Tonometry of partial carbon dioxide tension in gastric mucosa: use of saline, buffer solutions, gastric juice or air.
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Tonometry of gastric mucosal partial carbon dioxide tension (PCO2) has been forwarded as a clinically applicable tool to monitor regional perfusion adequacy during circulatory failure. The technique is still not used widely, partly because of methodological problems. Current measurement principles are reviewed, with help of the report on PCO2 measurements in gastric juice and tonometer in this issue. (+info)
Using heart-lung interactions to assess fluid responsiveness during mechanical ventilation.
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According to the Frank-Starling relationship, a patient is a 'responder' to volume expansion only if both ventricles are preload dependent. Mechanical ventilation induces cyclic changes in left ventricular (LV) stroke volume, which are mainly related to the expiratory decrease in LV preload due to the inspiratory decrease in right ventricular (RV) filling and ejection. In the present review, we detail the mechanisms by which mechanical ventilation should result in greater cyclic changes in LV stroke volume when both ventricles are 'preload dependent'. We also address recent clinical data demonstrating that respiratory changes in arterial pulse (or systolic) pressure and in Doppler aortic velocity (as surrogates of respiratory changes in LV stroke volume) can be used to detect biventricular preload dependence, and hence fluid responsiveness in critically ill patients. (+info)
Endotoxin, cytokines, and procalcitonin in febrile patients admitted to the hospital: identification of subjects at high risk of mortality.
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We prospectively examined 464 febrile patients (median age, 61 years) for predictors of in-hospital death, by use of univariate and multivariate logistic regression using clinical data (age, underlying disease, duration of fever, chills, and shock on admission) and plasma endotoxin, TNF-alpha, IL-6, IL-10, and procalcitonin levels. The mortality rate was 4.6-fold higher (95% confidence interval [CI], 1.8-12) in 31 patients with shock on admission, 7 of whom died; the strongest association with mortality was the endotoxin concentration (relative risk, 13.7; 95% CI, 1. 4-136), which predicted 5 of the deaths with a 5% false-positive rate. For 433 patients without shock on admission, mortality (26 deaths) was associated with age and underlying disease: clinical data predicted 30% of the deaths, whereas IL-6 and procalcitonin levels identified an extra 10% with a 5% false-positive rate. When febrile patients are screened on hospital admission to identify those with a high risk for mortality, clinical judgment on the basis of age, underlying disease, and recent history outweighs the predictive value of endotoxin, cytokine, and procalcitonin levels. Only in patients who present with shock will measurement of endotoxin levels help predict those who will likely die at the cost of few false-positive results. (+info)
Thrombosis and shock induced by activating antiplatelet antibodies in human Fc gamma RIIA transgenic mice: the interplay among antibody, spleen, and Fc receptor.
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Transgenic mouse lines were created that express Fc gamma RIIA on platelets and macrophages at human physiologic levels, and they were used to explore the consequences in vivo of activating antiplatelet antibodies. Anti-CD9 antibody activated platelets of Fc gamma RIIA transgenic (tg) mice and, following injection in vivo, caused more rapid severe thrombocytopenia than nonactivating antiplatelet antibody. Anti-CD9 injected into Fc gamma RIIA tg crossed with FcR gamma-chain knockout (gamma-KO) mice caused thrombosis and shock in all mice, and death in 16 of 18 mice. The shock depended on platelet Fc receptor density and antibody dose. On histologic examination, the lung vasculature of anti-CD9-treated Fc gamma RIIA tg x gamma-KO mice contained extensive platelet-fibrin thrombi. Thrombosis and shock in Fc gamma RIIA tg mice in the context of the FcR gamma-chain knockout suggested the importance of the interplay of intravascular platelet activation and splenic clearance. Reduction of splenic clearance surgically (splenectomy) or functionally (monoclonal antibody treatment) also facilitated anti-CD9-mediated shock in Fc gamma RIIA tg mice. The spleen, which clears nonactivating antibody-coated platelets leading to thrombocytopenia, appears to play a protective role in the thrombosis and shock observed with activating antiplatelet antibody. The data indicate that antibodies, which activate platelets in an Fc gamma RIIA-dependent manner, can lead to thrombosis, shock, and death. Furthermore, antibody titer, platelet Fc receptor density, and splenic clearance are likely important determinants of the outcome. (Blood. 2000;96:4254-4260) (+info)
Endothelial protective and antishock effects of a selective estrogen receptor modulator in rats.
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This study investigated whether idoxifene, a selective estrogen receptor modulator (SERM), exerted protective effects against ischemia-reperfusion-induced shock. Ovariectomized rats were treated with vehicle, idoxifene, or 17beta-estradiol for 4 days. Rats were subjected to splanchnic artery occlusion (SAO) followed by reperfusion (SOA/R). In vehicle-treated rats, SAO/R resulted in hypotension, hemoconcentration, increased plasma tumor necrosis factor (TNF)-alpha levels, intestinal neutrophil accumulation, and endothelial dysfunction. 17beta-Estradiol treatment increased plasma estradiol concentration and reduced SAO/R-induced tissue injury. Idoxifene treatment had no effect on plasma estradiol concentration but reduced SAO/R-induced hemoconcentration (+8.8 +/- 1.3 vs. +14 +/- 1.3% in the vehicle group, P < 0.01), TNF-alpha production (98 +/- 3.2 vs. 214 +/- 13 pg/ml, P < 0.01), and neutrophil accumulation (0.025 +/- 0.005 vs. 0.047 +/- 0.005 U/g protein, P < 0.01). It also improved endothelial function, prolonged survival time (172 +/- 3.5 vs. 147 +/- 8 min, P < 0.01), and increased survival rate (69 vs. 23%, P < 0.01). Moreover, treatment with 17beta-estradiol or idoxifene in vivo reduced TNF-alpha-induced endothelial dysfunction in vitro. Taken together, these results demonstrated that idoxifene exerted estrogen-like, endothelial-protective, and antishock effects in ovariectomized rats, suggesting that SERMs have therapeutic potential in tissue injury resulting from ischemia-reperfusion. (+info)
Urea sensitizes mIMCD3 cells to heat shock-induced apoptosis: protection by NaCl.
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Urea, with NaCl, constitutes the osmotic gradient that allows water reabsorption in mammalian kidneys. Because NaCl induces heat shock proteins, we tested the responses to heat shock of mIMCD3 cells adapted to permissive urea and/or NaCl concentrations. We found that heat-induced cell death was stronger after adaptation to 250 mM urea. This effect was reversible, dose dependent, and, interestingly, blunted by 125 mM NaCl. Moreover, we have shown that urea-adapted cells engaged in an apoptotic pathway upon heat shock, as shown by DNA laddering. This sensitization is not linked to a defect in the heat shock response, because the induction of HSP70 was similar in isotonic and urea-adapted cells. Moreover, it is not linked to the presence of urea inside cells, because washing urea away did not restore heat resistance and because applying urea and heat shock at the same time did not lead to heat sensitivity. Together, these results suggest that urea modifies the heat shock response, leading to facilitated apoptosis. (+info)
Antioxidant therapy: a new pharmacological approach in shock, inflammation, and ischemia/reperfusion injury.
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A vast amount of circumstantial evidence implicates oxygen-derived free radicals (especially superoxide and hydroxyl radical) and high-energy oxidants (such as peroxynitrite) as mediators of inflammation, shock, and ischemia/reperfusion injury. The aim of this review is to describe recent developments in the field of oxidative stress research. The first part of the review focuses on the roles of reactive oxygen species (ROS) in shock, inflammation, and ischemia/reperfusion injury. The second part of the review deals with the novel findings using recently identified pharmacological tools (e.g., peroxynitrite decomposition catalysts and selective superoxide dismutase mimetics (SODm) in shock, ischemia/reperfusion, and inflammation. 1) The role of ROS consists of immunohistochemical and biochemical evidence that demonstrates the production of ROS in shock, inflammation, and ischemia/reperfusion injury. ROS can initiate a wide range of toxic oxidative reactions. These include initiation of lipid peroxidation, direct inhibition of mitochondrial respiratory chain enzymes, inactivation of glyceraldehyde-3-phosphate dehydrogenase, inhibition of membrane sodium/potassium ATPase activity, inactivation of membrane sodium channels, and other oxidative modifications of proteins. All these toxicities are likely to play a role in the pathophysiology of shock, inflammation, and ischemia/reperfusion. 2) Treatment with either peroxynitrite decomposition catalysts, which selectively inhibit peroxynitrite, or with SODm, which selectively mimic the catalytic activity of the human superoxide dismutase enzymes, have been shown to prevent in vivo the delayed vascular decompensation and the cellular energetic failure associated with shock, inflammation, and ischemia/reperfusion injury. ROS (e.g., superoxide, peroxynitrite, hydroxyl radical, and hydrogen peroxide) are all potential reactants capable of initiating DNA single-strand breakage, with subsequent activation of the nuclear enzyme poly(ADP-ribose) synthetase, leading to eventual severe energy depletion of the cells and necrotic-type cell death. Antioxidant treatment inhibits the activation of poly(ADP-ribose) synthetase and prevents the organ injury associated with shock, inflammation, and ischemia/reperfusion. (+info)
Clinical features and predictors of in-hospital mortality in patients with acute and chronic pulmonary thromboembolism.
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OBJECTIVE: The differences in the clinical findings of patients with acute pulmonary thromboembolism (acute-PTE) and chronic pulmonary thromboembolism (chronic-PTE) were compared, and the association between the clinical findings and prognosis in the two groups was analyzed. PATIENTS: This study included 204 patients with PTE, 139 patients with acute-PTE and 65 patients with chronic-PTE. RESULTS: There were significant differences between acute-PTE and chronic-PTE in the predisposing factors of post operation (19.4 versus 1.5%, p = 0.0003), and electrocardiographic signs such as sinus tachycardia (73.7 versus 50.9 %, p = 0.007), ST-depression (25.3 versus 9.4%, p = 0.03), right ventricular hypertrophy (20.0 versus 47.2%, p = 0.0007), and right axis deviation (3.2 versus 22.6%, p = 0.0003). Thirty-one of the 139 acute-PTE patients died from PTE, as did 17 of the 65 chronic-PTE patients. The prognosis was poor in patients older than 70 years old (p = 0.01), with stroke (p = 0.008), syncope (p = 0.01), shock (p = 0.0006), hypocapnia (PaCO2 < or = 25 torr; p = 0.0006) and an elevation in total pulmonary resistance (TPR >1,000 dyne-sec cm(-5) (p = 0.02)) in acute-PTE, and in those with syncope (p = 0.03), shock (p = 0.008), and right ventricular hypertrophy on electrocardiogram (p = 0.03) in chronic-PTE. CONCLUSION: The results of this study indicate a relationship between the clinical features of patients with acute-PTE and chronic-PTE, and the predictors of in-hospital mortality. (+info)