scholarly journals Adenosine Deaminase Inhibitors Enhance Cerebral Anoxic Hyperemia in the Rat

1985 ◽  
Vol 5 (2) ◽  
pp. 295-299 ◽  
Author(s):  
J. W. Phillis ◽  
R. E. DeLong ◽  
J. K. Towner
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Adenosine Deaminase ◽  
Reactive Hyperemia ◽  
Low Doses ◽  
Venous Outflow ◽  
Vascular Regulation ◽  
Vascular Insufficiency ◽  
Basal Flow ◽  
Cerebral Vascular

Cerebral blood flow in the rat was monitored by a venous outflow technique with an extracorporeal circulation, which allows for the continuous recording of flow over periods of several hours. The adenosine deaminase inhibitors erythro-9-(2-hydroxy-3-nonyl)adenine (EHNA) (1.0–100 μg/kg) and deoxycoformycin (0.1–1 μg/kg) potentiated the reactive hyperemia elicited by a brief (24-s) anoxic challenge. Basal flow rate was unaltered by EHNA administration and slightly enhanced by deoxycoformycin. The results are consistent with the hypothesis that adenosine plays a significant role in cerebral vascular regulation and suggest that low doses of these deaminase inhibitors may be useful in the treatment of cerebral vascular insufficiency.

The assessment of pathological changes in cerebral blood flow in hypertensive rats with stress-induced intracranial hemorrhage using Doppler OCT: Particularities of arterial and venous alterations/Die Beurteilung von pathologischen Veränderungen der Hirndurchblutung bei hypertensiven Ratten mit Stress-induzierten intrakraniellen Blutungen mittels Doppler-OCT: Besonderheiten von arteriellen und venösen Veränderungen

2013 ◽  
Vol 2 (2) ◽  
Author(s):  
Oxana V. Semyachkina-Glushkovskaya ◽  
Vladislav V. Lychagov ◽  
Olga A. Bibikova ◽  
Igor A. Semyachkin-Glushkovskiy ◽  
Sergey S. Sindeev ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Hemorrhage ◽  
Venous Insufficiency ◽  
Hypertensive Rats ◽  
Arterial Tree ◽  
Venous Outflow ◽  
Venous Circulation ◽  
Latent Stage ◽  
Doppler Oct

AbstractHemorrhagic insult is a major source of morbidity and mortality in both adults and newborn babies in the developed countries. The mechanisms underlying the non-traumatic rupture of cerebral vessels are not fully clear, but there is strong evidence that stress, which is associated with an increase in arterial blood pressure, plays a crucial role in the development of acute intracranial hemorrhage (ICH), and alterations in cerebral blood flow (CBF) may contribute to the pathogenesis of ICH. The problem is that there are no effective diagnostic methods that allow for a prognosis of risk to be made for the development of ICH. Therefore, quantitative assessment of CBF may significantly advance the understanding of the nature of ICH. The aim of this study was to determine the particularities of alterations in arterial and venous cerebral circulation in hypertensive rats at different stages of stress-related development of ICH using three-dimensional Doppler optical coherence tomography (DOCT).Experiments were performed in mongrel adult rats. To induce ICH, hypertensive rats underwent stress (effect of severe sound, 120 dB during 2 h). To induce the renal hypertension (two kidneys, one clip) the rats were clipped at the left renal artery with a silver clip. Seven weeks after clipping, the hypertensive rats were used in the experiment. The monitoring of CBF was performed in anesthetized rats with fixed heads using a commercially available swept source OCT system (OCS1300SS; Thorlabs) in the masked period of ICH (4 h after stress) and during ICH (24 h after stress).It could be shown that in stressed rats, compared with non-stressed animals, the latent stage of stress-induced ICH (4 h after stress-off) is characterized by an increase in diameter of the superior sagittal vein with decrease in speed of the blood flow in the venous network, whereas no changes in the CBF in the arterial tree were found in this period. These facts suggest that the masked period of ICH is accompanied by decreasing venous outflow and the development of venous insufficiency. The incidence of ICH, 24 h after stress, is associated with progression of pathological alterations in cerebral venous circulation. All hypertensive rats with ICH demonstrated a greater increase in the diameter of the superior sagittal vein than stressed rats at the latent stage of ICH (in 2.5-fold,In summary, using DOCT we have shown that the latent stage of stress-induced ICH is characterized by a decrease in venous outflow. The incidence of ICH is associated with the progression of pathological alterations in cerebral venous circulation that is accompanied by a decrease in blood flow in the arterial tree. The evaluation of cerebral venous insufficiency is an important diagnostic approach for the prognosis of the risk of developing cerebral hypotension and ICH.

Role of adenosine in postprandial and reactive hyperemia in canine jejunum

1992 ◽  
Vol 263 (4) ◽  
pp. G487-G493 ◽  
Author(s):  
D. R. Sawmiller ◽  
C. C. Chou
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Adenosine Deaminase ◽  
Reactive Hyperemia ◽  
Concentration Difference ◽  
Adenosine Concentration ◽  
Anesthetized Dogs ◽  
Series Of Experiments ◽  
Increased Blood Flow

The role of adenosine in postprandial jejunal hyperemia was investigated by determining the effect of placement of predigested food into the jejunal lumen on blood flow and oxygen consumption before and during intra-arterial infusion of dipyridamole (1.5 microM arterial concn) or adenosine deaminase (9 U/ml arterial concn) in anesthetized dogs. Neither drug significantly altered resting jejunal blood flow and oxygen consumption. Before dipyridamole or deaminase, food placement increased blood flow by 30-36%, 26-42%, and 21-46%, and oxygen consumption by 13-22%, 21-22%, and 26-29%, during 0- to 3-, 4- to 7-, and 8- to 11-min placement periods, respectively. Adenosine deaminase abolished the entire 11-min hyperemia, whereas dipyridamole significantly enhanced the initial 7-min hyperemia (45-49%). Both drugs abolished the initial 7-min food-induced increase in oxygen consumption. Dipyridamole attenuated (14%), whereas deaminase did not alter (28%), the increased oxygen consumption that occurred at 8-11 min. Adenosine deaminase also prevented the food-induced increase in venoarterial adenosine concentration difference. In separate series of experiments, luminal placement of food significantly increased jejunal lymphatic adenosine concentration and release. Also, reactive hyperemia was accompanied by an increase in venous adenosine concentration and release. This study provides further evidence to support the thesis that adenosine plays a role in postprandial and reactive hyperemia in the canine jejunum.

scholarly journals Type A botulinum toxin (disport) in treatment of chronic forms of primary headache

2008 ◽  
Vol 7 (5-1) ◽  
pp. 270-275
Author(s):  
M. V. Napriyenko ◽  
V. Yu. Oknin ◽  
A. G. Sazonova ◽  
L. M. Kudayeva
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Botulinum Toxin ◽  
Pilot Study ◽  
Doppler Ultrasonography ◽  
Primary Headache ◽  
Arterial Blood Flow ◽  
Venous Outflow ◽  
Arterial Blood ◽  
Daily Headache

The aim of this investigation is to study the effect of BTA on the cerebral blood flow in patients with chronic daily headache. The analysis of Doppler ultrasonography and transcranial Dopplergraphy findings has shown the following: after the treatment 34% of the patients had no extravasal effect and in 66% of the patients it became moderate and after the treatment normal venous outflow was found in 58% of the patients . The results of the pilot study demonstrate the effect of BT-A injection on the cerebral blood flow by means of optimizing both the arterial blood flow and the venous outflow from the cavity of the skull.

Abstract P531: Cerebral Blood Flow Analysis Using Flow Wire Measurements and CFD Analysis

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Aichi Chien ◽  
Huy Dinh ◽  
Viktor Szeder ◽  
Fernando Vinuela
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Cfd Simulation ◽  
Cfd Analysis ◽  
Flow Data ◽  
Velocity Data ◽  
Mean Flow ◽  
Good Agreement ◽  
Cerebral Vascular

Introduction: Clinical reports show that cerebral blood flow conditions are indicative of cerebral vascular disease. While methods for characterizing cerebral vascular flow have been extensively reported in the past, comparative analyses between direct flow measurements (DM) and computational flow dynamic (CFD) analysis remain limited. We hypothesize that flow data can be reliably measured both directly and through CFD in normal vessels. Methods: A left heart replicator was used as a realistic cardiac pump which maintained systolic pressure at 120 mmHg and diastolic pressure at 80 mmHg. A stenotic model with 50% stenosis for the ICA was connected to the replicator. A ComboWire was used for DM and recorded flow pressure and velocity. CFD was used to study flow. Results: In areas at the proximal end of the stenosis, the pressure and flow velocity derived from DM and CFD were in good agreement. At the end of systole and diastole, DM pressure were 145.42 mmHg and 73.53 mmHg, respectively. CFD simulation for the same system obtained the pressure at the end of systole and diastole of 147.16 mmHg and 74.64 mmHg, respectively. The velocity data collected from DM was at 15.40 cm/s and 7.74 cm/s for systolic flow and mean flow velocity. CFD measured flow was 17.85 cm/s and 11.37 cm/s, respectively. In areas at the distal end of the stenosis, pressure data showed good agreement between DM and CFD analysis. The DM were 138 and 70.81 mmHg at the end of systole and diastole, respectively; CFD simulation yielded 145.95 and 74.51 mmHg, respectively. Variations in the velocity data were observed at this location (Fig, pink arrows). Conclusion: DM of pressure showed good agreement with CFD simulation in all areas of the vessel. DM of velocity using the flow wire were highly affected by location of the measurement. CFD analysis can provide more consistent flow data for flow information collection along the vasculature.

Vasopressin and prostanoid mechanisms in control of cerebral blood flow in hypotensive newborn pigs

1990 ◽  
Vol 258 (2) ◽  
pp. H408-H413 ◽  
Author(s):  
W. M. Armstead ◽  
C. W. Leffler ◽  
D. W. Busija ◽  
R. Mirro
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Vascular Resistance ◽  
Brain Regions ◽  
Cerebral Metabolic Rate ◽  
Cerebral Vasoconstriction ◽  
Newborn Pigs ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

The interaction between vasopressinergic and prostanoid mechanisms in the control of cerebral hemodynamics in the conscious hypotensive newborn pig was investigated. Indomethacin treatment (5 mg/kg) of hypotensive piglets caused a significant decrease in blood flow to all brain regions within 20 min. This decrease in cerebral blood flow resulted from increased cerebral vascular resistances of 52 and 198% 20 and 40 min after treatment, respectively. Cerebral oxygen consumption was reduced from 2.58 +/- 0.32 ml.100 g-1.min-1 to 1.01 +/- 0.12 and 0.29 +/- 0.08 ml.100 g-1.min-1 20 and 40 min after indomethacin, respectively, in hemorrhaged piglets. Treatment with the putative vascular (V1) receptor antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid-2-(O-methyl)tyrosine]arginine vasopressin (MEAVP) had no effect on regional cerebral blood flow, calculated cerebral vascular resistance, or cerebral metabolic rate either before or during hemorrhagic hypotension. However, decreases in cerebral blood flow and metabolic rate and increases in vascular resistance on treatment with indomethacin were blunted markedly in animals treated with MEAVP. These data are consistent with the hypothesis that the prostanoid system contributes to the maintenance of cerebral blood flow and cerebral metabolic rate during hypotension in the newborn pig, as reported previously, and implicate removal of vasopressinergic modulation by prostanoids as a potential mechanism for indomethacin-induced cerebral vasoconstriction in hypotensive newborn piglets.

scholarly journals Local Cerebral Blood Flow in the Recovery Period following Complete Cerebral Ischemia in the Rat

1983 ◽  
Vol 3 (2) ◽  
pp. 170-182 ◽  
Author(s):  
Erik Kågström ◽  
Maj-Lis Smith ◽  
Bo K. Siesjö
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Reactive Hyperemia ◽  
Recovery Period ◽  
Local Cerebral Blood Flow ◽  
Vessel Occlusion ◽  
No Reflow ◽  
Perfusion Defects ◽  
Ischemic Period ◽  
Complete Cerebral Ischemia

This study examines reflow patterns in the recirculation period following complete, global ischemia. Cerebrospinal fluid (CSF) compression ischemia was induced in ventilated rats for 5–30 min, and local cerebral blood flow (CBF) was measured autoradiographically after 5, 60, and 90 min of recirculation, Ischemia of 15 min duration was induced by four-vessel occlusion combined with arterial hypotension in two additional groups, with recovery periods of 5 or 60 min, In the immediate recirculation period (5 min), following 15 min of ischemia, local CBF was markedly heterogeneous, Thus, whereas most structures gave clear evidence of “reactive hyperemia,” others showed perfusion defects of the “no-reflow” type, Typically these defects affected the striatum, thalamus, and hippocampus, as well as the frontal, sensorimotor, and parietal cortices. Areas of no-reflow appeared after 10 min, were more extensive after 15 min, and occupied a major part of the brain after 30 min of ischemia. When recirculation was instituted for 60 or 90 min, following 15 min of ischemia, flow returned in previously unperfused areas. However, a delayed hypoperfusion developed, which differed widely between structures (range of CBF values, 20–80% of control). When the ischemic period was prolonged to 30 min, some perfusion defects remained, even after 90 min of recirculation.

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