Angiographically demonstrable coronary artery spasm could be provoked repeatedly by giving intracoronary or intravenous injections of histamine to miniature swine with experimentally induced atherosclerotic lesions of the coronary artery. The spasm induced in this way subsided either spontaneously or after the administration of nitroglycerin and was prevented by a calcium antagonist or an agent that blocks histamine H1 receptors. This model, which suggests that atherosclerotic changes may be one of the primary factors in the occurrence of coronary artery spasm, should facilitate studies on the pathogenesis of this condition.

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The present study was designed to elucidate the role of collateral development, per se, on reactive hyperemia without persistent coronary stenosis in instrumented conscious dogs. Functional states of coronary collaterals were augmented by repetitive 2 minutes of coronary occlusion every 30 minutes for 2-9 days. Regional shortening measured sonomicrometrically recovered from -1.2 +/- 6.5% of the preocclusive state at the end of the first coronary occlusion to 100.5 +/- 1.2% (n = 8, P less than 0.01) after repeated coronary occlusions. Before and after collateral development, transient coronary occlusions of 5, 10, 20, 30, 60, 90, and 120 seconds were randomly performed. The degree of regional dysfunction and the following reactive hyperemic response were measured. Up to 20 seconds of coronary occlusion, the flow ratio and duration of coronary reactive hyperemia increased similarly, both before and after collateral development. However, when the duration of coronary occlusion was over 30 seconds, flow ratio and debt repayment ratio were reduced progressively after the collateral development. Among the indices exhibiting reactive hyperemia, debt repayment ratio decreased initially and correlated well with the recovery of regional dysfunction during coronary occlusion. Thus, the augmentation of collateral function after repetitive coronary occlusion reduces reactive hyperemia even in the absence of significant coronary stenosis.

The effects of glyceryl trinitrate and dipyridamole on induced ischaemia were studied in awake dogs during transient coronary occlusion before and after collateral development. Seventeen dogs were instrumented under sterile conditions with a miniature pressure gauge to measure left ventricular pressure, a cannula for aortic pressure, and pairs of piezoelectric crystals towards the subendocardium of the left ventricle for regional segment length measurements. A hydraulic cuff occluder and Doppler flow probe were placed around the left circumflex coronary artery. Collateral function was increased by repeated 2 min coronary occlusions at 32 min intervals for 2-9 days until regional wall motion returned to preocclusive values, despite the persistence of coronary occlusion. The effects of glyceryl trinitrate and dipyridamole were studied after the initial haemodynamic changes had subsided. Collateral function was quantified by integrating changes in end systolic length of the ischaemic area during coronary occlusion. Before collateral development the end systolic length area was 29.4(2.4) cm X s and was unchanged by glyceryl trinitrate or dipyridamole. After the development of collaterals the end systolic length area decreased from 4.1(1.1) to 2.2(1.0) cm X s (p less than 0.01) after glyceryl trinitrate and increased to 14.9(1.7) cm X s (p less than 0.01) after dipyridamole. Therefore, glyceryl trinitrate acted directly on collaterals and improved the induced ischaemia, whereas dipyridamole exaggerated the regional wall motion abnormality.

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