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Biomedical subjects

S Lavy

Publications and source records attributed to S Lavy.

98 records · Page 6Linked to original sources
PubMedDate not supplied

The effect of incomplete cerebral ischemia on prostaglandin levels in rat brain.

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, PGE2 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. TXB2, 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 (43. +/- 0.9 min) and were more resistant to the induction of ischemia. We suggest that the reversibility of cortical activity may be correlated to the accumulation of TXB2 during ischemia and recirculation, and inhibition of its synthesis might improve the post-ischemic reflow.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

The effect of chronic propranolol therapy on regional cerebral blood flow in hypertensive patients.

In 31 hypertensive patients the effect of chronic oral administration of the beta blocking agent propranolol on regional cerebral blood flow (rCBF) was studied, using the non-invasive 133Xenon inhalation technique. The results of the measurements were compared to the rCBF obtained in an age-matched normal control group. Our study shows that during long-term therapy with low doses of propranolol (less than 120 mg/daily) the rCBF is unaffected, but it is increased significantly if higher doses (greater than 120 mg/daily) are used. In all six patients who served as their own control, as they had basic rCBF measurements before or during low-dose propranolol, the rCBF on high-dose propranolol became significantly increased. The possible mechanisms which may cause the increased rCBF on high-dose propranolol are discussed.

Administration, Oral↗
PubMedDate not supplied

The effect of cerebral infarction on the regional cerebral blood flow of the contralateral hemisphere.

Regional cerebral blood flow (rCBF) measurements were performed over the contralateral hemisphere by the 133Xe intracarotid injection method in 20 patients with acute cerebral infarction in the territory of the internal carotid artery. The rCBF was found to be reduced, sometimes remarkably, in all of the patients. The mean reduction was 30 percent to 36 percent from the lowest normal value for the mean age of these patients. In the younger age group (40 to 59) the reduction was greater, 40 percent to 47 percent from the lowest normal value for this age. tthe rCBF depression was not related to cerebral dominance, previous hypertension or arterial PCO2 levels. The occurred in both patients who were fully alert and those with disturbances or consciousness, although it tended to be more diminished in the latter. tit can be assumed that the flow reduction in the nonaffected hemisphere is part of a general phenomenon affecting the entire brain and caused by globally reduced cerebral metabolism.

Acute Disease↗
PubMedDate not supplied

Regional cerebral blood flow response to hypocapnia in the contralateral hemisphere of patients with acute cerebral infarction.

The rCBF response to hypocapnia induced by active short-term hyperventilation was determined in the contralateral hemispheres of ten patients with acute unilateral cerebral infarction. Overall rCBF reduction occurred in only two patients. Regional or widespread abnormal responses to Paco2 reduction manifested as either no change or a paradoxical increase in the rCBF were observed in eight patients. The hemispheric mean rCBF reduction following hypocapnia was diminished as compared with control subjects. Our findings suggest that an impairment of the chemical control of rCBF may occur in the non-infarcted hemisphere during the early period following the onset of cerebral infarction. The pathophysiological mechanisms which may underlie this abnormal rCBF reactivity to Paco2 reduction are considered.

Acute Disease↗