Hawthorn has been extensively studied, and there is good research evidence to support cardiovascular actions that include increasing the force of myocardial contraction (positive inotropic action), increasing coronary blood flow, reducing myocardial oxygen demand, protecting against myocardial damage, improving heart rate variability, as well as hypotensive and antiarrhythmic effects (Mills & Bone 2000). Hawthorn therefore differs from other inotropic agents, which reduce the refractory period and increase the risk of arrhythmias (Joseph et al 1995).
In vitro studies using isolated frog and guinea pig heart preparations, as well as in vivo studies on dogs and cats, report increased myocardial contractility and stroke volume. In vitro and in vivo studies on rats report an antiarrhythmic action and a significant cardioprotective effect during cardiac ischaemia (al Makdessi et al 1996, 1999, Jayalakshmi & Devaraj 2004, Min et al 2005, Veveris et al 2004).
Hawthorn flavonoids have also been shown to decrease the cytotoxicity of hypoxia to human umbilical vein endothelial cells in vitro (Lan et al 2005), as well as protect against delayed cell death caused by ischaemia/reperfusion brain injury in gerbils (Zhang et al 2004). These effects have been attributed to improving energy metabolism, scavenging oxygen free radicals and inhibiting production of free radicals in ischaemic myocardium (Min et al 2005, Zhang et al 2004).
Dose-dependent increases in coronary blood flow have been shown in isolated human coronary arteries and it has been suggested that this is caused by membrane hyperpolarisation of vascular smooth-muscle cells due to potassium channel activation (Siegel et al 1996). Other in vitro evidence suggests that phosphodiesterase inhibition may underlie the myocardial action of hawthorn (Schussler et al 1995).
Much of hawthorn's cardiovascular activity is attributed to its flavonoid constituents (Nemecz 1999) and hawthorn extract is classified as a flavonoid drug in Germany. Studies using isolated guinea pig hearts suggest that the oligomeric procyanidins contribute to the vasodilating and positive inotropic effects of hawthorn (Schussler et al 1995), and ischaemia-reperfusion studies in rats suggest that these compounds are also responsible for cardioprotective effects (Chatterjee et al 1997).
Several procyanidins have shown ACE inhibition in vitro, in a reversible and noncompetitive manner (Uchida et al 1987). Although the original study identifying this Hawthorn 682
activity tested isolated procyanidins from another herb, they are found in relatively high concentration in hawthorn extracts (Murray 1995).
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