The present study investigates the effect of strawberry antioxidants in beverage form on meal-induced postprandial inflammatory and insulin responses in human subjects. Overweight adults (n 24) consumed a high-carbohydrate, moderate-fat meal (HCFM) accompanied by either a strawberry or a placebo beverage in a cross-over design. Postprandial changes in plasma anthocyanins, their metabolites, insulin, glucose and inflammatory markers were assessed for 6 h. The postprandial concentrations of pelargonidin sulfate and pelargonidin-3-O-glucoside were significantly increased when the strawberry beverage was consumed concurrently with the HCFM compared with the placebo beverage (P,0·001). The strawberry beverage significantly attenuated the postprandial inflammatory response as measured by high-sensitivity C-reactive protein and IL-6 (P,0·05) induced by the HCFM. It was also associated with a reduction in postprandial insulin response (P,0·05). Collectively, these data provide evidence for favourable effects of strawberry antioxidants on postprandial inflammation and insulin sensitivity.

The aim of this study was to examine the effects of procyanidins derived from cocoa on vascular smooth muscle. Two hypotheses were tested: 1) extracts of cocoa, which are rich in procyanidins, cause endothelium-dependent relaxation (EDR), and 2) extracts of cocoa activate endothelial nitric oxide synthase (NOS). The experiments were carried out on aortic rings obtained from New Zealand White rabbits. The polymeric procyanidins (tetramer through decamer of catechin) caused an EDR. In addition, the Ca(2+)-dependent NOS activity, measured by the L-arginine to L-citrulline conversion assay, was significantly increased in aortic endothelial cells exposed to polymeric procyanidins, whereas monomeric compounds had no such effect. These findings demonstrate that polymeric procyanidins cause an EDR that is mediated by activation of NOS.

To determine whether the extent of left ventricular dysfunction and the degree of shape distortion can predict outcome in survivors of moderate-sized anterior Q wave myocardial infarction who are undergoing exercise training, these variables were measured by two-dimensional echocardiography before and after 12 weeks of a low level exercise training program starting 15 weeks after infarction in 13 patients (7 in group 1 and 6 in group 2) and 12 weeks apart in 24 matched control patients without training. By the end of training, the functional class score had increased in group 2 (from 2.25 to 2.67, p less than 0.005) but had not changed in group 1. Further discrimination of groups 1 and 2 was provided by an initial asynergy (akinesia or dyskinesia, or both) less than 18% or greater than or equal to 18%. Compared with group 1, group 2 had greater initial asynergy (32 versus 6%, p less than 0.001), expansion index (asynergic/normal endocardial segment length: 1.8 versus 1.6, p less than 0.025) and peak shape distortion index (12.2 versus 1.0 mm, p less than 0.005) but lower ejection fraction (43 versus 59%, p less than 0.05) and thinning ratio (asynergic/normal wall thickness: 0.61 versus 0.74, p less than 0.05). These variables did not change with training in group 1. However, in group 2, training caused significant increase in asynergy (from 32 to 40%, p less than 0.05), expansion index (from 1.8 to 2.0, p less than 0.01) and peak shape distortion (from 12.2 to 20.9 mm, p less than 0.05) associated with a decrease in thinning ratio (from 0.61 to 0.51, p less than 0.001) and ejection fraction (from 43 to 30%, p less than 0.005). Initial values for these variables were similar for corresponding control groups but did not change over the 12 weeks. Thus, patients with greater than or equal to 18% left ventricular asynergy on the initial echocardiogram showed more shape distortion, expansion and thinning before exercise training and developed further functional and topographic deterioration with training.

GSEs (grape seed extracts) which contain polyphenolic compounds cause an endothelium-dependent relaxation of blood vessels. The aim of the present study was to examine the mechanisms involved in this response. A well-characterized GSE was applied to rabbit aortic rings suspended in organ baths containing Krebs-Henseleit buffer maintained at 37 degrees C. In aortic rings pre-contacted with noradrenaline (norepinephrine), the extract produced a dose-dependent relaxation. The maximum relaxations elicited by the extract (71.9+/-1.0%) were similar to those elicited by acetylcholine (64.2+/-1.5%) (n=12 for each). As expected, the relaxations were abolished by removal of the endothelium and by prior incubation with L-NAME (N(G)-nitro-L-arginine methyl ester), confirming the essential role of eNOS (endothelial NO synthase) in the response. The responses to the GSE were also abolished by incubation with wortmannin and LY294002, which are inhibitors of PI3K (phosphoinositide 3-kinase). These compounds had no effect on the responses to acetylcholine. Using immunoblotting, we also demonstrated that the GSE induced the phosphorylation of both Akt and eNOS in HUVECs (human umbilical vein endothelial cells). Finally, the extract was modified by methylation of the hydroxy groups in the polyphenolic groups and was applied to the aortic rings. The modified extract failed to cause a relaxation. Taken together, these findings suggest that the endothelium-dependent relaxation induced by the GSE was mediated by activation of the PI3K/Akt signalling pathway through a redox-sensitive mechanism, resulting in phosphorylation of eNOS.

SUMMARY1. In dogs anaesthetized with chloralose, small latex balloons were positioned at the left pulmonary vein-atrial junctions so as to stretch this region. By recording action potentials from slips of the cervical vagi it was established that distension of these balloons stimulated receptor endings in the atrial endocardium which discharged into the myelinated branches of the vagi i.e. Paintal type A, type B and Intermediate type receptors.2. In other dogs, cooling the cervical vagus in steps of 2 'C reduced this response in vagal myelinated fibres. With twelve receptors the response to distension was reduced by 30 % when the vagus was cooled to 16 'C , by 70 % when cooled to 12 'C and abolished at 8-12 'C.3. In a third group of dogs, distension of balloons at the pulmonary vein-atrial junctions resulted in a reflex increase in heart rate. Cooling the cervical vagi in these dogs in stages to 8 'C reduced this increase in heart rate. In nine dogs the response was reduced by 20 % when the vagi was cooled to 16 'C, by 70 % when cooled to 12 'C and abolished between 12 and 8 TC.4. In a fourth group of dogs, distension of balloons at the pulmonary vein-atrial junctions was shown also to activate receptor endings in the atria which discharged into non-myelinated branches of the Vagi. In twelve receptors, cooling the cervical vagus in steps of 2 'C reduced this evoked increase in activity in non-myelinated fibres. These responses were abolished over a wide range of temperature unlike the responses observed above.5. It is concluded that the increase in heart rate which follows distension of balloons at the pulmonary vein-atrial junctions is mediated solely by the Paintaltype receptors which discharge into the myelinated fibres in the vagi.

SUMMARY1. The effects of an acute sustained increase in pulmonary venous pressure induced by partial obstruction of the mitral valve on the activity of

3. In the second series, eight type A units were selectively studied in twelve cats. Five were located in the atrial endocardium and all were converted. Of the other three units which were located at other sites in the chest, one could not be converted.4. In the third series, four type A units which could not be converted were selectively studied in twenty cats. All were located outside the atria.5. In the fourth series, three type B units which could not be converted were selectively studied in six cats. These units were located in the pulmonary veins and in the lateral walls of the atria.6. In the fifth series, fifty-five units were investigated in three anaesthetized spontaneously breathing cats. The proportion of the types of units were similar to that obtained in the artificially respired cats (first series).7. The present study has shown that atrial receptors with a type A pattern of discharge are relatively rare in the cat and that conversion of the patterns of discharge is a common phenomenon. Evidence is presented which suggests that there is one basic type of atrial receptor whose pattern of discharge is determined by their precise location in the vein-atrial system.

SUMMARY1. Distension of the atrial appendages resulted in a diuresis, an increase in the rate of Na+ excretion and an increase in heart rate.2. Both the urinary and heart rate responses to distension of the appendages were either abolished or much reduced by crushing the bases of the appendages.3. The diuresis in response to distension of the atrial appendages is similar to that previously described in response to distension of the pulmonary vein-atrial junctions by Ledsome & Linden (1968).4. It is concluded that stimulation of nerve endings within the atrial appendages results in a reflex increase in urine flow and heart rate.