Norepinephrine and nomega-monomethyl-L-arginine in porcine septic shock: effects on hepatic O2 exchange and energy balance
Autor: | Josef Vogt, Karen M. Rieger, Jens Adler, Thomas Iber, Karl Träger, Robert Grover, Ulrich Wachter, Michael Georgieff, Arnim Vlatten, Peter Radermacher, Borislav Santak |
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Rok vydání: | 1999 |
Předmět: |
Pulmonary and Respiratory Medicine
Male Mean arterial pressure Cardiac output medicine.medical_specialty Swine Hemodynamics Blood Pressure Critical Care and Intensive Care Medicine Norepinephrine (medication) Norepinephrine Oxygen Consumption Internal medicine Medicine Animals Enzyme Inhibitors omega-N-Methylarginine business.industry Septic shock medicine.disease Shock Septic Endotoxins medicine.anatomical_structure Endocrinology Glucose Liver Shock (circulatory) Vascular resistance Female Vascular Resistance medicine.symptom business Energy Metabolism Vasoconstriction medicine.drug Liver Circulation |
Zdroj: | American journal of respiratory and critical care medicine. 159(6) |
ISSN: | 1073-449X |
Popis: | We compared the effects of norepinephrine (NOR; n = 11) and the nonselective nitric oxide synthase inhibitor Nomega-monomethyl-L-arginine (L-NMMA; n = 11) on hepatic blood flow (Q liv), O2 exchange, and energy metabolism over 24 h of hyperdynamic, normotensive porcine endotoxic shock. Endotoxin (ETX; n = 8) caused a continuous fall in mean arterial pressure (MAP) despite a sustained 50% increase in cardiac output (Q) achieved by adequate fluid resuscitation. NOR maintained MAP at preshock levels owing to a further rise in Q, while the comparable hemodynamic stabilization during L-NMMA infusion resulted from systemic vasoconstriction, increasing the systemic vascular resistance (SVR) about 30% from shock level after 6 h of treatment concomitant with a reduction in Q to preshock values. Whereas NOR also increased Q liv and, hence, hepatic O2 delivery (hDO2), but did not affect hepatic O2 uptake (hVO2), L-NMMA influenced neither Q liv nor hDO2 and hVO2. Mean capillary hemoglobin O2 saturation (HbScO2) on the liver surface as well as HbScO2 frequency distributions, which mirror microcirculatory O2 availability, remained unchanged as well. Neither treatment influenced the ETX-induced derangements of cellular energy metabolism reflected by the progressive decrease in hepatic lactate uptake rate and increased hepatic venous lactate/pyruvate ratios. ETX nearly doubled the endogenous glucose production (EGP) rate, which was further increased with NOR, whereas L-NMMA nearly restored EGP to preshock levels. Nevertheless, despite the different mechanisms in maintaining blood pressure neither treatment influenced ETX-induced liver dysfunction. |
Databáze: | OpenAIRE |
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