Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Comparative Study
Does the timing of hypertonic saline resuscitation affect its potential to prevent lung damage?
Hypertonic saline (HS) resuscitation has been reported to prevent lung damage by suppressing neutrophil activation in animal models. Data on the effectiveness of HS to prevent organ damage in the clinical setting are inconsistent. We investigated whether the timing of HS administration relative to neutrophil activation could affect its potential to block neutrophil responses. ⋯ HS treatment caused a transient state of suppression during which neutrophil activation was suppressed; however, HS was unable to suppress cells that were stimulated with fMLP before HS was added. Accordingly, in vivo lung damage was greater in animals that received HS after they had been partially resuscitated with LR compared to mice that received HS before LR (P < 0.05). We conclude that timing of exposure to HS affects neutrophil responses in vitro and may reduce the potential of HS resuscitation to prevent lung injury in vivo.
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Comparative Study
Hypertonic/hyperoncotic resuscitation after intestinal superior mesenteric artery occlusion: early effects on circulation and intestinal reperfusion.
The objective of the study was to determine the early effects of hypertonic/hyperoncotic starch resuscitation after 2 h occlusion of the superior mesenteric artery (SMA) in comparison to animals reperfused without treatment and isotonic resuscitation. SMA was clamped (18 pigs, 19-23 kg) for 2 h followed by a 2-h reperfusion period, which was initiated with isotonic (ISO) (35 mL/kg 0.9% NaCl and 5 mL/kg 10% hydroxyethyl starch within 30 min) or hypertonic/hyperoncotic resuscitation (HHES) (7.5% NaCl/10% hydroxyethyl starch within 5 min). Cardiac output (CO), mean arterial blood pressure (MAP), serum lactate, antimesenteric serosal Laser-Doppler values (LD), and intramural pHi (tonometry) were measured. ⋯ With isotonic resuscitation LD values (21.8 +/- 2.1 LD units) and intramural pHi (7.09 +/- 0.14) decreased even more (P < 0.05) whereas the HHES group showed a significant hyperemic reaction and a normalization of the intramural pHi and serum lactate within 30 min. Hypertonic/hyperoncotic resuscitation significantly improves MAP and CO during reperfusion shock and induces an immediate hyperemic reperfusion reaction of the intestinal microcirculation. Adequate isotonic fluid replacement in order to restore the postischemic plasma volume loss may cause a pronounced deterioration of intestinal perfusion.
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Blood lactate elevation in critically ill patients commonly is taken as a sign of impaired tissue perfusion. Simultaneous elevation of lactate to pyruvate ratio (L/P ratio) may be helpful in discriminating between different mechanisms of hyperlactatemia and thus in determining the relevance of the finding. We studied prospectively the prevalence and the time pattern of hyperlactatemia and simultaneous L/P ratio elevation in 98 consecutive emergency admission patients in a 23-bed surgical-medical University Hospital intensive care unit. ⋯ We conclude that hyperlactatemia is common in emergency admission patients. Hyperlactatemia with L/P ratio elevation and lactic acidosis is likely to be associated with inadequate tissue perfusion. Hyperlactatemia persisting more than 6 h and simultaneous elevation of L/P ratio are associated with increased mortality.
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The objective of the study was to evaluate the tissue oxygenation and hemodynamic effects of NOS inhibition in clinical severe septic shock. Eight patients with septic shock refractory to volume loading and high level of adrenergic support were prospectively enrolled in the study. Increasing doses of NOS inhibitors [N(G)-nitro-L-arginine-methyl ester (L-NAME) or N(G)-monomethyl-L-arginine (L-NMMA)] were administered as i.v. bolus until a peak effect = 10 mmHg on mean blood pressure was obtained or until side effects occurred. ⋯ Blood lactate and the difference between tonometric gastric and arterial PCO2 remained unchanged. There were 4/8 ICU survivors. We conclude that nitric oxide synthase inhibition in severe septic shock was followed with a progressive correction of the vasoplegic hemodynamic disturbances with finally normalization of cardiac output and systemic vascular resistances without any demonstrable deterioration in tissue oxygenation.
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During circulatory shock, activating factors for cells in the microcirculation can be detected in plasma. But the source of such activators has remained uncertain. We have demonstrated recently that homogenates derived from the pancreas but not other peritoneal organs activate naive leukocytes. ⋯ Neutrophil pseudopod formation and plasma peroxide production, an additional index of cellular activation, were significantly lower in Futhan-treated SAO shock plasma (P < 0.05) than levels in non-treated SAO shock animals. These results demonstrate that activating factors for leukocyte are released in SAO shock and can be mitigated by pretreatment with the serine protease inhibitor Futhan. Proteolytically derived plasma factors released during SAO shock may contribute to leukocyte activation and ensuing organ dysfunction.