scholarly journals Comparative evaluation of anesthesia methods for reconstructive carotid surgery

2020 ◽  
Vol 17 (5) ◽  
pp. 15-24
Author(s):  
M. I. Neymark ◽  
V. V. Shmelyov ◽  
Z. A. Titova ◽  
S. A. Khaustova ◽  
B. A. Shadymov

The objective: to assess the impact of total intravenous and combined anesthesia (consisting of regional block and inhalation anesthesia with sevoflurane) on higher mental functions, frequency and nature of postoperative complications in carotid endarterectomy.Subjects and methods. A total of 190 patients with ipsilateral carotid stenosis exceeding 70%, or with the unstable atheromatous plaque were examined. CE was performed in 140 (73.6%) patients, while 50 (26.4%) patients underwent plasty with the autovenous patch. 60 patients had total intravenous anesthesia. The other 60 patients had combination anesthesia (cervical plexus block as per A. Yu. Paschuk + non-inhalation anesthesia with thiopental sodium). In 70 patients, low-flow inhalation anesthesia with sevoran and potentiation of the analgesic effect by bolus administration of fentanyl was performed. The parameters of central hemodynamics, cerebral blood flow, markers of cerebral damage, and state of higher mental functions were assessed.Results. Inhalation anesthesia with sevoflurane was characterized by decrease of total peripheral resistance index by 20% (p = 0.002) and SBP by 13% (p = 0.004) compared to baseline values. Moderate reduction of afterload was accompanied by normalization of cardiac and stroke indices. Optimization of the central hemodynamic parameters led to high levels of the linear velocity of cerebral blood flow and cerebral perfusion pressure which at the main stages of the operation did not differ from the control values. At the end of the operation, a statistically significant insignificant increase in intracranial pressure was noted (on average, by 4 mm Hg exceeded values at the previous stages, p = 0.014) and levels of markers of ischemic neuronal damage: the levels of antibodies to protein S-100 increased by 14% (p = 0.043), and NSE – by 2.8 μg/L. During inhalation anesthesia with sevoflurane, the lowest number of postoperative neurological and cardiac complications was recorded; they developed only in 6 (8.6%) patients and distributed equally. However, more pronounced postoperative cognitive dysfunction was noted when this method of anesthesia was used.Conclusion. Each method of anesthesia provided an unequal level of cerebral protection from ischemic damage which was manifested by a difference in the severity of disorders of higher mental functions, the number and nature of postoperative neurological complications.

1978 ◽  
Vol 56 (2) ◽  
pp. 115-117 ◽  
Author(s):  
Lars Gustafson ◽  
Jarl Risberg ◽  
Margareth Johanson ◽  
Margareta Fransson ◽  
V. Alexander Maximilian

2013 ◽  
Vol 33 (6) ◽  
pp. 954-962 ◽  
Author(s):  
Cenk Ayata ◽  
Hwa Kyoung Shin ◽  
Ergin Dileköz ◽  
Dmitriy N Atochin ◽  
Satoshi Kashiwagi ◽  
...  

Hyperlipidemia is a highly prevalent risk factor for coronary and cervical atherosclerosis and stroke. However, even in the absence of overt atherosclerosis, hyperlipidemia disrupts endothelial and smooth muscle function. We investigated the impact of hyperlipidemia on resting-brain perfusion, fundamental cerebrovascular reflexes, and dynamic perfusion defect during acute focal ischemia in hyperlipidemic apolipoprotein E knockout mice before the development of flow-limiting atherosclerotic stenoses. Despite elevated blood pressures, absolute resting cerebral blood flow was reduced by 20% in apolipoprotein E knockout compared with wild type when measured by [14C]-iodoamphetamine technique. Noninvasive, high spatiotemporal resolution laser speckle flow imaging revealed that the lower autoregulatory limit was elevated in apolipoprotein E knockout mice (60 vs. 40 mm Hg), and cortical hyperemic responses to hypercapnia and functional activation were attenuated by 30% and 64%, respectively. Distal middle cerebral artery occlusion caused significantly larger perfusion defects and infarct volumes in apolipoprotein E knockout compared with wild type. Cerebrovascular dysfunction showed a direct relationship to the duration of high-fat diet. These data suggest that hyperlipidemia disrupts cerebral blood flow regulation and diminishes collateral perfusion in acute stroke in the absence of hemodynamically significant atherosclerosis.


2020 ◽  
pp. 0271678X2096745
Author(s):  
Zhao Liming ◽  
Sun Weiliang ◽  
Jia Jia ◽  
Liang Hao ◽  
Liu Yang ◽  
...  

Our aim was to determine the impact of targeted blood pressure modifications on cerebral blood flow in ischemic moyamoya disease patients assessed by single-photon emission computed tomography (SPECT). From March to September 2018, we prospectively collected data of 154 moyamoya disease patients and selected 40 patients with ischemic moyamoya disease. All patients underwent in-hospital blood pressure monitoring to determine the mean arterial pressure baseline values. The study cohort was subdivided into two subgroups: (1) Group A or relative high blood pressure (RHBP) with an induced mean arterial pressure 10–20% higher than baseline and (2) Group B or relative low blood pressure (RLBP) including patients with mean arterial pressure 10–20% lower than baseline. All patients underwent initial SPECT study on admission-day, and on the following day, every subgroup underwent a second SPECT study under their respective targeted blood pressure values. In general, RHBP patients showed an increment in perfusion of 10.13% (SD 2.94%), whereas RLBP patients showed a reduction of perfusion of 12.19% (SD 2.68%). Cerebral blood flow of moyamoya disease patients is susceptible to small blood pressure changes, and cerebral autoregulation might be affected due to short dynamic blood pressure modifications.


1993 ◽  
Vol 56 (3) ◽  
pp. 515-519 ◽  
Author(s):  
Rafael Astudillo ◽  
Jan van der Linden ◽  
Rolf Ekroth ◽  
Örjan Wesslén ◽  
Stefan Hallhagen ◽  
...  

2000 ◽  
Vol 93 (4) ◽  
pp. 1085-1094 ◽  
Author(s):  
Richard N. Upton ◽  
Guy L. Ludbrook ◽  
Cliff Grant ◽  
David J. Doolette

Background Thiopental and propofol are highly lipid-soluble, and their entry into the brain often is assumed to be limited by cerebral blood flow rather than by a diffusion barrier. However, there is little direct experimental evidence for this assumption. Methods The cerebral kinetics of thiopental and propofol were examined over a range of cerebral blood flows using five and six chronically instrumented sheep, respectively. Using anesthesia (2.0% halothane), three steady state levels of cerebral blood flow (low, medium, and high) were achieved in random order by altering arterial carbon dioxide tension. For each flow state, 250 mg thiopental or 100 mg propofol was infused intravenously over 2 min. To quantify cerebral kinetics, arterial and sagittal sinus blood was sampled rapidly for 20 min from the start of the infusion, and 1.5 h was allowed between consecutive infusions. Various models of cerebral kinetics were examined for their ability to account for the data. Results The mean baseline cerebral blood flows for the "high" flow state were over threefold greater than those for the low. For the high-flow state the normalized arteriovenous concentration difference across the brain was smaller than for the low-flow state, for both drugs. The data were better described by a model with partial membrane limitation than those with only flow limitation or dispersion. Conclusions The cerebral kinetics of thiopental and propofol after bolus injection were dependent on cerebral blood flow, despite partial diffusion limitation. Higher flows produce higher peak cerebral concentrations.


2002 ◽  
Vol 97 (6) ◽  
pp. 1521-1527 ◽  
Author(s):  
Andreas W. Loepke ◽  
Margaret A. Priestley ◽  
Steven E. Schultz ◽  
John McCann ◽  
Jeffrey Golden ◽  
...  

Background Despite improvements in neonatal heart surgery, neurologic complications continue to occur from low-flow cardiopulmonary bypass (LF-CPB) and deep hypothermic circulatory arrest (DHCA). Desflurane confers neuroprotection against ischemia at normothermia and for DHCA. This study compared neurologic outcome of a desflurane-based with a fentanyl-based anesthetic for LF-CPB. Methods Thirty piglets aged 1 week received either fentanyl-droperidol (F/D), desflurane 4.5% (Des4.5), or desflurane 9% (Des9) during surgical preparation and CPB. Arterial blood gases, glucose, heart rate, arterial pressure, brain temperature, and cerebral blood flow (laser Doppler flowmetry) were recorded. After CPB cooling (22 degrees C brain) using pH-stat strategy, LF-CPB was performed for 150 min followed by CPB rewarming, separation from CPB, and extubation. On postoperative day 2, functional and histologic outcomes were assessed. Results Cardiovascular variables were physiologically similar between groups before, during, and after LF-CPB. Cerebral blood flow during LF-CPB (13% of pre-CPB value) did not differ significantly between the groups. Functional disability was worse in F/D than in Des9 (P = 0.04) but not Des4.5 (P = 0.1). In neocortex, histopathologic damage was greater in F/D than in Des4.5 (P = 0.03) and Des9 (P = 0.009). In hippocampus, damage was worse in F/D than in Des9 (P = 0.01) but not Des4.5 (P = 0.08). The incidences of ventricular fibrillation during LF-CPB were 90, 60, and 10% for F/D, Des4.5 (P = 0.06), and Des9 (P = 0.0002), respectively. Conclusions Desflurane improved neurologic outcome following LF-CPB compared with F/D in piglets, indicated by less functional disability and less histologic damage, especially with Des9. Desflurane may have produced cardiac protection, suggested by a lower incidence of ventricular fibrillation.


1996 ◽  
Vol 24 (1) ◽  
pp. 26-31 ◽  
Author(s):  
G. L. Ludbrook ◽  
R. N. Upton ◽  
C. Grant ◽  
E. C. Gray

The effects of bolus administration of propofol (50 mg, 100 mg and 200 mg) on cerebral blood flow and cerebral metabolic rate for oxygen were examined in a chronically catheterized sheep preparation. Depth of anaesthesia was simultaneously measured using a withdrawal response to a noxious electrical stimulus and it was demonstrated that the 100 mg dose induced moderate sedation while the 200 mg dose induced relatively deep anaesthesia. Propofol caused transient dose-dependent decreases in cerebral blood flow, despite minimal changes in blood pressure. These were accompanied by parallel decreases in cerebral metabolic rate but no change in cerebral oxygen extraction. As cerebrovascular responses in the sheep appear similar to those in man, the parallel changes in cerebral blood flow and metabolic rate demonstrated in this study supports the suitability of propofol as a neuroanaesthetic agent.


Author(s):  
Kaja Falkenhain ◽  
Nancy E. Ruiz-Uribe ◽  
Mohammad Haft-Javaherian ◽  
Muhammad Ali ◽  
Pietro E. Michelucci ◽  
...  

ABSTRACTExercise exerts a beneficial effect on the major pathological and clinical symptoms associated with Alzheimer’ s disease in humans and mouse models of the disease. While numerous mechanisms for such benefits from exercise have been proposed, a clear understanding of the causal links remains elusive. Recent studies also suggest that cerebral blood flow in the brain of both Alzheimer’ s patients and mouse models of the disease is decreased and that the cognitive symptoms can be improved when blood flow is restored. We therefore hypothesized that the mitigating effect of exercise on the development and progression of Alzheimer’ s disease may be mediated through an increase in the otherwise reduced brain blood flow. To test this idea, we examined the impact of three months of voluntary wheel running in ∼1-year-old APP/PS1 mice on short-term memory function, brain inflammation, amyloid deposition, and cerebral blood flow. Our findings that exercise led to improved memory function, a trend toward reduced brain inflammation, markedly increased neurogenesis in the dentate gyrus, and no changes in amyloid-beta deposits are consistent with other reports on the impact of exercise on the progression of Alzheimer’ s related symptoms in mouse models. Notably, we did not observe any impact of wheel running on overall cortical blood flow nor on the incidence of non-flowing capillaries, a mechanism we recently identified as one contributing factor to cerebral blood flow deficits in mouse models of Alzheimer’ s disease. Overall, our results replicate previous findings that exercise is able to ameliorate certain aspects of Alzheimer’ s disease pathology, but show that this benefit does not appear to act through increases in cerebral blood flow.


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