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B R Clower

Publications and source records attributed to B R Clower.

49 records · Page 3Linked to original sources
PubMedDate not supplied

The hippocampus and stress induced 17-OHCS elevations.

The physiologic contribution of the limbic brain to emotionally induced stress is still poorly understood. The present study is designed to more specifically evaluate the role of the hippocampus in stress induced plasma 17-OHCS elevations. The conditional reflex to a sequential presentation of tone and shock was used as the stress agent in adult mongrel dogs. Plasma 17-OHCS levels were determined by the Porter-Silber method. Control and stress levels of 17-OHCS were determined before and after unilateral (left) hippocampectomy, and subsequent contralateral (right) hippocampectomy. A unilateral posterior hippocampal lesion partially attenuated (20%) the normal 17-OHCS stress response. In contrast to unilateral lesions, equivalent bilateral posterior hippocampal lesions abolished the normal 17-OHCS stress response. These observations support the thesis that the elevated 17-OHCS levels in response to the conditioning paradigm is dependent on the hippocampus. Furthermore, it is dependent upon the continuity of the hippocampal circuit and not upon the volumetric steroid binding capacity of the hippocampus. These studies also suggest that a unilaterally functioning hippocampus may be adequate to meet the physiologic needs of stress, as reflected by the 17-OHCS response.

11-Hydroxycorticosteroids↗
PubMedDate not supplied

Limbic hypertension induced by stress and septal stimulation. Stress-locked-in hypertension.

For this study, it was postulated that hypertension of emotional origin is generated within the limbic system. To validate this thesis, septal induced blood pressure elevations were combined with a stressful experience in adult rats (spontaneously hypertensive and Wistar Kyoto rats). Stress consisted of intermittent confinement in a plexiglass tube. The results revealed that hypertension induced by electric stimulation of the septum during the stressful state could subsequently be elicited by the stressful state alone, without electric stimulation of the septum. It was postulated that the cortically modulated stress circuit converged with the electrically activated limbic pressor circuit at the level of the septum. This convergence resulted in the formation of one cortico-limbic circuitry which could be activated by stress alone. This underlying mechanism may be considered as a model of neural sensitization in the production of stress-induced limbic hypertension.

Animals↗
PubMedDate not supplied

Constrictive endarteropathy following experimental subarachnoid hemorrhage.

Rhesus monkeys were subjected to subarachnoid hemorrhage by either the introduction of blood into the subarachnoid space or by mechanically rupturing the middle cerebral artery. Local cerebral blood flow, vascular compliance studies, and histological studies (light and electron microscope) were made of the vessels of all animals. In animals hemorrhaged via vascular rupture, subintimal swelling and thickening was minimally present by 3 days, becoming progressively more severe by one month. Such changes consisted of severe subintimal proliferation, fibrosis of the medial smooth muscle layer and interruption of the internal elastic membrane. Cells in the subintimal proliferative areas examined by electronmicroscopy were seen to have ultrastructural characteristics of smooth muscle. In the subarachnoid-injected hemorrhaged animals, there was no evidence of intimal proliferation or other vascular changes, which was also true of all control vessels. There was a decrease in wall elasticity of vessels exposed to mechanical rupture when compared to those exposed only to injected subarachnoid blood or normal vessels. Local cerebral blood flow was affected very little following the 2 methods of subarachnoid hemorrhage.

Animals↗
PubMedDate not supplied

The angiopathy of subarachnoid hemorrhage: angiographic and morphologic correlates.

In patients with subarachnoid hemorrhage, particularly hemorrhage due to aneurysmal rupture, there was a positive significant relation between angiographic vessel constriction and vessel pathology (angiopathy). Furthermore, there was a positive relationship between post-hemorrhage survival time and the severity of angiopathy. Factors such as age, sex, operations, steroid and CSF pressure seemed to have little affect on angiopathy following hemorrhage. Pathological changes were primarily limited to the involved major cerebral vessels themselves, with their branches rarely being affected. While intramural vascular hemorrhage was a common pathological feature in vessels showing severe pathology, the mere presence of blood surrounding an artery seemed to have little influence on vessel alterations.

Cerebral Angiography↗
PubMedDate not supplied

The angiopathy of subarachnoid hemorrhage I. Role of vessel wall catecholamines.

Subarachnoid hemorrhage (SAH) due to rupture of the right middle cerebral artery (RMCA) produced specific anatomical and biophysiological responses in the involved feline vessels. The RMCA showed morphological alterations that became progressively more severe with time and were widespread within the cerebral vascular tree. SAH also resulted in an acute depletion of vessel catecholamine levels which remained depressed over a 30 day period. When the cerebral vessels of cats were severely depleted of catecholamines (using reserpine) prior to induced SAH, morphological alterations were significantly reduced both in severity and in degree of spread within the cerebral vascular network. The results of this study suggest that the concentration of norepinephrine within the vessel at the time of hemorrhage plays a significant role in the production of the angiopathy that follows SAH.

Angiography↗