Clonidine reduces sympathetic activity but maintains baroreflex responses in normotensive humans.

Clonidine, an alpha 2-adrenergic agonist, has been shown to modify the hemodynamic responses to surgery. To examine further the mechanism underlying this action, we evaluated the neurocirculatory effects of oral clonidine and the ability of clonidine to alter the hemodynamic and sympathetic responses to a noxious stimulus (cold pressor test) and to baroreceptor perturbations in nine healthy men (ages 20-29 yr). Heart rate (ECG), blood pressure (radial artery catheter), central venous pressure (jugular vein), and cardiac output (impedance cardiography) were monitored before and after oral clonidine (0.3 mg) or placebo. Plasma norepinephrine was measured with high-performance liquid chromatography. Sympathetic nerve activity (SNA) to skeletal muscle blood vessels was recorded from a Tungsten needle positioned within the peroneal nerve. Baroreceptor testing was carried out by intravenous bolus injections of nitroprusside (100 micrograms) followed 60 s later by intravenous phenylephrine (150 micrograms). The slope of the linear relationship between the change in R-R interval versus the change in mean pressure (cardiac baroslope) or change in SNA versus change in diastolic pressure (sympathetic baroslope) was determined at baseline and 75 min after clonidine or placebo. In addition, peak responses to the cold pressor test (60-s hand immersion in ice water) were determined at the same intervals. Clonidine progressively decreased blood pressure and muscle SNA over the 75-min session. Clonidine subtly reduced the sympathoexcitation produced by the cold pressor test but did not alter the gain of the baroreceptor reflex regulating cardiac interval or peripheral SNA; baroslope relationships were simply shifted leftward (to operate at lower pressures).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac disease and the patient with burns.

Cardiac disease has many manifestations that may complicate burn care. A review of 2477 consecutive acute burn admissions was conducted to determine the types and incidence of cardiac complications in this patient population. Nearly one half of patients with a prior cardiac history manifested some form of cardiac dysfunction, most frequently arrhythmias. Eight percent had an in-hospital myocardial infarction. Only 6% of patients without a prior cardiac history manifested cardiac dysfunction. The in-hospital mortality rate after myocardial infarction for both groups was 3.5 to 4 times that of patients without burns. Except for patients with prosthetic valves, for whom anticoagulation and infection prophylaxis are required, burn care of the cardiac patient is expectant with selective use of invasive monitoring and therapy as determined by the patient's clinical course.