The Pathophysiology And Treatment Of Subarachnoid Hemorrhage In The Cynomolgus Monkey

Author : Charles Sheldon Rothberg
Publisher :
ISBN 13 :
Total Pages : 0 pages
Book Rating : 4.:/5 (144 download)

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Download or read book Pathophysiology and Treatment of Subarachnoid Hemorrhage in the Cynomolgus Monkey written by Charles Sheldon Rothberg and published by . This book was released on 1979 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: In an experimental model using the cynomolg the pathophysiological responses to induced suba hemorrhage and the effectiveness of treatment of subsequent cerebrovascular abnormalities were st Using the intra-arterial 133 Xenon clearanc for regional cerebral blood flow measurement, th work involves two major investigations. In the f pathophysiological responses to increasing volum subarachnoid blood were documented. Comparative the acute effects of increasing volumes of subdu and of subarachnoid injections of a large volume artifical CSF were also performed. The second major investigation concerned th effectiveness of the treatment combination of so nitroprusside and phenylephrine in improving cer flow, cerebrovascular resistance, cerebral vasos neurological grade post-subarachnoid and post-su hemorrhage. Subarachnoid hemorrhage caused a reduction cerebral blood flow which was more marked and mo persistent in the larger hemorrhage volume group the immediate post-hemorrhage period (ca 2 1/2 h regional cerebral blood flow generally recovered lower hemorrhage volume groups, whereas in the 1 us monkey rachnoid the udied. a technique e reported irst, the es of studies of ral blood, of e di um ebral blood pasm and bdural in regional re s. During ours) in the arger volume groups it remained low for the duration of the experiment. Other significant experimental findings in the immediate post-hemorrhage period were: decreased cerebral perfusion pressure; increased cerebrovascular resistance; cerebral vasospasm, and elevated intracranial pressure. The larger hemorrhage volume groups showed a more marked and a longer duration of elevation of cerebrovascular resistance, and a longer duration of elevated intracranial pressure. Cerebral vasospasm was initially similar for these groups, but after 2 1/2 hours a better recovery of vessel caliber was demonstrated by the lower hemorrhage volume groups. Cerebral perfusion pressure recovered in all groups. Following the insult in the subdural hemorrhage groups regional cerebral blood flow was unchanged for the lower volume group but decreased at the larger hemorrhage volume. Cerebral perfusion pressure was reduced in the immediate post-hemorrhage period but subsequently recovered for both groups. Cerebrovascular resistance was increased for the larger hemorrhage volume group but reduced for animals receiving the lower volume. Vasospasm was present in both groups in the post-insult period, and to the same degree as for corresponding volume subarachnoid hemorrhage groups. After 2 1/2 hours, vessel caliber recovery was more complete in the smaller volume subdural hemorrhage group than for the larger volume group. The magnitude of intracranial pressure elevation in these groups was also similar to that in the subarachnoid hemorrhage groups but was of shorter duration In the post-insult period for the group receiving artificial CSF there was a minimal reduction in regional cerebral blood flow, no change in cerebral perfusion pressure, and minimal increase in cerebrovascular resistance. No change in vessel caliber was found. Intracranial pressure elevation was similar to, but of shorter duration than that occurring in the subarachnoid and subdural hemorrhage groups. Post-insult apnea was a experimental studies, the du was greater in the larger su groups. finding common to all our ration and frequency of which barachnoid hemorrhage volume In general, during the post-insult period, we found hypoxemia, hypocapnia and elevated alveolar-arterial oxygen differences which were more marked and of longer duration in the larger subarachnoid hemorrhage volume groups. The changes observed in arterial oxygenation were directly related to the duration of elevation of intracranial pressure and of right ventricular pressure. These findings generally correlated well with the pulmonary pathology, consisting of intra-alveolar and interstitial edema. In general, those animals receiving large volumes of subarachnoid blood fared worse in all respects than animals in other groups. In these investigations a total of six animals died acutely (within five hours of the intracranial insult) all with large subarachnoid hemorrhage volumes. These animals demonstrated decreases in regional cerebral blood flow, increases in cerebrovascular resistance, decreases in arterial oxygen and increases in alveolar-arterial oxygen difference of greater magnitude than the surviving animals. The degree of vasospasm was not different for the two subgroups. In the second major investigation regional cerebral blood flow was significantly decreased following both subarachnoid and subdural hemorrhage insults. During the combination treatment regime of sodium nitroprusside and phenylephrine, administered post-hemorrhage, regional cerebral blood flow remained significantly reduced, cerebral perfusion pressure remained low, cerebrovascular resistance elevation was persistent and cerebral vasospasm unchanged. The post-insult cerebrovascular abnormalities were not different from those in the large hemorrhage volume untreated groups. Following cessation of treatment, cerebral perfusion pressure recovered, regional cerebral blood flow remained significantly below control, cerebrovascular resistance was elevated and cerebral vasospasm was peristent. No difference in the neurological grade or survival was found between the same insult volume treated and untreated groups. In the experimental group that was treated but did not receive an intracranial insult, regional cerebral blood flow and cerebral perfusion pressure were slightly diminished, cerebrovascular resistance was unchanged and no cerebral vessel spasm or vasodilation was observed. On completion of the therapy, both regional cerebral blood flow and cerebral perfusion pressure remained low, while cerebrovascular resistance and vessel caliber remained unchanged. Our experimental findings suggest the following conclusions: 1. Subarachnoid hemorrhage is associated with reduced cerebral blood flow, elevated cerebrovasular resistance and cerebral vasospasm. 2. Subarachnoid hemorrhage impairs autoregulation. 3. The treatment regime of sodium nitroprusside and phenylephrine: (i)is ineffective in improving both post subarachnoid hemorrhage and post-subdural hemorrhage reduced cerebral blood flow, elevated cerebrovascular resistance and cerebral vasospasm. (ii)impairs autoregulation (iii)can be toxic (lethal) 4. Cerebral vasospasm plays only a small part in the reduction of cerebral blood flow and elevation of cerebrovascular resistance, with the cerebral microcirculation playing the major role. 5. Pulmonary pathology, giving rise to poor arterial oxygenation, and respiratory centre dysfunction evidenced by post-insult apnea and other respiratory pattern aberrations, are present in the period immediately following both subarachnoid and subdural hemorrhages. These pathophysiological responses are directly related to the duration of elevation of the intracranial pressure. 6. Morbidity and mortality from subarachnoid hemorrhage are, at least in part, related either singly or in combination to reduced cerebral perfusion, poor arterial oxygenation and respiratory centre dysfunction.