Brain adenosine production in rat during sustained alteration in systemic blood pressure

1980 ◽  
Vol 239 (5) ◽  
pp. H636-H641 ◽  
Author(s):  
H. R. Winn ◽  
J. E. Welsh ◽  
R. Rubio ◽  
R. M. Berne
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Autoregulation ◽  
Adenine Nucleotides ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Arterial Blood ◽  
Adenosine Concentration ◽  
Severe Hypotension

Brain production of adenosine and its metabolites, inosine and hypoxanthine was determined in 46 rats during sustained (5 min) reduction in mean arterial blood pressure (MABP) caused by hemorrhage. Also measured were ATP, ADP, AMP, phosphocreatine (PCr), and lactate. Brain tissue was obtained by the freeze-blowing technique. Ventilation was controlled to maintain constant arterial O2 tension, CO2 tension, and pH. When MABP was decreased from 135 + 3 (SE) mmHg to 72 +/- 2 mmHg, within the range of cerebral autoregulation, brain adenosine concentration doubled from 0.55 +/- 0.12 to 1.16 +/- 0.13 nmol/g (P < 0.015). Unlike the changes in adenosine concentrations, adenine nucleotides and PCr remained stable. Lactate varied inversely with MABP. With moderate to severe hypotension (MABP = 45 +/- 3 mmHg), adenosine levels increased almost sixfold. The increment in brain adenosine concentration within the autoregulatory range supports a role for this potent dilator of pial vessels in the regulation of cerebral blood flow.

Cerebral blood flow and interstitial fluid adenosine during hemorrhagic hypotension

1988 ◽  
Vol 255 (5) ◽  
pp. H1211-H1218 ◽  
Author(s):  
D. G. Van Wylen ◽  
T. S. Park ◽  
R. Rubio ◽  
R. M. Berne
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Adenosine Receptor ◽  
Cerebral Autoregulation ◽  
Interstitial Fluid ◽  
Adenosine Receptor Antagonist ◽  
Arterial Blood ◽  
Artificial Cerebrospinal Fluid ◽  
Adenosine Concentration ◽  
Group 2

This study was designed to assess the role of adenosine in autoregulation of cerebral blood flow (CBF) with the use of the brain dialysis technique to sample cerebral interstitial fluid (ISF) and hydrogen clearance to measure local CBF in ketamine-anesthetized rats. In group 1 (n = 11), animals were hemorrhaged to reduce mean arterial blood pressure (MABP) from control levels (MABP = 101.1 +/- 2.6) to 80, 70, 60, 50, 40, and 30 mmHg. Cerebral autoregulation was evidenced by no significant decrease in CBF until MABP decreased to 60 mmHg. However, dialysate adenosine concentration did not increase until MABP decreased to 50 mmHg. In group 2 (bilateral dialysis; n = 11), in which the left carotid artery was ligated before reductions in MABP, left-side dialysate adenosine concentration increased at a MABP of 70 mmHg. In group 3 (bilateral dialysis; n = 6), one dialysis probe was perfused with artificial cerebrospinal fluid containing 10(-3) M 8(p-sulfophenyl)theophylline (8-SPT), an adenosine receptor antagonist, during reduction of MABP to 50 mmHg. Although there were similar reductions in CBF with or without adenosine receptor blockade, dialysate adenosine concentration was greater on the side of locally infused 8-SPT at a MABP of 50 mmHg. These data suggest that adenosine is not responsible for cerebral autoregulation at blood pressures greater than 50 mmHg but may contribute to the decrease in cerebral vascular resistance observed at arterial pressures below the autoregulatory range.

Baroreceptor influence on postural changes in blood pressure and carotid blood flow

1963 ◽  
Vol 205 (2) ◽  
pp. 360-364 ◽  
Author(s):  
Francis L. Abel ◽  
John H. Pierce ◽  
Warren G. Guntheroth
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Sinus ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Carotid Blood Flow ◽  
Postural Changes ◽  
Nembutal Anesthesia

The effects of 30° head-down and head-up tilting on mean systemic blood pressure, carotid blood flow, and heart rate were studied in 16 dogs under morphine and Nembutal anesthesia. The tilting procedure was further repeated after denervation of the carotid sinus and aortic arch baroreceptors and after administration of a dihydrogenated ergot alkaloid mixture (Hydergine). The results indicate that the drop in pressure in the head-down position is primarily due to baroreceptor activity and that the baroreceptors are necessary for compensatory vasoconstriction on head-up tilting. Carotid blood flow decreased in both tilted positions in the control animals; the possible relationship to cerebral blood flow is discussed.

Acute cerebral blood flow response to dopamine-induced hypertension after subarachnoid hemorrhage

1994 ◽  
Vol 80 (5) ◽  
pp. 857-864 ◽  
Author(s):  
Joseph M. Darby ◽  
Howard Yonas ◽  
Elizabeth C. Marks ◽  
Susan Durham ◽  
Robert W. Snyder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Systemic Blood Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Fine Print

✓ The effects of dopamine-induced hypertension on local cerebral blood flow (CBF) were investigated in 13 patients suspected of suffering clinical vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The CBF was measured in multiple vascular territories using xenon-enhanced computerized tomography (CT) with and without dopamine-induced hypertension. A territorial local CBF of 25 ml/100 gm/min or less was used to define ischemia and was identified in nine of the 13 patients. Raising mean arterial blood pressure from 90 ± 11 mm Hg to 111 ± 13 mm Hg (p < 0.05) via dopamine administration increased territorial local CBF above the ischemic range in more than 90% of the uninfarcted territories identified on CT while decreasing local CBF in one-third of the nonischemic territories. Overall, the change in local CBF after dopamine-induced hypertension was correlated with resting local CBF at normotension and was unrelated to the change in blood pressure. Of the 13 patients initially suspected of suffering clinical vasospasm, only 54% had identifiable reversible ischemia. The authors conclude that dopamine-induced hypertension is associated with an increase in flow in patients with ischemia after SAH. However, flow changes associated with dopamine-induced hypertension may not be entirely dependent on changes in systemic blood pressure. The direct cerebrovascular effects of dopamine may have important, yet unpredictable, effects on CBF under clinical pathological conditions. Because there is a potential risk of dopamine-induced ischemia, treatment may be best guided by local CBF measurements.

scholarly journals Possible Neuroprotective Properties of Flunarizine Infused after Asphyxia in Fetal Lambs Are Not Explained by Effects on Cerebral Blood Flow or Systemic Blood Pressure

1993 ◽  
Vol 34 (3) ◽  
pp. 379-384 ◽  
Author(s):  
Harmen H De Haan ◽  
Jos L H Van Reempts ◽  
Marcel Borgers ◽  
Jelte De Haan ◽  
Johan S H Vles ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Systemic Blood Pressure ◽  
Systemic Blood

Pericardial concentrations of adenosine, inosine and hypoxanthine in an experimental canine model of spastic ischaemia

2002 ◽  
Vol 103 (s2002) ◽  
pp. 198S-201S ◽  
Author(s):  
Violetta KÉKESI ◽  
Endre ZIMA ◽  
Erzsébet BARÁT ◽  
Éva HUSZÁR ◽  
Andrea NAGY ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Coronary Spasm ◽  
Systemic Blood Pressure ◽  
Canine Model ◽  
Pericardial Fluid ◽  
Metabolic Adaptation ◽  
Systemic Blood ◽  
Arterial Blood ◽  
Adenosine Concentration ◽  
Experimental Canine

It has been shown that the adenosine concentration in the pericardial fluid of the normal heart is higher by one order of magnitude than that of the venous plasma. A further increase in the pericardial adenosine concentration was also demonstrated in myocardial ischaemia or hypoxia. It was proposed that pericardial nucleoside levels may represent the interstitial concentrations of the adenine nucleosides. An experimental model was designed to determine the intrapericardial concentrations of adenosine, inosine and hypoxanthine during coronary spasm provoked by intracoronary administration of endothelin-1 (ET-1; 0.08±0.02nmol/g of myocardial tissue). In the in situ dog heart (n = 10), adenosine, inosine and hypoxanthine concentrations were determined by HPLC in fluid samples collected from the closed pericardial sac before and after ET-1 administration, and from the systemic arterial blood. Systemic blood pressure, heart rate and standard ECG were registered continuously. We found that the nucleoside concentrations in the infusate samples increased significantly during coronary spasm [adenosine, 1.49±0.44 compared with 0.37±0.07µM (P<0.05); inosine, 27.43±11.51 compared with 0.47±0.11µM (P<0.05); hypoxanthine, 21.17±6.49 compared with 4.91±1.24µM (P<0.05)], while a significant decrease in blood pressure and an elevation in ECG ST segments were observed. The levels of the purine metabolites did not change in the systemic blood. The data indicate that changes in adenine nucleoside levels measured in pericardial infusate samples reflect activation of coronary metabolic adaptation in this model of spastic ischaemia, and that pericardial nucleoside levels may characterize alterations in interstitial adenine nucleoside concentrations.

Sign in / Sign up

Export Citation Format

Share Document