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Axillary buds of pea (Pisum sativum L. cv. Alaska) do not grow on intact plants. Dormant axillary buds can be stimulated to grow rapidly after decapitation. Here, we isolated cDNAs of PCNA, cyclinB, cyclinD, and cdc2 from pea. The mRNA expression levels of these genes were very low in dormant axillary buds, whereas they remarkably increased after decapitation. Based on the mRNA accumulation patterns of these genes, we found that most cells in dormant axillary buds are arrested at the Gi phase in the cell cycle. There are four buds at the second node on pea seedlings. After decapitation, mRNAs became abundant in the large and small buds and were kept during the following 3 d. After 4 d, mRNAs were still present in the large bud, but not in the small bud. However, after removal of the large bud, the mRNA levels started to increase again in the small bud. These mRNA accumulation patterns were the same as those after the first decapitation. These results suggested that most cells in axillary buds at the second node are arrested at the G] phase again and have the capacity to undergo multiple cycles of dormancy and growth. Moreover, in situ hybridization analyses demonstrated that PCNA mRNA increased in all parts of the axillary buds after decapitation.

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In spontaneously hypertensive rats, we studied the participation of xanthine oxidase-linked free radical in ischemia and reperfusion-induced cerebral injury, using allopurinol, a xanthine oxidase inhibitor. The loss of righting reflex was noted in some animals after a 4 hour occlusion of bilateral common carotid arteries and 19 of 25 animals died within 72 hours after reperfusion. One hour after reperfusion, the cerebral water content increased significantly, with an increase in sodium content and a decrease in potassium content. In 7 animals treated with oral administrations of allopurinol (200 mg/kg) 24 hours and 1 hour before occlusion, no death was found either during occlusion or after reperfusion, and the loss of righting reflex was noted in only one animal 24-72 hours following reperfusion. The increase in cerebral water content and accompanied changes in electrolyte contents were clearly prevented by allopurinol. These results suggest the possibility that the production of xanthine oxidase-linked free radical participates in cerebral injury due to ischemia and reperfusion in spontaneously hypertensive rats.