There is experimental evidence that the bimodally distributed ventricular arrhythmias (phases Ia and Ib) during the first 30 min after coronary occlusion (CO) in dogs are not due to the same mechanism. In 39 dogs we related the incidence of phases Ia and Ib to the time courses of excitation thresholds (ET), refractoriness (REFR), conduction times (CT) and effective refractory periods (ERP) at 6-12 epicardial electrode sites within the ischemic zone. The regional collateral myocardial blood flow (RMBF-tracer microsphere technique) was determined in 14 out of the dogs. This measurement only served for rough grouping into dogs with low and higher RMBF at the electrode sites during ischemia. REFR was determined as temporal recovery of excitability at a constant current strength of 4-6 times preocclusion ET. ERP was intermittently measured at 2.0-8.0 mA. At low RMBF ET, REFR and CT increased very inhomogeneously (dispersion of ET increased from 0.06 to 2.42 mA) 2-8 min after CO, leading to Ia-arrhythmias (also depending on infarct size) which terminated as ET, REFR and CT partially recovered 10-30 min after CO, their dispersions being still markedly elevated. With further recovery of these electrophysiological parameters the phases Ib subsided. On the other hand, the ERP diminished for the most part within the first 10 min after CO with only minor further decrease. Remarkably the dispersion of ERP did not significantly increase within the ischemic zone (from mean = 15 +/- 5 ms to 22 +/- 8 ms at low RMBF and from 14 +/- 6 ms to 18 +/- 9 ms at higher RMBF, p = ns). As a consequence of the homogeneous and constant shortening of the ERP, the time course of REFR mainly was determined by the nonhomogeneous alterations of ET. At a higher RMBF there were only minor electrophysiological alterations, and Ia- or Ib-arrhythmias did not emerge. These results indicate a strong relation of the Ia- and Ib-arrhythmias to the ischemia-induced time courses and dispersions of ET, REFR and CT but not of ERP within the ischemic area. Although the phases Ia relate to a strong increase of ET, REFR and CT and the Ib-arrhythmias to a partial recovery of these parameters, both the Ia- and Ib-arrhythmias seem to depend on a "critical" extent of electrophysiological inhomogeneity within a "critical" mass of ischemic but excitable myocardium.

It has been implied that the increase of myocardial extracellular potassium activity [( K+]e) in the early stage of acute myocardial ischemia is a major cause of the increased likelihood of arrhythmia after acute coronary artery occlusion. There is also experimental evidence that some calcium antagonists reduce the occurrence of ischemia-induced early ventricular arrhythmias. In order to clarify the antiarrhythmic effect of gallopamil during the early phase of acute LAD occlusion, the influence of this calcium antagonist on the time course of [K+]e during acute ischemia was measured in open-chest anesthetized dogs using a K+-selective surface multielectrode. The regional myocardial blood flow was determined with 9 micron radioactive tracer microspheres. After application of gallopamil (bolus 25 micrograms/kg and infusion 2.5 micrograms/kg.min for 30 min) the maximal and mean rate of rise of [K+]e as well as the plateau of [K+]e reached during ischemia were significantly diminished compared with the control occlusions. 90 min after gallopamil, the rate of rise of [K+]e as well as the plateau of [K+]e reached were still significantly reduced, but 180 min after the gallopamil application, no significant differences between the time course of [K+]e and that of the two control occlusions could be found. Gallopamil significantly elevated myocardial blood flow in the non-ischemic area, but did not influence blood flow in the ischemic region. While collateral perfusion remains unchanged, the slowed and reduced increase of myocardial [K+]e during acute coronary artery occlusion may be an important component of the antiarrhythmic effect of gallopamil during early ischemia.

Recent reports have shown considerably differing results for myocardial shunting of 9 microns and 15 microns tracer microspheres (TMs) under various conditions. This could restrict the use of TMs for myocardial, especially collateral blood flow measurements. To determine the importance of coronary collateral blood flow and its early changes during the first 30 minutes after acute coronary artery occlusion (i.e. the 1st arrhythmic phase), we studied the shunting of 9 microns and 15 microns TMs from the ischemic myocardium during acute LAD ligation. In anesthetized dogs these TMs and subsequently Ringer solution were infused into the occluded coronary artery just distal to the ligation with constant low perfusion pressure. TM shunting (%S) into the lungs was then determined (%S = total lung radioactivity . 100/radioactivity infused). During a single LAD occlusion lasting 35 minutes (series I, n = 10) 9 microns TMs were infused immediately and 30 minutes after ligation, 15 microns TMs being infused after 15-20 minutes. In series II (n = 6) 9 microns TMs were infused immediately during the 1st, short (5 minutes) LAD occlusion. Following 90 minutes of reperfusion a 2nd LAD ligation (35 minutes) was performed with 9 microns TMs being infused immediately and 30 minutes after occlusion. During the first 30 minutes of acute coronary artery occlusion, TM shunting from the ischemic myocardium is negligible for 15 microns TMs (%S less than 0.5%; n = 5), whereas the mean 9 microns TM shunt of the early applied TM (i.e. A1, series I; n = 9; B2, series II; n = 6) amounts to a maximum of 1.21 +/- 0.2% (X +/- SEM). After 30 minutes of occlusion the mean 9 microns TM shunt amounts only to 0.71 +/- 0.15% (i.e. C1, series I; n = 4; C2, series II; n = 4). - In a coronary artery occlusion repeated once, 9 microns TM shunting, while increasing slightly due to the 90 minutes of reperfusion, still amounts to only 1.73 +/- 0.41% (n = 6). In three experiments 9 microns TMs were infused into the unoccluded, normally perfused LCX coronary artery during LAD occlusion. The mean LCX shunt value of 4% after a mean time of 25 minutes following TM infusion is in very good agreement with the 9 microns TM shunt values in the literature. These results clearly demonstrate that the TM technique with 9 microns microspheres is suitable for measuring changes in coronary collateral blood flow at least for a short time period after acute coronary artery occlusion.

An attempt was made in a survey‐type trial to combine perennial ryegrass with cocksfoot, meadow fescue and timothy together in the same sward, without the association being dominated by the ryegrass. It is concluded from this work that such non‐dominant ryegrass swards can be obtained by limiting the seeding rate of the ryegrass to 1 lb. per acre in a seeds mixture sown at the rate of about 20 lb. per acre.

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