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Non-conjugated catecholamines were measured in morning urine samples from 111 healthy, non-hospitalized subjects aged 8-18 y and in 16 hospitalized, healthy subjects aged 12 16 y. The catecholamines were extracted by cation exchange columns and alumina adsorption and quantitated with HPLC with electrochemical detection. The concentration of catecholamines was related both to the urinary creatinine concentration and to the collecting period and body surface area. Linear regression analysis was used to estimate continuous age-related reference centiles based upon the measurements from the 111 non-hospitalized subjects. The upper limits for the adrenaline/creatinine and noradrenaline/creatinine ratios were lower than in previous studies. The excretion of adrenaline and noradrenaline per hour and m2 body surface area was higher in the 16 hospitalized than in the 74 age-matched non-hospitalized subjects. The excretion of the catecholamines expressed per hour and m2 body surface area and expressed relative to creatinine excretion, decreased with increasing age, and the excretion of adrenaline and noradrenaline per hour and m2 body surface area was higher in boys than in girls. In conclusion, standardization of urine sampling leads to more narrow ranges for urinary adrenaline and noradrenaline excretion in healthy children and adolescents.

The regulation of beta-adrenergic function in circulating mononuclear leukocytes was evaluated during an episode of haemorrhagic shock treated by intra-osseous infusion of a small volume of hyperosmotic fluid. Two groups of piglets (n = 14) were anaesthetized with ketamine and bled to a mean arterial pressure of 40 mmHg. After 45 min the animals were randomized to receive 100 ml of either hyperosmotic (2.4 mol l-1) or iso-osmotic (0.29 mol l-1) fluid (equal volumes of glucose/sodium chloride) into the tibial bone marrow. Observations of haemodynamic variables and levels of plasma catecholamines and cAMP of circulating mononuclear leukocytes were carried out for 70 min. Infusion of hyperosmotic fluid enhanced the circulatory performance and attenuated the plasma catecholamine release significantly (p < 0.05) compared to the corresponding values in the animals that had iso-osmotic fluid infusion. Measurements of unstimulated and isoprenaline-stimulated cAMP levels in mononuclear lymphocytes indicated that the high plasma catecholamine levels in the iso-osmotic treatment group induced a desensitization of the beta-adrenoceptors 70 min after initiation of the shock. This effect was not seen in animals that had undergone hyperosmotic infusion.

Objective: To evaluate the plasma and urinary catecholamine concentrations after episodes of haemorrhagic shock treated by intraosseous infusion of a small volume of hyperosmotic fluid, followed by whole blood, in a standard porcine model., Design: Randomised open study., Setting: University hospital, Norway., Material: 18 piglets., Interventions: All animals were bled to an arterial systolic pressure of 60 mm Hg. After 30 minutes 100 ml hyperosmotic (2.4 mol/l) fluid (glucose/sodium chloride) was given either intraosseously (n = 6) or intravenously (n = 6). Ninety minutes later the animals were again bled to a systolic pressure of 60 mm Hg, and after 30 minutes an autologous whole blood transfusion was given by either intraosseous or intravenous infusion. Six animals acted as untreated controls., Main Outcome Measures: Changes in haemodynamic variables and plasma and urinary catecholamine concentrations., Results: Two pigs in the control group died. The hyperosmotic infusion improved the circulatory performance significantly (p < 0.05). Thirty minutes after both bleeds the plasma catecholamine concentrations were increased by 10-15 times, but returned to the reference range in all groups 90 minutes after the hyperosmotic infusion. Two hours after the whole blood infusion the catecholamine concentrations of the treated animals were at baseline values, significantly lower than those of the controls. The corresponding urinary catecholamine concentrations of the controls were significantly increased. There were no differences between the two treatment groups., Conclusion: The catecholamine measurements indicate that there may possibly be protective renal excretion of excess shock-induced plasma catecholamines after acute haemorrhage.

The effects of therapeutic plasma concentrations of lidocaine on blood platelet function and plasma catecholamine levels were assessed in 9 healthy subjects. There were no significant effects on plasma levels of beta-thromboglobulin, collagen and adenosine diphosphate-stimulated platelet aggregation, thromboxane-B2-concentration in plasma after collagen and ADP stimulated platelet aggregation, or on plasma nor-adrenaline and adrenaline. No significant correlation could be demonstrated between any of the variables tested. Thus, it appeared that lidocaine had no effect on platelets that could be of benefit in acute myocardial infarction. It should be possible to use lidocaine, in combination with thrombolytic therapies without increasing the risk of bleeding complications.

In the present study equilibrium dialysis has been used to determine the degree of protein binding of the catecholamines adrenaline and noradrenaline and the adrenergic receptor blockers, prazosin and propranolol in diabetics. The binding of the catecholamines in plasma from Type I and II diabetic patients was not significantly different from that of healthy subjects. The ratio of the bound and free catecholamine concentrations was correlated with the level of albumin (HSA). Significantly reduced protein binding of prazosin was observed in Type I and II diabetic subjects compared to healthy volunteers. The binding of propranolol was significantly reduced in Type I patients. The ratios between the bound and unbound concentrations of prazosin and propranolol were significantly correlated with the levels of alpha 1-acid glycoprotein (AAG). The results suggest that non-enzymatic glycosylation of plasma proteins may increase the unbound fraction of the adrenergic blockers prazosin and propranolol.

The binding of catecholamines in human serum was determined by equilibrium dialysis at 37 degrees. For serum concentrations of 10-15 nM the bound fractions were 28.8 +/- 2.2%, 25.7 +/- 1.7% and 22.2 +/- 2.2% for (+/-)-isoproterenol (IPR), (+/-)-norepinephrine (NE) and (+/-)-epinephrine (EPI), respectively. At higher serum concentrations saturation occurred. Alpha-1 acid glycoprotein (AAG) possessed one high affinity binding site and approximately 10 low affinity sites. The catecholamines were bound to AAG with the same order of potency for both classes of binding sites: IPR (Kd1: 100 microM Kd2: 2.2 mM) greater than NE (Kd1: 120 microM, Kd2: 6.5 mM) greater than EPI (Kd1: 140 microM, Kd2: 14 mM). Human serum albumin (HSA) and lipoproteins (SLP) interacted with the catecholamines in a non-saturable manner. IPR showed the strongest and EPI the weakest association to both of these serum protein fractions. (-)-Propranolol was able to inhibit the binding of IPR in serum and to isolated AAG, but not to HSA or to SLP. The present results show that AAG is an important catecholamine-binding protein in human serum. AAG, but not HSA or SLP, possesses binding sites shared by adrenergic receptor stimulators and blockers.