Cerebral and systemic circulatory effects of arterial hypotension induced by adenosine

Kassell, Neal F.; Boarini, David J.; Olin, Julie J.; Sprowell, James A.

doi:10.3171/jns.1983.58.1.0069

Cited by 56 publications

(22 citation statements)

References 47 publications

(1 reference statement)

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“…29 It has been reported that large doses of intravenous adenosine and dipyridamole can induce severe arterial hypotension, severe enough to be out of the range of cerebral autoregulation and hence cause a decrease in CBF. 18 However, no changes in blood pressures were observed between the dipyridamole stress and the rest conditions in the present study.…”

Section: Ito Et Al Effect Of Dipyridamole On Cbfcontrasting

confidence: 70%

Effect of Intravenous Dipyridamole on Cerebral Blood Flow in Humans

Ito

Kinoshita

Tamura

et al. 1999

Stroke

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Background and Purpose-Dipyridamole increases the concentration of circulating adenosine, which is a potent vasodilator, by inhibition of uptake of adenosine into the erythrocytes, and hence produces coronary vasodilation. However, the effects of dipyridamole on cerebral circulation is not pronounced. This study investigates the effects of intravenous dipyridamole on cerebral blood flow (CBF) in humans with use of positron emission tomography (PET). Methods-In each of 13 healthy subjects, CBF was measured using 15 O-labeled water and PET at rest and during hypercapnia, hypocapnia, and dipyridamole stress; corresponding CBF values were then compared. Results-CBF values during dipyridamole stress were significantly lower than those measured at rest. The dipyridamole stress PaCO 2 was also significantly lower than the resting PaCO 2 . The change in CBF during dipyridamole stress relative to PaCO 2 closely followed the relationship between CBF and PaCO 2 during hypocapnia. Conclusions-These results indicate that the observed decrease in CBF during dipyridamole stress was caused by a decrease in PaCO 2 rather than by any direct action of dipyridamole on CBF. The decrease in PaCO 2 during dipyridamole stress was most likely due to hyperventilation, which was a side effect of adenosine. These results support the hypothesis that circulating adenosine is largely prevented from binding to adenosine receptors of cerebral vessels by the blood-brain barrier. (Stroke. 1999;30:1616-1620.)

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Section: Ito Et Al Effect Of Dipyridamole On Cbfcontrasting

confidence: 70%

Effect of Intravenous Dipyridamole on Cerebral Blood Flow in Humans

Ito

Kinoshita

Tamura

et al. 1999

Stroke

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“…It should further be noted that the cardiovascular responses to adenosine in dogs (3,4) also differed from those obtained in the present study, as well as previous human studies (1,2), indicating species variability in the systemic adenosine response as well. Cardiac output was increased by 34% in this study, but was significantly decreased in dogs (3,4), while SVR was more effectively reduced than CVR in both species. Thus, in roinmon with dogs, the vasodilatory response in the patients was less prominent in the cerebral than in the systemic circulation, indicating decreased blood flow distribution to the brain.…”

Section: Circulatory Efjcectscontrasting

confidence: 69%

Cerebral blood flow and metabolism during adenosine–induced hypotension in patients undergoing cerebral aneurysm surgery

Lagerkranser

Bergstrand

Gordon

et al. 1989

Acta Anaesthesiol Scand

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The effects of adenosine-induced hypotension on cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and cerebral lactate production, together with systemic haemodynamics, were studied in 10 patients undergoing cerebral aneurysm surgery in neurolept anaesthesia with controlled hyperventilation. CBF changes were determined in six of the patients with a retrograde thermodilution technique in the jugular vein. Hypotension was induced with a continuous infusion of adenosine in the superior vena cava. The dose range was 0.06-0.35 mg/kg/min, and this caused a 42% reduction in mean arterial blood pressure (MABP) from 79 +/- 4 to 46 +/- 1 mmHg (10.5 +/- 0.5 to 6.1 +/- 0.1 kPa) through a profound reduction in systemic vascular resistance (SVR), which amounted to 61%. No significant change occurred in CBF. Whole body AV-difference of oxygen was decreased by 37%, and cerebral AV-difference by 28%, corresponding to reductions in whole body oxygen uptake and CMRO2 of 16 and 17%, respectively. Cerebral AV-difference of lactate did not change. In the posthypotensive period MABP was increased by 10%, together with a minor increase in CBF (15%). It is concluded, that adenosine-induced hypotension at MABP levels between 40-50 mmHg (5.3-6.7 kPa) does not affect cerebral oxygenation unfavourably, and may even offer a protective effect by reducing cerebral oxygen demand. The slight CBF increase in the posthypotensive period was probably secondary to an increase in MABP together with a blunted autoregulation, but in no case was this effect considered to be harmful for the patient.

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“…Further studies are required to evaluate the safety of the latter condition in hearts with stenotic coronary arteries. side, and trimethaphan, which include cyanide toxicity, tachyphylaxis, reflex tachycardia, rebound hypertension, and excessive cerebral vasodilation (2)(3)(4)(5), have stimulated interest in the use of exogenous adenosine to induce controlled hypotension (2,(7)(8)(9).…”

mentioning

confidence: 99%

Myocardial Blood Flow and Oxygen Consumption during Isovolemic Hemodilution Alone and in Combination with Adenosine-Induced Controlled Hypotension

Crystal

Rooney

Salem

1988

Anesthesia & Analgesia

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CRYSTAL GJ, ROONEY MW, SALEM MR. Myocardial blood flow and oxygen consumption during isovolemic hemodilution alone and in combination with adenosine-induced controlled hypotension. Anesth Analg 1988:67:53947.Recent reports have proposed combining isovolemic hemodilution and controlled hypotension to limit blood loss during surgery. Before such a technique can be considered for clinical use, it must be demonstrated that it does not endanger maintenance of adequate myocardial oxygenation. Accordingly, measurements of left ventricular myocardial blood flow and oxygen consumption were obtained during isovolemic hemodilution alone and in combination with adenosine-induced controlled hypotension in ten pentobarbital-anesthetized, open chest dogs with normal corona y circulation. Hemodilution to a hematocrit of 21.7% was produced by isovolemic exchange of whole blood for 5% dextran. In the presence of hemodilution, adenosine was infused intravenously at a rate sufficient to decrease mean aortic pressure to 51 mm Hg. Myocardial blood flow was measured with radioactive microspheres and used to calculate global left ventricular myocardial oxygen consumption and oxygen supply. Hemodilution alone increased aortic blood flow (+43%) but had no effect on aortic pressure, left atrial pressure, heart rate, or left ventricular dPldt,,; an increase in myocardial blood flow (+130%) maintained oxygen supply and consumption at the baseline level. Adenosine-induced hypotension during hemodilution decreased heart rate (-35%), left ventricular dPldt max (-28%), and aortic blood flow (-14%). These systemic responses were accompanied by reduced myocardial oxygen consumption (-29%) and increased myocardial blood flow (+54%) and myocardial oxygen supply (+72%). These latter effects resulted in reduction in the coronary arteriovenous oxygen content difference and in an attendant rise in coronary sinus Po, (+66%), which are signs of luxuriant myocardial perfusion. The present study demonstrated in anesthetized dogs that 1) myocardial oxygenation is well maintained during isovolemic hemodilution alone and, 2) myocardial oxygenation is influenced favorably when isovolemic hemodilution is combined with adenosine-induced controlled hypotension. Further studies are required to evaluate the safety of the latter condition in hearts with stenotic coronary arteries.Adenosine, a metabolic breakdown product of adenosine triphosphate, is an endogenous vasodilator that has been implicated in local regulation of coronary blood flow (1). The drawbacks of currently used hypotensive drugs, halothane, nitroglycerin, nitroprusside, and trimethaphan, which include cyanide toxicity, tachyphylaxis, reflex tachycardia, rebound hypertension, and excessive cerebral vasodilation (2-5), have stimulated interest in the use of exogenous adenosine to induce controlled hypotension (2,7-9).Intravenous infusion of adenosine causes arterial hypotension that is rapidly achieved, easily controlled, short-lived and, furthermore, is not associated with any apparent hematologic or...

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Cerebral and systemic circulatory effects of arterial hypotension induced by adenosine

Cited by 56 publications

References 47 publications

Effect of Intravenous Dipyridamole on Cerebral Blood Flow in Humans

Effect of Intravenous Dipyridamole on Cerebral Blood Flow in Humans

Cerebral blood flow and metabolism during adenosine–induced hypotension in patients undergoing cerebral aneurysm surgery

Myocardial Blood Flow and Oxygen Consumption during Isovolemic Hemodilution Alone and in Combination with Adenosine-Induced Controlled Hypotension

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