Endothelial function can be preserved during cryo-storage of human saphenous vein.

Endothelial functional integrity was quantified in human saphenous vein by measurement of stimulated (vortex-mixing) rates of prostacyclin production. Prostacyclin production was not inhibited by dimethylsulphoxide (DMSO), glycerol or sucrose at concentrations normally used for cryopreservation. Rapid freezing followed by storage for 3-4 weeks and thawing of veins pretreated with 15% (v/v) dimethylsulphoxide significantly impaired prostacyclin production. In contrast, slow freezing and thawing in the presence, but not the absence, of DMSO led to complete retention of prostacyclin production. We conclude that endothelial function can be preserved during cryostorage.

Nature and pressure dependence of damage induced by distension of human saphenous vein coronary artery bypass grafts.

Surgical preparation of human saphenous vein for coronary artery bypass grafting involving distension and storage in iso-osmotic sodium chloride solution reduced tissue adenosine triphosphate (ATP) (mean(SEM] concentration from 280(20) nmol.g-1 wet wt (n = 25) to 140(30) nmol.g-1 wet wt (n = 12) and the adenosine triphosphate to adenosine diphosphate (ATP:ADP) concentration ratio from 2.4(0.1) to 1.2(0.2). Since removal of endothelium from freshly isolated vein did not affect ATP concentration or ATP:ADP ratio, these changes quantified medial damage. Distension of the vein at a pressure of 150 mmHg caused no change in ATP concentration or ATP:ADP ratio, but these values were reduced progressively by distension at 300 mmHg and 600 mmHg. Damage was not reversed but was exacerbated by subsequent incubation of the distended vein in blood. Distension of the vein at 600 mmHg caused release of tissue lactate dehydrogenase. The data show that acute medial damage can result from distension of the vein but that this does not occur at pressure equivalent to normal arterial pressure. Distension induced medial damage is unlikely to be rapidly reversible.

Intravenous adenosine in the treatment of supraventricular tachycardia: a dose-ranging study and interaction with dipyridamole.

Increasing doses of adenosine were given by rapid intravenous bolus to seven patients with spontaneous supraventricular tachycardia. Adenosine restored sinus rhythm in 10 of 14 episodes of narrow complex tachycardia. In those patients in whom adenosine produced only transient ventricular slowing the underlying rhythm was atrial flutter. Transient dyspnoea occurred in all patients. In two patients taking dipyridamole the mean dose of adenosine which produced an electrophysiologic effect (restoration of sinus rhythm or ventricular slowing to under 100 beats min-1) was 1.0 +/- 0.52 mg, whereas in other patients the mean dose was 8.8 +/- 2.6 mg, suggesting potentiation of the action of adenosine by dipyridamole.