title: Left-sided stellate ganglion ablation or "rate-controlled" vagal nerve stimulation decreases regional myocardial metabolic impairment during acute ischemia in dogs.
abstract: This study was designed to see whether during ischemia a metabolic advantage results with left-sided ablation of the stellate ganglion (SGA), an available clinical technique. Its effects on hemodynamics and regional metabolism during myocardial ischemia were compared with those of electrical stimulation of the left vagus nerve (VS), a nonclinical technique, and those of a control condition (ischemia without intervention). The left anterior descending coronary artery (LADa) of 30 dogs was constricted to reduce blood flow by 50% and then 75% from that before constriction and after autonomic intervention (baseline). Electrocardiogram, left-ventricular (LV) first-time derivative (dP/dt), and systemic, LADa, and LV end-diastolic pressures were continuously recorded. Before and during each constriction, cardiac output and regional myocardial blood flow (by microspheres), blood gas tensions, pH, hemoglobin O2 saturation, lactate, glucose, sodium, and potassium concentrations were measured. During ischemia, SGA and VS each decreased heart rate, myocardial contractility (dP/dt), and filling pressures, the decrease in each variable being greater with VS. Also during ischemia, myocardial O2 delivery and consumption decreased to the same extent in the ischemic zone with VS, but the O2 delivery/consumption ratio was higher only with SGA. In addition, ischemic lactate production was lower with SGA and VS than with no autonomic intervention. It is concluded that left-sided SGA or VS to a heart rate of 80 to 90 beats per minute similarly mitigated metabolic impairment during myocardial ischemia. Although the study was only designed to compare modification of ischemia by two different techniques, the results suggest that ischemic zone O2 delivery/consumption ratio and hemodynamic stability were better with SGA.
authors.affiliation: Department of Anesthesiology, University of Florida College of Medicine, Gainesville 32610-0254, USA.
authors.forename: A
authors.initials: A
authors.lastname: Sidi
authors.forename: R T
authors.initials: RT
authors.lastname: Gehrig
authors.forename: W
authors.initials: W
authors.lastname: Rush
authors.forename: R F
authors.initials: RF
authors.lastname: Davis
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D002302:Cardiac Output; D003326:Coronary Circulation; D004285:Dogs; D004558:Electric Stimulation; D004562:Electrocardiography; D005260:Female; D006339:Heart Rate; D006454:Hemoglobins / Q000378:metabolism; D007773:Lactates / Q000097:blood; D008297:Male; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D011188:Potassium / Q000097:blood; D012964:Sodium / Q000097:blood; D013233:Stellate Ganglion / Q000502:physiology* / Q000601:surgery*; D014630:Vagus Nerve / Q000502:physiology*; D016277:Ventricular Function, Left; D017725:Ventricular Pressure
chemical_list: D001786:Blood Glucose; D006454:Hemoglobins; D007773:Lactates; D012964:Sodium; D011188:Potassium; D010100:Oxygen