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- Haney, Michael, et al.
(författare)
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Method of preload reduction during LVPVR analysis of systolic function : airway pressure elevation and vena cava occlusion
- 2002
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Ingår i: Anesthesiology. ; 97:2, s. 436-46
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: A graded preload reduction during analysis of the left ventricular pressure-volume relationship (LVPVR) is required for derivation of end-systolic elastance (Ees) and preload recruitable stroke work (PRSW). The authors aimed to measure serial changes in these systolic function parameters before and during planned circulatory interventions using two different methods of preload alteration: a positive airway pressure plateau (APP) and inferior vena cava occlusion (IVCO). METHODS: In eight animals, measurements were made at 38 degrees, 30 degrees, 32 degrees, 34 degrees, and posthypothermia 38 degrees C. In an additional eight animals, isoflurane, adrenaline, and aorta occlusion (balloon catheter occluder) were administered in series, each with a preintervention control measurement. Left ventricular volume was measured by conductance. Paired measurements of the systolic function parameters Ees and PRSW, each derived with two preload methods, were analyzed for bias. RESULTS: Circulatory alterations were achieved with the temperature, isoflurane, adrenaline, and aorta occlusion interventions. Measured changes in Ees and PRSW from control to intervention showed a strong correlation and no significant bias for APP in relation to IVCO. The APP-derived absolute values for Ees and PRSW demonstrated a consistent positive bias compared with IVCO. CONCLUSION: The APP method for preload reduction during LVPVR analysis detected changes in Ees and PRSW during the circulatory interventions in this model that were not different than those detected using another preload reduction method, IVCO. APP and IVCO are not interchangeable methods for preload reductions during LVPVR absolute quantitation of systolic function, and each needs to be used serially.
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| 2. |
- Lehtipalo, Stefan, et al.
(författare)
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Does dopexamine influence regional vascular tone and oxygenation during intestinal hypotension?
- 2002
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Ingår i: Acta Anaesthesiol Scand. ; 46:10, s. 1217-26
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Local effects of dopexamine on intestinal vascular tone and oxygenation were investigated during intestinal hypotension. To this end, we employed an experimental model, in which the superior mesenteric arterial pressure (PSMA) was controlled by an adjustable perivascular clamp. This approach enabled us to keep the intestinal perfusion pressure (IPP) constant in the face of any systemic circulatory alterations. METHODS: In 11 barbiturate-anesthetized pigs, we instrumented the superior mesenteric circulation for assessments of vascular resistance (RMES), IPP, jejunal mucosal perfusion (Laser Doppler) and intestinal tissue oxygenation (microoximetry). Measurements were carried out before and during dopexamine infusions (0.5 and 1.0 micro g.kg-1.min-1) at a freely variable PSMA (i.e. the perivascular clamp fully open) and at a PSMA of 50 mmHg and 30 mmHg. RESULTS: At a constant PSMA of 50 mmHg, dopexamine had no significant intestinal vascular effects. However, at a constant PSMA of 30 mmHg, both doses of dopexamine were associated with decreases in RMES. Effects of dopexamine on intestinal oxygen delivery and extraction were minimal during these procedures, while a minor decrease in intestinal tissue oxygen tension was observed during dopexamine administration at the lowest IPP level. CONCLUSION: At very low intestinal perfusion pressures (approximately 30 mmHg) dopexamine produces intestinal vasodilation in excess of what is produced by intrinsic autoregulation. This suggests that there is a vasodilatory reserve in the intestine under such conditions and that a pharmacological vasodilator like dopexamine may improve intestinal circulation during regional severe hypotension.
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| 3. |
- Österlund, Barbro, et al.
(författare)
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Myocardial ischemia induces coronary t-PA release in the pig
- 2002
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Ingår i: Acta Anaesthesiol Scand. ; 46:3, s. 271-8
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Tissue-type plasminogen activator (t-PA) is the key factor in initiating endogenous fibrinolysis in the vascular compartment. Regulated release of t-PA from endothelial stores is rapidly induced by several humoral factors as well as coagulation activation products. The aim of the present study was to test the hypothesis that regional myocardial ischemia induces regulated release of t-PA in the coronary vasculature in vivo. METHODS: Healthy anesthetized (pentobarbital) pigs (n=8) were studied before and after a 10-min left anterior descending region coronary artery occlusion (LAD). Coronary fluxes of lactate, total t-PA antigen (ELISA, detecting both complex bound and free fraction) and active t-PA (functional assay detecting biological free fraction) were determined at 1, 3, 5 and 10 min of reflow. RESULTS: Coronary occlusion induced myocardial lactate production in all animals. Net coronary release of total t-PA, which was 21 ng/min during control, increased rapidly during reflow with a peak after only 1 min (136 ng/min), and returned to baseline within 3 min. Net release of active t-PA mirrored the overall net release response, but fell short of statistical significance. CONCLUSION: Data indicate a local myocardial profibrinolytic response following regional ischemia, which may serve as a prompt defence against coronary thromboembolic events.
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