scholarly journals The Effect of Infusions of Adrenaline, Noradrenaline and Dopamine on Cerebral Autoregulation under Isoflurane Anaesthesia in an Ovine Model

2003 ◽  
Vol 31 (3) ◽  
pp. 259-266 ◽  
Author(s):  
J. A. Myburgh ◽  
R. N. Upton ◽  
C. Grant ◽  
A. Martinez

The effects of infusions of adrenaline, noradrenaline and dopamine on cerebral autoregulation under steady-state isoflurane anaesthesia were compared with the awake state. Six studies each were conducted in two cohorts of adult ewes: awake sheep and those anaesthetized with 2% isoflurane anaesthesia. In random order, each animal received ramped infusions of adrenaline, noradrenaline (0-40 μg/min) and dopamine (0-40 μg/kg/min). Cerebral blood flow was measured continuously from changes in Doppler velocities in the sagittal sinus. Autoregulation was determined by linear regression analysis between cerebral blood flow and mean arterial pressure. Isoflurane did not significantly alter cerebral blood flow relative to pre-anaesthesia values (P>0.05). All three catecholamines significantly and equivalently increased MAP from baseline in a dose dependent manner in both the awake and isoflurane cohorts. Although adrenaline significantly increased cerebral blood flow from baseline in the awake cohort (P< 0.01), none of the catecholamines significantly increased cerebral blood flow during isoflurane anaesthesia. No significant differences were demonstrated between the slopes and intercepts of regression lines for adrenaline, noradrenaline and dopamine within either cohort (ANCOVA). Inter-cohort comparisons between the two autoregulation curves demonstrated no significant difference between the slopes of the autoregulation curves for the awake (pooled slope=0.39) and isoflurane cohorts (pooled slope=0.28) (P>0.05). Over a specific dose range, systemic hypertension induced by adrenaline, noradrenaline and dopamine did not significantly increase cerebral blood flow under 2% isoflurane anaesthesia. The concomitant administration of isoflurane and the catecholamines was not associated with altered autoregulatory function compared to the awake state.

2002 ◽  
Vol 30 (4) ◽  
pp. 413-421 ◽  
Author(s):  
J. A. Myburgh ◽  
R. N. Upton ◽  
G. L. Ludbrook ◽  
A. Martinez ◽  
C. Grant

Propofol and isoflurane are commonly used in neuroanaesthesia. Some published data suggest that the use of these agents is associated with impaired cerebral blood flow/carbon dioxide (CO 2 ) reactivity. Cerebrovascular CO 2 reactivity was therefore measured in three cohorts of adult merino sheep: awake (n=6), anaesthetized with steady-state propofol (15 mg/min; n=6) and anaesthetized with 2% isoflurane (n=6). Changes in cerebral blood flow were measured continuously from changes in velocities of blood in the sagittal sinus via a Doppler probe. Alterations in the partial pressure of carbon dioxide in arterial blood (P a CO 2 ) over the range 18–63 mmHg were achieved by altering either the inspired CO 2 concentration or the rate of mechanical ventilation. Cerebral blood flow/CO 2 relationships were determined by linear regression analysis, with changes in cerebral blood flow expressed as a percentage of the value for a P a CO 2 of 35 mmHg. Propofol decreased cerebral blood flow by 55% relative to pre-anaesthesia values (P=0.0001), while isoflurane did not significantly alter cerebral blood flow (88.45% of baseline, P=0.39). Significant linear relationships between cerebral blood flow and CO 2 tension were determined in all individual studies (r 2 ranged from 0.72 to 0.99). The slopes of the lines were highly variable between individuals for the awake cohort (mean 4.73, 1.42–7.12, 95% CI). The slopes for the propofol (mean 2.67, 2.06–3.28, 95% CI) and isoflurane (mean 2.82, 2.19–3.45, 95% CI) cohorts were more predictable. However, there was no significant difference between these anaesthetic agents with respect to the CO 2 reactivity of cerebral blood flow.


1997 ◽  
Vol 17 (12) ◽  
pp. 1309-1318 ◽  
Author(s):  
Naoaki Horinaka ◽  
Tang-Yong Kuang ◽  
Hazel Pak ◽  
Robert Wang ◽  
Jane Jehle ◽  
...  

The possibility that adenosine and ATP-sensitive potassium channels (KATP) might be involved in the mechanisms of the increases in cerebral blood flow (CBF) that occur in insulin-induced hypoglycemia was examined. Cerebral blood flow was measured by the [14C]iodoantipyrine method in conscious rats during insulin-induced, moderate hypoglycemia (2 to 3 mmol/L glucose in arterial plasma) after intravenous injections of 10 to 20 mg/kg of caffeine, an adenosine receptor antagonist, or intracisternal infusion of 1 to 2 μmol/L glibenclamide, a KATP channel inhibitor. Cerebral blood flow was also measured in corresponding normoglycemic and drug-free control groups. Cerebral blood flow was 51% higher in untreated hypoglycemic than in untreated normoglycemic rats ( P < 0.01). Caffeine had a small, statistically insignificant effect on CBF in normoglycemic rats, but reduced the CBF response to hypoglycemia in a dose-dependent manner, i.e., 27% increase with 10 mg/kg and complete elimination with 20 mg/kg. Chemical determinations by HPLC in extracts of freeze-blown brains showed significant increases in the levels of adenosine and its degradation products, inosine and hypoxanthine, during hypoglycemia ( P < 0.05). Intracisternal glibenclamide had little effect on CBF in normoglycemia, but, like caffeine, produced dose-dependent reductions in the magnitude of the increases in CBF during hypoglycemia, i.e., +66% with glibenclamide-free artificial CSF administration, +25% with 1 μmol/L glibenclamide, and almost complete blockade (+5%) with 2 μmol/L glibenclamide. These results suggest that adenosine and KATP channels may play a role in the increases in CBF during hypoglycemia.


2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Marike Zwienenberg ◽  
Kee D Kim ◽  
Kiarash Shahlaie

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity


2021 ◽  
Author(s):  
Laurent Guillon ◽  
Marc Kermorgant ◽  
Thomas Charvolin ◽  
Fabrice Bonneville ◽  
Marie-Pierre Bareille ◽  
...  

Abstract Purpose Neuro-ophthalmological changes defined as spaceflight-associated neuro-ocular syndrome have been reported after long duration space flights. The pathophysiology of this syndrome remains unclear, with the possible involvement of elevated intracranial pressure. Changes in blood flow in the brain, evaluated indirectly by Doppler, have been reported in flight. However, the effects of microgravity on regional cerebral blood flow (rCBF) are not known. We therefore investigated changes in rCBF in a 5-day dry immersion (DI) model. Moreover, we tested thigh cuffs as a countermeasure to prevent potential microgravity-induced modifications in rCBF.Methods 18 healthy male participants underwent 5-day DI with or without a thigh cuffs countermeasure. They were randomly allocated to a control (n = 9) or cuffs (n = 9) group. rCBF was measured 4 days before DI (Pre-DI) and at the end of the fifth day of DI (Post-DI), using single-photon emission computed tomography (SPECT) with radiopharmaceutical 99mTc-hexamethyl propylene amine oxime (HMPAO). SPECT images were processed using statistical parametric mapping (SPM12) software.Results At DI5, we observed a significant decrease in rCBF in 32 cortical and subcortical patterns, with greater hypoperfusion in the occipital region (occipital peak level: z = 4.51, puncorr < 0.001) and basal ganglia (putamen peak level: z = 4.71, puncorr < 0.001; caudate nuclei peak level: z = 3.80, puncorr < 0.001). No significant difference was found between the control and cuffs groups on variations in rCBF at DI5.Conclusion 5-day DI induces a relative decrease in rCBF in cortical and subcortical regions. Nevertheless, the consequences of this decrease for brain function and mechanisms need further investigation.


Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
E B Gould ◽  
Rebecca McCourt ◽  
Sana Vahidy ◽  
Negar Asdaghi ◽  
Michael D Hill ◽  
...  

Background: Treatment of hypertension during acute intracerebral hemorrhage (ICH) is controversial. There are concerns that in the context of disrupted cerebral autoregulation, blood pressure (BP) reduction may cause decreased cerebral blood flow (CBF), particularly in the perihematoma region. CBF was assessed using serial CT perfusion (CTP) studies. We hypothesized that CBF would remain stable following BP reduction. Methods: Acute primary ICH patients were imaged pre and post BP treatment. Perfusion maps were calculated from CTP source images. Mean CBF was measured in a 1cm perihematoma region, contralateral homologous regions and in both hemispheres. Mean cerebral blood volume (CBV), mean transit time (MTT), and time to drain (TTD) were calculated in the same manner. Relative measures (i.e. rCBF) were calculated as ratios/differences between ipsilateral and contralateral regions. Results: Sixteen patients (median age 75 (54-91)) were imaged with CTP (median time from onset 19.4 (2.0-72.2) h) and re-imaged 2.0 (1.1-3.3) h later. Median NIHSS at baseline was 9 (2-24); this remained stable at the time of the second CTP (10 (2-24), P=0.14). Baseline hematoma volume was 24.8±19.9 ml and there was no change at the time of the second CTP (26.3±22.1 ml, P=0.16). Patients were recruited from an ongoing trial, in which they were randomly treated to a target systolic BP of <150mmHg (n=9) or <180mmHg (n=7). Four patients received no antihypertensives as BP was below target at the time of randomization. Mean systolic BP in treated patients (n=12) decreased significantly between the first (165±23 mmHg) and second (143±18 mmHg, P<0.0001) CTP scans. Mean perihematoma CBF in treated patients was stable with BP reduction (pre=35.1±7.1 vs. post=35.4±6.2 ml/100g/min, P=0.87). Ipsilateral hemispheric CBF was also stable (pre=47.3±7.2 vs. post=46.4±7.1 ml/100g/min, P=0.66). Although perihematoma CBF was lower than in contralateral homologous regions (rCBF=0.72±0.11), BP reduction did not decrease this further (0.74±0.14 post-treatment, P=0.58). Ipsilateral hemispheric rCBF (0.96±0.06) was also unaffected by BP treatment (0.95±0.08, P=0.64). Perihematoma rCBF decreased in 5 treated patients, but never by >12%. Linear regression showed no relationship between changes in systolic BP and perihematoma rCBF (R=-0.002, [-0.005, 0.001], P=0.18). Perihematoma rCBV (pre=0.77±0.11 vs. post=0.79±0.10, P=0.20), rMTT (pre=0.51±0.54s vs. post=0.70±0.65s, P=0.26) and rTTD (pre=0.71±1.01s vs. post=0.89±0.84s, P=0.42) also remained stable following BP treatment. Conclusions: Acute BP reduction does not appear to exacerbate perihematoma oligaemia. Stability of CBF following acute BP treatment suggests preservation of cerebral autoregulation in ICH, within the range of arterial pressures studied. These findings support the safety of early BP treatment in ICH.


2019 ◽  
pp. 3-3
Author(s):  
Peter Novak

This chapter lists the main syndromes and patterns seen during autonomic testing, based on classification according to physiology and/or functional anatomy. Although the classification is arbitrary, it is useful in that it allows the diagnostician to see classify patterns in test results that assist in the correct interpretation of the results. Presented in a series of easy to access lists, the most common patterns are autonomic failure, autonomic overactivity, paroxysmal dysautonomia orthostatic hypotension syncope, hyperventilation, cerebral hypoperfusion, cerebral blood flow velocity, and cerebral autoregulation disorders.


2020 ◽  
Vol 9 (12) ◽  
pp. 4088
Author(s):  
Shyan-Lung Lin ◽  
Shoou-Jeng Yeh ◽  
Ching-Kun Chen ◽  
Yu-Liang Hsu ◽  
Chih-En Kuo ◽  
...  

Postural orthostatic tachycardia syndrome (POTS) typically occurs in youths, and early accurate POTS diagnosis is challenging. A recent hypothesis suggests that upright cognitive impairment in POTS occurs because reduced cerebral blood flow velocity (CBFV) and cerebrovascular response to carbon dioxide (CO2) are nonlinear during transient changes in end-tidal CO2 (PETCO2). This novel study aimed to reveal the interaction between cerebral autoregulation and ventilatory control in POTS patients by using tilt table and hyperventilation to alter the CO2 tension between 10 and 30 mmHg. The cerebral blood flow velocity (CBFV), partial pressure of end-tidal carbon dioxide (PETCO2), and other cardiopulmonary signals were recorded for POTS patients and two healthy groups including those aged >45 years (Healthy-Elder) and aged <45 years (Healthy-Youth) throughout the experiment. Two nonlinear regression functions, Models I and II, were applied to evaluate their CBFV-PETCO2 relationship and cerebral vasomotor reactivity (CVMR). Among the estimated parameters, the curve-fitting Model I for CBFV and CVMR responses to CO2 for POTS patients demonstrated an observable dissimilarity in CBFVmax (p = 0.011), mid-PETCO2 (p = 0.013), and PETCO2 range (p = 0.023) compared with those of Healthy-Youth and in CBFVmax (p = 0.015) and CVMRmax compared with those of Healthy-Elder. With curve-fitting Model II for POTS patients, the fit parameters of curvilinear (p = 0.036) and PETCO2 level (p = 0.033) displayed significant difference in comparison with Healthy-Youth parameters; range of change (p = 0.042), PETCO2 level, and CBFVmax also displayed a significant difference in comparison with Healthy-Elder parameters. The results of this study contribute toward developing an early accurate diagnosis of impaired CBFV responses to CO2 for POTS patients.


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