scholarly journals Cerebral Blood Flow–Guided Manipulation of Arterial Blood Pressure Attenuates Hippocampal Apoptosis After Asphyxia‐Induced Cardiac Arrest in Rats

2020 ◽  
Vol 9 (13) ◽  
Author(s):  
Chih‐Hung Wang ◽  
Wei‐Tien Chang ◽  
Chien‐Hua Huang ◽  
Min‐Shan Tsai ◽  
Shing‐Hwa Liu ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Neuronal Damage ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Arterial Blood ◽  
Induced Cardiac Arrest

Background In most post–cardiac arrest patients, the autoregulation mechanism of cerebral blood flow ( CBF ) is dysregulated. We examined whether recovery of CBF by adjusting mean arterial pressure mitigates post–cardiac arrest neuronal damage. Methods and Results Wistar rats that underwent 8‐minute asphyxia‐induced cardiac arrest and resuscitation were computer‐randomized to norepinephrine or control groups. The CBF was measured at the dorsal hippocampal CA 1 region of the left hemisphere. In the norepinephrine group, the mean arterial pressure was adjusted to recover CBF to 80% to 100% of baseline. Twenty‐four hours following resuscitation, neurological outcomes were assessed, and brain tissues and blood samples were harvested for neuronal apoptosis and injury assessment. Thirty resuscitated rats were randomized into 2 groups, each containing 12 rats that completed the experiments. Norepinephrine infusion effectively prevented posthyperemia hypoperfusion and recovered CBF to pre‐arrest baseline levels; a moderate positive linear correlation between mean arterial pressure and CBF during this period was also observed ( P <0.001). There were no significant between‐group differences in neurological recovery. In the norepinephrine group compared with the control group, upregulated cleaved caspase‐3 protein expression in brain tissue determined by Western blot was reduced ( P =0.02) and the densities of apoptotic cells in hippocampal CA 1 and CA 3 regions determined by terminal deoxynucleotidyl transferase‐mediated dUTP biotin nick‐end labeling were decreased ( P <0.001). No significant differences in serum neuron‐specific enolase or S100β levels were detected between the 2 groups. Conclusions CBF recovery demonstrated neuroprotective effects by reducing activation of cerebral apoptosis and number of apoptotic neurons. However, these effects did not significantly improve clinical neurological function, necessitating further investigation.

Abstract 9934: High Mean Arterial Pressure Aggravates Cerebral Hemodynamics After Extracorporeal Resuscitation in Swine

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Yael Levy ◽  
Alice Hutin ◽  
Nicolas Polge ◽  
fanny lidouren ◽  
Matthias Kohlhauer ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cerebral Hemodynamics ◽  
Reactivity Index ◽  
Extracorporeal Cardiopulmonary Resuscitation ◽  
Standard Map ◽  
Arterial Blood

Introduction: Extracorporeal cardiopulmonary resuscitation (E-CPR) is used for the treatment of refractory cardiac arrest but the optimal target to reach for mean arterial pressure (MAP) remains to be determined. Hypothesis: We hypothesized that MAP levels modify cerebral hemodynamics during E-CPR. Accordingly, we tested two MAP targets (65-75 vs 80-90 mmHg) in a porcine model of E-CPR. Methods: Pigs were anesthetized and instrumented for the evaluation of cerebral and systemic hemodynamics. They were submitted to 15 min of untreated ventricular fibrillation followed by 30 min of E-CPR. Electric attempts of defibrillation were then delivered until resumption of spontaneous circulation (ROSC). Extracorporeal circulation was initially set to an average flow of 40 ml/kg/min with a standardized volume expansion in both groups. The dose of epinephrine was set to reach either a standard or a high MAP target level (65-75 vs 80-90 mmHg, respectively). Animals were followed during 120 min after ROSC. Results: Six animals were included in both groups. After cardiac arrest, MAP was maintained at the expected level (Figure). During E-CPR, high MAP transiently improved carotid blood flow as compared to standard MAP. This blood flow progressively decreased after ROSC in high vs standard MAP, while intra-cranial pressure increased. Interestingly, this was associated with a significant decrease in cerebral oxygen consumption (26±8 vs 54±6 L O 2 /min/kg at 120 min after ROSC, respectively; p<0.01) (Figure). The pressure reactivity index (PRx), which is the correlation coefficient between arterial blood pressure and intracranial pressure, became positive in high MAP (0.47±0.02) vs standard MAP group (-0.16±0.10), demonstrating altered cerebral autoregulation with high MAP. Conclusion: Increasing MAP above 80 mmHg with epinephrine aggravates cerebral hemodynamics after E-CPR. Figure: Mean arterial pressure (MAP), cerebral blood flow and oxygen consumption (*, p<0.05)

Increased vascular resistance in paralyzed legs after spinal cord injury is reversible by training

2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Cord Injury

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.

Direct Cerebral Vasodilatory Effects of Sevoflurane and Isoflurane 

1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
End Tidal

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P&lt;0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.

Local cerebral blood flow and glucose utilization after blood exchange with a hemoglobin-based O2 carrier in conscious rats

1993 ◽  
Vol 265 (4) ◽  
pp. H1243-H1248 ◽  
Author(s):  
K. Waschke ◽  
H. Schrock ◽  
D. M. Albrecht ◽  
K. van Ackern ◽  
W. Kuschinsky
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Utilization ◽  
Brain Structures ◽  
Control Group ◽  
Local Cerebral Blood Flow ◽  
Conscious Rats ◽  
Cerebral Glucose Utilization ◽  
Arterial Blood ◽  
Blood Exchange

The effects of a blood exchange on cerebral blood flow and glucose utilization were studied. A near to total blood exchange (hematocrit < 3%) was achieved in conscious rats by isovolemic hemodilution. Ultrapurified, polymerized, bovine hemoglobin (UPBHB) served as a blood substitute. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 34 brain structures of conscious rats by means of the ido[14C]antipyrine and the 2-[14C]-deoxy-D-glucose methods. A group of rats without blood exchange served as control. After blood exchange LCBF increased from 36 to 126% in the different brain structures resulting in a nearly doubled mean cerebral blood flow (+82%). LCGU increased only moderately by 0-24%. Significant increases in LCGU were observed in 16 brain structures. Mean cerebral glucose utilization slightly increased (+14%). The relationship between LCGU and LCBF was found to be tight both in the control group (r = 0.95) as well as after blood replacement (r = 0.94), although it was reset to a higher overall LCBF-to-LCGU ratio. The profound increases in LCBF observed after blood exchange, which were not paralleled by comparable increases in LCGU, might be explained by a reduction of blood viscosity after blood exchange. Additional effects of blood exchange observed in the present study were an increase of mean arterial blood pressure and a decline of heart rate. The results indicate that replacement of blood with the hemoglobin-based oxygen carrier UPBHB appears to meet the cerebral circulatory and metabolic demands of the brain tissue.

Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension

1985 ◽  
Vol 63 (6) ◽  
pp. 937-943 ◽  
Author(s):  
David J. Boarini ◽  
Neal F. Kassell ◽  
James A. Sprowell ◽  
Julie J. Olin ◽  
Hans C. Coester
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Hypotension ◽  
Content Type ◽  
Blood Flows ◽  
Before And After ◽  
Regional Blood Flows ◽  
Fine Print

✓ Profound arterial hypotension is à commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

scholarly journals Impact of blood pressure changes in cerebral blood perfusion of patients with ischemic Moyamoya disease evaluated by SPECT

2020 ◽  
pp. 0271678X2096745
Author(s):  
Zhao Liming ◽  
Sun Weiliang ◽  
Jia Jia ◽  
Liang Hao ◽  
Liu Yang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Moyamoya Disease ◽  
Emission Computed Tomography ◽  
Study Cohort ◽  
Pressure Changes ◽  
The Impact

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.

Relationship between Cardiopulmonary Bypass Flow Rate and Cerebral Embolization in Dogs 

1999 ◽  
Vol 91 (5) ◽  
pp. 1387-1387 ◽  
Author(s):  
Hulya Sungurtekin ◽  
Walter Plöchl ◽  
David J. Cook
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cardiopulmonary Bypass ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Rank Order ◽  
Brain Regions ◽  
Pump Flow ◽  
Cerebral Embolization ◽  
The Brain

Background Cerebral embolization is a primary cause of cardiac surgical neurologic morbidity. During cardiopulmonary bypass (CPB), there are well-defined periods of embolic risk. In theory, cerebral embolization might be reduced by an increase in pump flow during these periods. The purpose of this study was to determine the CPB flow-embolization relation in a canine model. Methods Twenty mongrel dogs underwent CPB at 35 degrees C with alpha-stat management and a fentanyl-midazolam anesthetic. In each animal, CPB flow was adjusted to achieve a mean arterial pressure of 65-75 mmHg. During CPB, an embolic load of 1.2 x 10(5) 67 microm fluorescent microspheres was injected into the arterial inflow line. Before and after embolization, cerebral blood flow was determined using 15-microm microspheres. Tissue was taken from 12 brain regions and microspheres were recovered. The relation between pump flow and embolization/g of brain was determined. Results The mean arterial pressure at embolization was 67 +/-4 mmHg, and the range of pump flow was 0.9-3.5 l x min(-1)x m(-2). Cerebral blood flow was independent of pump flow. At lower pump flow, the percentage of that flow delivered to the brain increased. There was a strong inverse relation between pump flow and cerebral embolization (r = -0.708, P &lt; 0.000 by Spearman rank order correlation). Conclusions Cerebral embolization is determined by the CPB flow. At an unchanged mean arterial pressure, as pump flow is reduced, a progressively greater proportion of that flow is delivered to the brain.

Sign in / Sign up

Export Citation Format

Share Document