Objective: To study the effect of epinephrine (EPI) infusion on vital organ blood flow and metabolic variables during sepsis.
Design And Setting: Randomised placebo-controlled animal trial in an animal laboratory.
Animals: Seven merino cross-ewes.
Interventions: Chronic implantation of flow probes (aorta, renal, mesenteric and coronary artery and sagittal sinus). Induction of sepsis by intravenous injection of E. coli. Random allocation of sheep to EPI (0.4 microg kg(-1) min(-1)) or vehicle for 6 h.
Measurements And Results: E. coli induced hypotension and hyperlactataemia and increased cardiac output, renal, mesenteric and coronary blood flows. Compared to vehicle, EPI restored mean arterial blood pressure (69 vs. 86 mmHg) and further increased cardiac output (6.4 vs. 7.1 l/min). EPI, however, decreased renal blood flow (330 vs. 247 ml/min) and renal conductance. EPI also reduced mesenteric and coronary conductance without changes in flows. Compared to vehicle, EPI increased urine output (293 vs. 544 ml/6 h) but not creatinine clearance. EPI increased lactate (1.8 vs. 15.7 mmol/l) with accompanying acidosis (serum bicarbonate: 25.2 vs. 15.7 mmol/l), hyperglycaemia (2.6 vs. 13.5 mmol/l) and hypokalaemia (4.3 vs. 3.0 mmol/l).
Conclusions: Hyperdynamic sepsis increased blood flow to heart, gut and kidney. Although EPI infusion further increased cardiac output, blood pressure and myocardial performance, it was also associated with potent metabolic effects, decreased mesenteric, coronary and renal conductance and a significant reduction in renal blood flow.
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http://dx.doi.org/10.1007/s00134-005-2580-x | DOI Listing |
Comput Methods Biomech Biomed Engin
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Shenzhen Key Laboratory of Cardiovascular Disease, Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen, Guangdong Province, China.
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Academic Model Providing Access to Healthcare (AMPATH), Eldoret, Kenya.
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Henan Key Laboratory of Medical Tissue Regeneration, Xinxiang Medical University, Xinxiang, China.
Cardiovascular diseases (CVD) are the leading cause of morbidity and mortality globally, with elevated low-density lipoprotein cholesterol (LDL-C) levels being a major risk factor. Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a critical role in regulating LDL-C levels by promoting the degradation of hepatic low-density lipoprotein receptors (LDLR) responsible for clearing LDL-C from the circulation. PCSK9 inhibitors are novel lipid-modifying agents that have demonstrated remarkable efficacy in reducing plasma LDL-C levels and decreasing the incidence of CVD.
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View Article and Find Full Text PDFJ Clin Med
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Department of Cardiovascular & Thoracic Anaesthesia and Critical Care, University Hospital of Martinique, F-97200 Fort-de-France, Martinique, France.
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