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Adrenaline infusion evokes increased thromboxane B 2 production by platelets in healthy men: the effect of beta‐adrenoceptor blockade
Author(s) -
LAUSTIOLA K.,
KAUKINEN S.,
SEPPÄLÄ E.,
JOKELA T.,
VAPAATALO H.
Publication year - 1986
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1986.tb02164.x
Subject(s) - pindolol , practolol , platelet , medicine , endocrinology , stimulation , chemistry , thromboxane b2 , prostacyclin , epinephrine , thromboxane , propranolol
Abstract. The effects of direct adrenergic stimulation, achieved by 60‐min adrenaline infusion (0·1–0·2 μg kg ‐1 min ‐1 ), on thromboxane B 2 (TxB 2 ) production by platelets in whole blood ex vivo and on ADP‐induced platelet aggregation were studied in seven healthy male volunteers. The effects of two beta‐adrenergic blocking agents, pindolol and practolol, on the adrenaline‐induced changes were furthermore analyzed. Adrenaline administration resulted in an about ten‐fold elevation in plasma adrenaline, and an about threefold increase in TxB 2 production by platelets at 30 min of infusion. The increased TxB 2 production persisted throughout the entire adrenaline infusion, and up to 30 min of postinfusion period (recovery). Pindolol blunted markedly the effects of adrenaline on platelet TxB 2 production, whereas practolol seemed to have only a weak effect. The sensitivity of platelets to ADP‐induced aggregation did not change during the 60 min of adrenaline infusion. However, at 60 min of recovery the platelets showed a significantly increased sensitivity to ADP. Correspondingly, pindolol treatment did not affect platelet sensitivity during the infusion period, but at 60 min of recovery it had caused a significantly decreased sensitivity of platelets to ADP‐stimulation. Plasma‐free fatty acids increased markedly during the adrenaline infusion. This increase was totally blocked by pindolol, but only partly by practolol. The present results demonstrate that adrenaline, at plasma levels seen for example, in complicated myocardial infarction, stimulates platelet TxB 2 production and increases the sensitivity of platelets to ADP after the infusion. Pindolol, but not practolol, inhibits these adrenaline‐induced changes in platelet behaviour.