scholarly journals Cerebral Circulatory Effects of a Dopaminergic Agonist (Apomorphine) in the Dog

1982 ◽  
Vol 2 (3) ◽  
pp. 369-372 ◽  
Author(s):  
Ph. Jauzac ◽  
A. Blasco ◽  
F. Vigoni ◽  
P. Valdiguie ◽  
A. Bès

Dopaminergic influence upon cerebral circulation was studied in 12 adult mongrel dogs, local cerebral blood flow (lCBF) being measured by the microspheres method. The intravenous injection of apomorphine (0.1 mg/kg) produced heterogeneous effects on lCBF; an increase in lCBF reaching the level of statistical significance was observed in frontal and sensory motor cortices, whereas blood flow was not significantly altered in the other regions examined. When the animals are considered individually, a widespread response was generally observed. Local cerebral blood flow increased from 16% to 85% (depending on the regions examined) in 4 animals, and tended to decrease (particularly in the caudate nucleus) in the 8 others. These opposite effects cannot be related with changes in general metabolic or hemodynamic parameters (Paco2, Pao2, pH, and arterial pressure). It is thus concluded that the effect of dopaminergic stimulation upon cerebral circulation is more complex than previously reported. These effects could only be partly mediated via vascular receptors and could be the result of modifications of the local metabolic level.

1984 ◽  
Vol 4 (1) ◽  
pp. 88-95 ◽  
Author(s):  
Tsuyoshi Maekawa ◽  
Concezione Tommasino ◽  
Harvey M. Shapiro

Local cerebral blood flow (LCBF) was evaluated with the [14C]iodoantipyrine quantitative autoradiographic technique in 29 brain structures in conscious control rats and during fentanyl-induced electroencephalographic (EEG) spike and/or seizure activity and in the postseizure EEG suppression phase. During spike activity, LCBF increased in all structures; the increase reached statistical significance (p < 0.05) in the superior colliculus, sensorimotor cortex, and pineal body (+ 130%, + 187%, and + 185% from control, respectively). With progressive development of seizure activity, LCBF significantly increased in 24 brain structures (range, +58% to +231% from control). During the postseizure EEG suppression phase, LCBF remained elevated in all structures (+80% to +390% from control). The local cerebrovascular resistance (LCVR) significantly decreased in 10 of 29 structures with the onset of spike activity (range, –24% to –64%), and remained decreased in all brain structures during seizure activity (range, –34% to –67%) and during the EEG suppression phase (range, –24% to –74%). This reduction of LCVR represents a near maximal state of cerebrovasodilation during fentanyl-induced EEG seizure or postseizure suppression activity. The global nature of the LCBF elevation indicates that factors other than local metabolic control are responsible for CBF regulation during local seizure activity.


2018 ◽  
Vol 08 (03) ◽  
Author(s):  
Yasuyuki Matsuura ◽  
Toru Tanimura ◽  
Daisuke Iida ◽  
Hiroki Takada

1988 ◽  
Vol 10 (3) ◽  
pp. 151-155 ◽  
Author(s):  
Bruce I. Tranmer ◽  
Cordell E. Gross ◽  
Geoff R. Adey ◽  
Ted S. Keller ◽  
Ken Nagata ◽  
...  

1992 ◽  
Vol 114 (1) ◽  
pp. 974-977
Author(s):  
G. A. Chernysheva ◽  
M. B. Plotnikov ◽  
�. A. Bisenieks ◽  
N. V. Makarova ◽  
Ya. R. Uldriks ◽  
...  

2018 ◽  
Vol 129 (1) ◽  
pp. 241-246 ◽  
Author(s):  
Aditya Vedantam ◽  
Claudia S. Robertson ◽  
Shankar P. Gopinath

OBJECTIVEFew studies have reported on changes in quantitative cerebral blood flow (CBF) after decompressive craniectomy and the impact of these measures on clinical outcome. The aim of the present study was to evaluate global and regional CBF patterns in relation to cerebral hemodynamic parameters in patients after decompressive craniectomy for traumatic brain injury (TBI).METHODSThe authors studied clinical and imaging data of patients who underwent xenon-enhanced CT (XeCT) CBF studies after decompressive craniectomy for evacuation of a mass lesion and/or to relieve intractable intracranial hypertension. Cerebral hemodynamic parameters prior to decompressive craniectomy and at the time of the XeCT CBF study were recorded. Global and regional CBF after decompressive craniectomy was measured using XeCT. Regional cortical CBF was measured under the craniectomy defect as well as for each cerebral hemisphere. Associations between CBF, cerebral hemodynamics, and early clinical outcome were assessed.RESULTSTwenty-seven patients were included in this study. The majority of patients (88.9%) had an initial Glasgow Coma Scale score ≤ 8. The median time between injury and decompressive surgery was 9 hours. Primary decompressive surgery (within 24 hours) was performed in the majority of patients (n = 18, 66.7%). Six patients had died by the time of discharge. XeCT CBF studies were performed a median of 51 hours after decompressive surgery. The mean global CBF after decompressive craniectomy was 49.9 ± 21.3 ml/100 g/min. The mean cortical CBF under the craniectomy defect was 46.0 ± 21.7 ml/100 g/min. Patients who were dead at discharge had significantly lower postcraniectomy CBF under the craniectomy defect (30.1 ± 22.9 vs 50.6 ± 19.6 ml/100 g/min; p = 0.039). These patients also had lower global CBF (36.7 ± 23.4 vs 53.7 ± 19.7 ml/100 g/min; p = 0.09), as well as lower CBF for the ipsilateral (33.3 ± 27.2 vs 51.8 ± 19.7 ml/100 g/min; p = 0.07) and contralateral (36.7 ± 19.2 vs 55.2 ± 21.9 ml/100 g/min; p = 0.08) hemispheres, but these differences were not statistically significant. The patients who died also had significantly lower cerebral perfusion pressure (52 ± 17.4 vs 75.3 ± 10.9 mm Hg; p = 0.001).CONCLUSIONSIn the presence of global hypoperfusion, regional cerebral hypoperfusion under the craniectomy defect is associated with early mortality in patients with TBI. Further study is needed to determine the value of incorporating CBF studies into clinical decision making for severe traumatic brain injury.


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