| 1. |
- Åneman, A., et al.
(författare)
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Specific angiotensin II receptor blockage improves intestinal perfusion during graded hypovolemia in pigs
- 2000
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Ingår i: Critical Care Medicine. - : Ovid Technologies (Wolters Kluwer Health). - 0090-3493 .- 1530-0293. ; 28:3, s. 818-823
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To investigate the potential of specific angiotensin II subtype 1 (AT1) receptor blockade to modify the mesenteric hemodynamic response to acute hypovolemia and retransfusion. DESIGN: Prospective, randomized, controlled experimental study. SETTING: University-affiliated animal research laboratory. SUBJECTS: Fasted, anesthetized, ventilated, juvenile domestic pigs of both sexes. INTERVENTIONS: Acute, graded hypovolemia by 20% and 40% of the total estimated blood volume followed by retransfusion in control animals (CTRL; n = 10) and animals pretreated with the AT1 receptor blocker candesartan (CAND; n = 10). MEASUREMENTS AND MAIN RESULTS: Invasive monitoring of arterial and central venous blood pressures, cardiac output, portal venous blood flow, and jejunal mucosal blood flow. Blood gases were repeatedly analyzed to calculate oxygen delivery and consumption. Thirty minutes after each level of hypovolemia at 20% and 40%, cardiac output was decreased in CTRL animals from a baseline of 2.9 +/- 0.1 to 1.8 +/- 0.2 and 1.1 +/- 0.2 L/min, with no differences compared with CAND animals. Cardiac output was restored to 3.0 +/- 0.3 L/min 30 mins after retransfusion in CTRL animals, with no significant intergroup differences. Baseline portal venous blood flow (Q(MES)) and jejunal mucosal perfusion (PU(JEJ)) were greater in CAND animals compared with CTRL animals. During graded hypovolemia, CAND animals maintained Q(MES) and PU(JEJ) at significantly higher levels compared with CTRL animals, particularly after 40% hemorrhage (+221% and + 244%, respectively, relative to the mean values in CTRL animals). The same pattern was observed after retransfusion. Moreover, the calculated mesenteric critical oxygen delivery was significantly greater in CTRL animals (74 mL/min) compared with CAND animals (34 mL/min). No animals died in the CAND group, whereas four animals died during 40% hypovolemia or retransfusion in the CTRL group. CONCLUSIONS: Specific AT1 blockade before acute hypovolemia significantly ameliorated mesenteric and, in particular, jejunal mucosal hypoperfusion. In addition, cardiovascular stability was improved, and mortality in conjunction with acute hypovolemia and retransfusion could be completely avoided. These findings support a fundamental role of the renin-angiotensin system in the mesenteric response to acute hypovolemia and indicate a substantial interventional potential for candesartan in conjunction with circulatory stress.
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| 2. |
- Düring, J., et al.
(författare)
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Lactate, lactate clearance and outcome after cardiac arrest : A post-hoc analysis of the TTM-Trial
- 2018
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Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 62:10, s. 1436-1442
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Tidskriftsartikel (refereegranskat)abstract
- Background: Admission lactate and lactate clearance are implemented for risk stratification in sepsis and trauma. In out-of-hospital cardiac arrest, results regarding outcome and lactate are conflicting. Methods: This is a post-hoc analysis of the Target Temperature Management trial in which 950 unconscious patents after out-of-hospital cardiac arrest were randomized to a temperature intervention of 33°C or 36°C. Serial lactate samples during the first 36 hours were collected. Admission lactate, 12-hour lactate, and the clearance of lactate within 12 hours after admission were analyzed and the association with 30-day mortality assessed. Results: Samples from 877 patients were analyzed. In univariate logistic regression analysis, the odds ratio for death by day 30 for each mmol/L was 1.12 (1.08-1.16) for admission lactate, P <.01, 1.21 (1.12-1.31) for 12-hour lactate, P <.01, and 1.003 (1.00-1.01) for each percentage point increase in 12-hour lactate clearance, P =.03. Only admission lactate and 12-hour lactate levels remained significant after adjusting for known predictors of outcome. The area under the receiver operating characteristic curve was 0.65 (0.61-0.69), P <.001, 0.61 (0.57-0.65), P <.001, and 0.53 (0.49-0.57), P =.15 for admission lactate, 12-hour lactate, and 12-hour lactate clearance, respectively. Conclusions: Admission lactate and 12-hour lactate values were independently associated with 30-day mortality after out-of-hospital cardiac arrest while 12-hour lactate clearance was not. The clinical value of lactate as the sole predictor of outcome after out-of-hospital cardiac arrest is, however, limited.
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| 3. |
- Frost, Steven A, et al.
(författare)
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Unplanned admission to the intensive care unit in the very elderly and risk of in-hospital mortality.
- 2010
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Ingår i: Critical care and resuscitation. - 1441-2772. ; 12:3, s. 171-6
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Unplanned admission to the intensive care unit has been shown to significantly increase the risk of inhospital mortality. Medical advances and increased expectations have resulted in a greater number of very elderly patients (80 years and over) being admitted to the ICU. The risk of in-hospital death associated with unplanned admission to the ICU in very elderly patients has not been clearly defined. OBJECTIVE: To estimate the risk of in-hospital mortality associated with unplanned admission to the ICU in patients aged 80 years and over. DESIGN, SETTING AND PARTICIPANTS: Retrospective review of an adult intensive care database. The setting was Liverpool Hospital, a large teaching hospital in Sydney, Australia, with a 28-bed ICU that has about 2000 admissions per year. We analysed data on very elderly patients (n = 1680), aged 80 years or more, admitted to the ICU between 1 January 1997 and 31 December 2007. MAIN OUTCOME MEASURES: Baseline risk factors for inhospital mortality. RESULTS: Mortality among patients with unplanned ICU admissions was 47%, compared with 25% in patients with planned admissions (adjusted rate ratio [RR], 1.92 [95% CI, 1.59-2.32]). An estimated 50% of the overall risk of inhospital death among very elderly patients was attributable to a combination of unplanned admission to the ICU, the presence of at least one comorbid condition, acute renal failure and respiratory failure requiring intubation. CONCLUSION: Unplanned admission to the ICU increases the risk of in-hospital mortality in very elderly patients. At least 50% of the risk of in-hospital death in this age group is attributable to a combination of unplanned ICU admission, comorbidity (≥1 comorbid condition), acute renal failure and respiratory failure.
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| 4. |
- Åneman, Anders, 1965, et al.
(författare)
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Tezosentan normalizes hepatomesenteric perfusion in a porcine model of cardiac tamponade.
- 2009
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Ingår i: Acta anaesthesiologica Scandinavica. - : Wiley. - 1399-6576 .- 0001-5172. ; 53:2, s. 203-9
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: To investigate endothelin-1 (ET-1)-dependent hepatic and mesenteric vasoconstriction, and oxygen and lactate fluxes in an acute, fixed low cardiac output (CO) state. METHODS: Sixteen anesthetized, mechanically ventilated pigs were studied. Cardiac tamponade was established to reduce portal venous blood flow (Q(PV)) to 2/3 of the baseline value. CO, hepatic artery blood flow (Q(HA)), Q(PV), hepatic laser-Doppler flow (LDF), hepatic venous and portal pressure, and hepatic and mesenteric oxygen and lactate fluxes were measured. Hepatic arterial (R(HA)), portal (R(HP)) and mesenteric (R(mes)) vascular resistances were calculated. The combined ET(A)-ET(B) receptor antagonist tezosentan (RO 61-0612) or normal saline vehicle was infused in the low CO state. Measurements were made at baseline, after 30, 60, 90 min of tamponade, and 30, 60, 90 min following the infusion of tesozentan at 1 mg/kg/h. Results: Tamponade decreased CO, Q(PV), Q(HA), LDF, hepatic and mesenteric oxygen delivery, while hepatic and mesenteric oxygen extraction and lactate release increased. R(HA), R(HP) and R(mes) all increased. Ninety minutes after tesozentan, Q(PV), LDF and hepatic and mesenteric oxygen delivery and extraction increased approaching baseline values, but no effect was seen on CO or Q(HA). Hepatic and mesenteric handling of lactate converted to extraction. R(HA), R(HP) and R(mes) returned to baseline values. No changes were observed in these variables among control animals not receiving tesozentan. Conclusion: In a porcine model of acute splanchnic hypoperfusion, unselective ET-1 blockade restored hepatomesenteric perfusion and reversed lactate metabolism. These observations might be relevant when considering liver protection in low CO states.
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