SUMMARY Regional cerebral blood flow (rCBF) was measured by the '"Xenon inhalation method in a selected group of 44 normal non-hospitalized, normotensive subjects aged 19 to 79 years. rCBF was computed as the initial slope index value (ISI). Advancing age was associated with significant reductions in the mean brain and mean hemispheric ISI as well as in individual ISI levels measured from all areas in both hemispheres. Our findings suggest that decline of rCBF is not limited to normal elderly subjects but that it is a progressive phenomenon which begins at an earlier age.

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Fifty-two stroke patients, 43 with cerebral ischemia and nine with cerebral hemorrhage, underwent continuous cardiac monitoring in an Intensive Stroke Care Unit shortly after the onset of the acute cerebrovascular accident. In the group of patients with no evidence of pre-existing heart disease, eight of 18 with cerebral ischemia and five of seven with hemorrhage developed ECG abnormalities. Additional ECG changes were noted in 21 of 25 patients with cerebral ischemia and two of two with hemorrhage who were known to have previous heart disease. Both disturbances in rhythm and conduction and "ischemic" ST-T alterations were detected and the frequency of the former exceeded that of the latter. The ECG alterations were transient in 32 patients and permanent in four. New electrocardiographical abnormalities in patients without evidence of heart disease prior to the stroke were associated with poorer prognosis. The pathogenetic mechanisms leading to the appearance of cardiac abnormalities in stroke patients are considered.

in infants with coarctation of the aorta. J Thorac Vase Surg 81: [323][324][325] 1981 8. Liberfhson RR: Congenital Heart Disease in the Child, Adolescent and Adult Patient. In: The Practice of Cardiology, Johnson RA, Haber E, Austin WG (eds.) Boston, Little Brown, 1980, pp. 760-761 during 30 minutes of recirculation. They also observed a marked (3-fold) increase in the relative content of arachidonic acid. During the recirculation period following ischemia the neurophysiological and metabolic functions might be restored if no irreversible cell damage occurred. A prerequisite for recovery is an adequate perfusion, whereas immediate or delayed perfusion defects might be the cause for irreversibility of brain function.14 ' I5Hossmann 16 reviewed various factors that may contribute to delayed hypoperfusion thus increasing the primary ischemic region. Among these factors are blood coagulation and vascular spasm.The maintenance of normal tissue perfusion depends on a balanced interaction of two prostaglandins which have opposite effects at the blood-endothelial interface, namely thromboxane A 2 (TXA 2 ) and prostaglandin I 2 (PGI 2 ). 17 ' 18 Both prostaglandins have the same precursor, cyclic-endoperoxide (PGH 2 ), but while TXA 2 is a potent platelet aggregator and vasoconstrictor, 19 PGI 2 inhibits platelet aggregation and is a vasodilator. 20 Thus, any interruption in the balanced production of these compounds which might result in an increase of TXA 2 could diminish local blood flow. Hallenbeck and Furlow 21 have shown that dogs exposed to complete ischemia had low post ischemic blood flow with focal zones of greatly impaired reperfusion. A significant increase in the blood flow during the post ischemic period was observed in animals receiving either indomethacin prior to ischemia or a combination of indomethacin and PGI 2 after ischemia. Gaudet and Levine have demonstrated that gerbils pre- The Effect of Incomplete Cerebral Ischemia on Prostaglandin Levels in Rat BrainE, SHOHAMI, PH.D., J. ROSENTHAL, M.SC, AND S. LAW, M.D.* SUMMARY Rats were subjected to severe incomplete cerebral ischemia followed by recirculation. The levels of several of the cyclooxygenase products of arachidonic acid were measured at 5 and 15 minutes of ischemia and at 30 minutes of recirculation following 15 minutes of ischemia, PGE 2 accumulated during the first 5 min. of ischemia and its level declined at 15 min. and returned to control level at 30 min. of recirculation. TXB 2 , on the other hand, increased during the whole time course of the experiment and at the end of the post ischemic period its level was 5 times higher than control. Treatment of the animals with indomethacin (4 mg/Kg, i.v.) prior to ischemia reduced the levels of these products without altering the pattern of their changes. During the ischemic period the EEG was isoelectric and the mean recovery time of electrical cortical activity after 15 min. of ischemia was 10.4 ± 3.5 min. in the control rats. The rats which received indomethacin recovered faster (4.3 ± 0....

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