The effect of sympathetic denervation on cerebral CO2 sensitivity.
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Biomedical subjects
Publications and source records attributed to M E Raichle.
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The effect of chronic, unilateral superior cervical ganglionectomy on cerebral blood flow and blood flow autoregulaiton to changes in perfusion pressure was examined in seven phencyclidine anesthetized monkeys. Ten to 14 days prior to the experiments Doppler ultrasonic flow transducers were placed on both carotid arteries after ligation of the external carotid branches and removal of one superior cervical ganglion. Autoregulation was tested by exsanguination and metaraminol infusion with the monkeys inspiring from air, 9% and 12% carbon dioxide in air. Immediately following experimentation the cerebral vessels were examined for the presence of noradrenergic fibers. The results of the study demonstrate that: (1) superior cervical ganglionectomy produces a significant reduction in the noradrenergic innervation of ipsilateral extraparenchymal arteries: (2) the peripheral sympathetic nervous system contrivutes to overall cerebral vascular resistance primarily by affecting resistance in extraparenchymal arteries; and (3) as a result, it determines the contribution of the extraparenchymal arteries to overall cerebral blood flow autoregulation.
Thirty-one patients with acute cerebral infarction were treated with the thrombolytic agent urokinase for either a single or a double infusion period, each of ten hours. The effects of urokinase therapy administered at dosage rates of 1,200, 1,500 or 1,700 CTA urokinase units per pound of body weight per hour were followed by serial blood coagulation and other biochemical studies. In the dosage used, urokinase produced a prompt sustained increase, 20-fold to 40-fold, of plasma thrombolytic activity with relatively minor disturbance of the blood coagulation system. Nevertheless, hemorrhagic complications occurred in several patients and distinctly favorable therapeutic effects were not observed.
Plasma fibrinogen chromatography is a method for quantification of high molecular weight fibrinogen complexes (HMWFC), native fibrinogen and other fibrinogen derivatives in plasma. Enchanced formation of fibrin, intravascular coagulation, thrombus formation, etc., are reflected by elevation of plasma HMWFC, and the method distinguishes between subjects with normal and pathological rates of fibrin formation. Serial standard blood coagulation assays, including plasma fibrinogen chromatography, and neurological studies were performed on 220 patients admitted to a stroke unit. Findings from patients with cerebral infarction were compared against those of three control groups: (1)normals, (2)a stroke control group and(3)a stroke risk factor group. Plasma HMWFC findings were significantly (p less than 0.001) higher in the stroke risk factor group than in the normals. Plasma HMWFC values were significantly higher (p less than 0.001) in the cerebral infarction patients than in any of the control groups, and plasma fibrinogen, plasminogen, alpha1-antitrypsin and alpha2-macroglobulin also were significiantly higher (p less than 0.001) in the patients. The greater the degree of initial neurological deficit, the greater were plasma HMWFC values (p less than 0.001), and high HMWFC values were associated with poor clinical outcome. Plasma HMWFC values were significantly higher (p less than 0.001) in patients with intracerebral hemorrhage, subarachnoid hemorrhage and cerebral embolism. These findings docunment the fact that a high proportion of stroke patients have coagulopathy, characterized by pathological enhancement of fibrin formation.