Plasma epinephrine

It is not surprising that intramuscular injection of epinephrine into the vastus lateralis produces a prompt peak plasma epinephrine concentration, because of the large size and excellent vascularization of this muscle. It is also not surprising that subcutaneous injection of epinephrine potentially leads to delayed absorption, because of the potent Ui-adrenergic agonist vasoconstrictor effects in the skin and subcutaneous tissue, as evidenced by skin blanching at the injection site [19, 20]. 

Caffeine causes a rise in plasma epinephrine and norepinephrine in subjects unused to caffeine beverages. 

This blood pressure and the plasma epinephrine and norepinephrine (2 and 3 above) effect of caffeine disappear after a few days, even if heavy coffee consumption continues. 

The answer is d, (Hardman, pp 855-856.) Propranolol, as well as other non selective beta blockers, tends to slow the rate of recovery in a hypoglycemic attack caused by insulin. Beta blockers also mask the symptoms of hypoglycemia and may actually cause hypertension because of the increased plasma epinephrine in the presence of a vascular beta2 blockade. 

There is evidence that y-aminobutyric acid A receptors may be modified during SE and become less responsive to endogenous agonists and antagonists. Two phases of GCSE have been identified. During phase I, each seizure produces marked increases in plasma epinephrine, norepinephrine, and steroid concentrations that may cause hypertension, tachycardia, and cardiac arrhythmias. Muscle contractions and hypoxia can cause acidosis, and hypotension, shock, rhabdomyolysis, secondary hyperkalemia, and acute tubular necrosis may ensue. 

Ketamine is the only intravenous anesthetic that possesses analgesic properties and produces cardiovascular stimulation. Heart rate, arterial blood pressure, and cardiac output are usually significantly increased. The peak increases in these variables occur 2-4 minutes after intravenous injection and then slowly decline to normal over the next 10-20 minutes. Ketamine produces its cardiovascular stimulation by excitation of the central sympathetic nervous system and possibly by inhibition of the reuptake of norepinephrine at sympathetic nerve terminals. Increases in plasma epinephrine and norepinephrine levels occur as early as 2 minutes after intravenous ketamine and return to baseline levels 15 minutes later. 

Intoxicating amounts of alcohol stimulate the release of cortisol, although the effect is more related to the intoxication than to the alcohol per se. SympatheticomeduUary activity is increased by acute alcohol ingestion but without detectable effect on the plasma epinephrine concentration and only a mild effect on norepinephrine. With intoxication, plasma concentrations of catecholamines are substantially increased. Acute ingestion of alcohol leads to a sharp reduction in the plasma testosterone in men, with an increase in the plasma luteinizing hormone concentration. 

Chalew SA, McLaughhn JV, Mersey JH, Adams AJ, Cornblath M, Kowarski AA. The use of the plasma epinephrine response in the diagnosis of idiopathic postprandial syndrome. JAMA 1984 251 612-5. 

R. Mora-Rodriguez and E.F. Cole, Effects of plasma epinephrine on fat metabolism during exercise interactions with exercise intensity. Am. J. Physiol. Endocrinol. Metab., 2000, 278, 669-676. 

This has been defined (B5) as the smallest single result which, with some assurance, can be distinguished from zero, or, in statistical terms, the smallest single result whose fiducial limits for, say, P = 0.05 do not include zero. This review will be primarily concerned with clinical chemical methods that have acceptable levels of sensitivity, and to which therefore statistical methods of quality control can be applied throughout the range of concentrations which may be encountered in physiological and pathological conditions. To take an extreme example, therefore, the statistical methods of quality control discussed in this review would not be fully applicable to determinations of plasma epinephrine or... 

A.Yamatodani and H. Wada, Automated analysis for plasma epinephrine and norepinephrine by hquid chromatography, including a sample cleanup procedure. Clin. Chem., 27, 1983-1987 (1981). 

Granados G. Garay-Sevilla ME, Malacara JM, et al Plasma epinephrine and norepinephrine response to... 

In addition to studying hemodynamic changes caused by liberated histamine, plasma epinephrine and norepinephrine levels have been investigated following injection of morphine. In a study of a patient who experienced an anaphylactoid response following the intravenous injection of morphine 0.3 mg/kg, plasma catecholamines were increased and this was accompanied by decreases in systemic vascular resistance and arterial blood pressure. In another study, intravenous morphine increased cardiac output, histamine, and epinephrine plasma concentrations and decreased arterial blood pressure and systemic vasculature resistance in adult subjects with no history of drug allergy or clinical evidence of cardiovascular, pulmonary, or metabolic disease. 

---