Effect of increased cardiac output on hepatic and intestinal microcirculatory blood flow, oxygenation, and metabolism in hyperdynamic murine septic shock

Albuszies, Gerd; Radermacher, Peter; Vogt, J.; Wachter, Ulrich; Weber, Sandra; Schoaff, M.; Georgieff, Michael; Barth, Eberhard

doi:10.1097/01.ccm.0000182817.20977.e9

Cited by 63 publications

(40 citation statements)

References 53 publications

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“…Tao et al (39) have shown that cardiac function was significantly reduced in CLP mice with fluid resuscitation. Albuszies et al (1) reported that a combination of fluid resuscitation and norepinephrine resulted in significantly increased cardiac output in CLP-induced septic mice. Collectively, these data suggest that prevention of cardiac dysfunction could be an important strategy in management of septic shock.…”

Section: Discussionmentioning

confidence: 99%

Glucan phosphate attenuates cardiac dysfunction and inhibits cardiac MIF expression and apoptosis in septic mice

Ha¹,

Fang²,

Grant³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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. Glucan phosphate attenuates cardiac dysfunction and inhibits cardiac MIF expression and apoptosis in septic mice. Am J Physiol Heart Circ Physiol 291: H1910 -H1918, 2006. First published June 9, 2006 doi:10.1152/ajpheart.01264.2005.-Myocardial dysfunction is a major consequence of septic shock and contributes to the high mortality of sepsis. We have previously reported that glucan phosphate (GP) significantly increased survival in a murine model of cecal ligation and puncture (CLP)-induced sepsis. In the present study, we examined the effect of GP on cardiac dysfunction in CLP-induced septic mice. GP was administered to ICR/HSD mice 1 h before induction of CLP. Sham surgically operated mice served as control. Cardiac function was significantly decreased 6 h after CLP-induced sepsis compared with sham control. In contrast, GP administration prevented CLPinduced cardiac dysfunction. Macrophage migration inhibitory factor (MIF) has been implicated as a major factor in cardiomyocyte apoptosis and cardiac dysfunction during septic shock. CLP increased myocardial MIF expression by 88.3% (P Ͻ 0.05) and cardiomyocyte apoptosis by 7.8-fold (P Ͻ 0.05) compared with sham control. GP administration, however, prevented CLP-increased MIF expression and decreased cardiomyocyte apoptosis by 51.2% (P Ͻ 0.05) compared with untreated CLP mice. GP also prevented sepsis-caused decreases in phospho-Akt, phospho-GSK-3␤, and Bcl-2 levels in the myocardium of septic mice. These data suggest that GP treatment attenuates cardiovascular dysfunction in fulminating sepsis. GP administration also activates the phosphoinositide 3-kinase/Akt pathway, decreases myocardial MIF expression, and reduces cardiomyocyte apoptosis.

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Section: Discussionmentioning

confidence: 99%

Glucan phosphate attenuates cardiac dysfunction and inhibits cardiac MIF expression and apoptosis in septic mice

Ha¹,

Fang²,

Grant³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…Systolic blood pressure was read in anesthesia after catheterization of the carotid artery (Albuszies et al, 2005) in mice loaded with IgE on the previous day. After intravenous antigen challenge, the mean blood pressure rose from $95 mm Hg to $170 mm Hg within 2 min, followed by a sudden and massive drop to $60 mm Hg, from where it slowly recovered ( Figure 3A).…”

Section: Ablation Of Connective Tissue Mast Cells By Expression Of Crmentioning

confidence: 99%

Cre-Mediated Cell Ablation Contests Mast Cell Contribution in Models of Antibody- and T Cell-Mediated Autoimmunity

et al. 2011

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Immunological functions of mast cells remain poorly understood. Studies in Kit mutant mice suggest key roles for mast cells in certain antibody- and T cell-mediated autoimmune diseases. However, Kit mutations affect multiple cell types of both immune and nonimmune origin. Here, we show that targeted insertion of Cre-recombinase into the mast cell carboxypeptidase A3 locus deleted mast cells in connective and mucosal tissues by a genotoxic Trp53-dependent mechanism. Cre-mediated mast cell eradication (Cre-Master) mice had, with the exception of a lack of mast cells and reduced basophils, a normal immune system. Cre-Master mice were refractory to IgE-mediated anaphylaxis, and this defect was rescued by mast cell reconstitution. This mast cell-deficient strain was fully susceptible to antibody-induced autoimmune arthritis and to experimental autoimmune encephalomyelitis. Differences comparing Kit mutant mast cell deficiency models to selectively mast cell-deficient mice call for a systematic re-evaluation of immunological functions of mast cells beyond allergy.

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“…Nevertheless, this technique reflected the effect of iloprost on microcirculation by showing significant differences between treatment groups and the control group and between the different treatment groups. This method has not been used in pig IECR thus far, but measurements in mouse livers 13 and pig 15 and human 29 intestinal mucosa during sepsis episodes have been performed, providing evidence that microcirculatory disturbances can be measured. Ischemia-reperfusion, reflected by compromised nutritional perfusion and leukocyte adherence, can be decreased significantly by prostacyclin donor bolus pretreatment, as shown previously in a rat liver transplant model using intravital microscopy for microcirculatory measurements.…”

Section: Discussionmentioning

confidence: 99%

“…The technique and reliability testing were described previously. [13][14][15][16][17] Microvascular blood flow (recorded in arbitrary units [AU]) was derived from the power spectra of back scattered laser light representing the distribution of Doppler shifts of the erythrocyte velocities. The rHb and SO 2 values were derived from light spectra detected after tissue illumination and back scattering.…”

Section: Assessment Of Microcirculationmentioning

confidence: 99%

Untitled

2015

Exp Clin Transplant

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Objectives: Iloprost has the potential to protect the liver transplant graft before and during cold ischemia. We studied iloprost administration during organ procurement and reperfusion in an extracorporeal pig liver perfusion model. Materials and Methods: German Landrace pigs (n = 7/group; 22-26 kg each) were used as donors. Preservation was performed by aortic perfusion with 2L Bretschneiders' Histidine-Tryptophan-Ketoglutarate solution HTK and cold ischemia time (4°C) 20 hours followed by normothermic extracorporeal perfusion for 8 hours. Untreated controls (1) were compared to iloprost (2) donor bolus-treatment (1 μg/kg body weight), (3) addition of iloprost to Bretschneiders´ Histidine-Tryptophan-Ketoglutarate solution HTK (0.0125 μg/mL), (4) continuous infusion during reperfusion (2 ng/kg/min), and (5) combined treatment (2) and (4). Results: Iloprost donor treatment led to significantly higher bile production. Addition of iloprost to the preservation solution significantly improved hepatic artery perfusion and was accompanied by improvements of microcirculation and bile production. Iloprost reperfusion treatment alone significantly improved bile production. Enzyme levels were positively affected by all treatment regimens.Combined use of iloprost before and after ischemia improved hepatic artery flow and microcirculation and showed significantly lower hypoxia staining versus controls. Conclusions: Iloprost donor treatment and use of iloprost in the preservation solution significantly improved graft perfusion and function. The effects of graft treatment seemed greater before than after reperfusion. Combined treatment did not reveal a synergistic advantage. Key words: End-stage liver disease, Graft, Prostaglandin, Transplant IntroductionThe use of iloprost clinically and experimentally is widely accepted after liver transplant. 1-4 However, although beneficial clinically and experimentally, its use in donor pretreatment is uncommon and the exact recommendations about type of application are pending. [5][6][7] The purpose of this study was to compare 4 different iloprost treatment regimens to a control group and to determine their effect on liver injury and function after extended cold ischemia time (CIT) (20 h) in an isolated 8-hour extracorporeal pig liver perfusion model. The following parameters were assessed:• Liver perfusion (macro-and microcirculation). Materials and Methods Animals and anesthesiaGerman Landrace pigs aged 10 to 16 weeks with a mean body weight (BW) 23.7 ± 1.56 kg (range, 22-26 kg) were used as organ donors. Animals were purchased (Fa. Sommerfeld, Brandenburg, Germany) and housed in our animal facility located at Charité Campus Virchow Klinikum, Berlin, Germany, approximately 1 week before each experiment. Animals were examined after delivery and kept species-appropriate with free access to water. Twice daily they were fed with standard pig nutrition pellets (Mpig-H, Sniff Spezialitäten GmbH, Soest, Germany) and housed at a day and night cycle of 12 hours and mean temperature ...

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Effect of increased cardiac output on hepatic and intestinal microcirculatory blood flow, oxygenation, and metabolism in hyperdynamic murine septic shock

Cited by 63 publications

References 53 publications

Glucan phosphate attenuates cardiac dysfunction and inhibits cardiac MIF expression and apoptosis in septic mice

Glucan phosphate attenuates cardiac dysfunction and inhibits cardiac MIF expression and apoptosis in septic mice

Cre-Mediated Cell Ablation Contests Mast Cell Contribution in Models of Antibody- and T Cell-Mediated Autoimmunity

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