellular L-arginine (3). An alternative...

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“…Дисфункция легких возникает в результате остро-го системного и легочного воспалительного отве-та [45,46]. Легочный кровоток останавливается, кровь подвергается воздействию гипотермии, кар-диоплегического раствора, чужеродных поверх-ностей и механическому воздействию в контуре аппарата ИК.…”

Section: клиническая кардиологияunclassified

Prevention of Respiraotry Complications in Subjects With Coronary Artery Disease When Performing Planned Coronary Artery Bypass Grafting

Баздырев¹,

Иванов²,

Pavlova³

et al. 2016

Kompleks. probl. serdečno-sosud. zabol.

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1 Федеральное государственное бюджетное научное учреждение «Научно-исследовательский институт комплексных проблем сердечно-сосудистых заболеваний», Кемерово, Россия 2 Государственное образовательное учреждение высшего профессионального обучения «Кемеровская государственная медицинская академия» Министерства здравоохранения Российской Федерации, Кемерово, Россия Сердечно-сосудистые заболевания, в первую очередь ишемическая болезнь сердца (ИБС), остаются главной причиной смертности как в России, так и в других индустриально развитых странах. К наиболее эффективному методу лечения ИБС относит-ся коронарное шунтирование (КШ). Несмотря на усовершенствования техники кардиохирургических операций, в послеоперацион-ных осложнениях одно из лидирующих мест занимают бронхолегочные осложнения, увеличивая пребывание пациента в стацио-наре, стоимость их лечения, повышая смертность. В обзоре представлен методологический подход к подготовке пациентов с ИБС к КШ, а также предложены методы, направленные на снижение послеоперационных респираторных осложнений.Ключевые слова: ишемическая болезнь сердца, коронарное шунтирование, респираторные осложнения, реабилитация, предоперационная подготовка. Cardiovascular diseases especially coronary artery disease (CAd) remains the major cause of death both in Russian and in other industrialized countries. the most effective method of CAd treatment is a coronary artery bypass grafting (CABG). despite the technological improvement of cardiac surgery operations, one of the leading position in postoperative complications are taken by bronchopulmonary complications which lengthen a subject's hospital stay, increasing treatment cost and mortality rate. A review provides a methodological approach to the preparation of CAd subjects for CABG, as well as proposes the methods aimed at reducing the postoperative respiratory complications. PREVENTION OF RESPIRAOTRY COMPLICATIONS IN SUBJECTS WITH CORONARY ARTERY DISEASE WHEN PERFORMING PLANNED CORONARY ARTERY BYPASS GRAFTING

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Inter-individual differences in cytokine release in patients undergoing cardiac surgery with cardiopulmonary bypass

Cited by 52 publications

References 51 publications

Interleukin-6 Causes Myocardial Failure and Skeletal Muscle Atrophy in Rats

Interleukin-6 Causes Myocardial Failure and Skeletal Muscle Atrophy in Rats

Receptor-mediated activation of nitric oxide synthesis by arginine in endothelial cells

Prevention of Respiraotry Complications in Subjects With Coronary Artery Disease When Performing Planned Coronary Artery Bypass Grafting

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