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

Abstract

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.

Vasodilatory effect of adenosine triphosphate does not change cerebral blood flow: a PET study with 15O-water

“…No increase in cortical CBF, rather a slight non-significant decrease, after the ATP injection was observed, although vasodilatory change at basal major vessels was indicated according to SPM analysis. The relaxation of vascular smooth muscles by the stimulation of the A2 receptors [7,23] did not change CBF in the cerebral cortices, which goes in line with previous reports studied with adenosine [24,25]. This no change in CBF despite vasodilation in the major vessels is considered to be caused by systemic hypotension due to vasodilation in peripheral arteries and the cerebral microvascular autoregulation which preserves intracranial perfusion pressure [22].…”

Cardiovascular selectivity of adenosine receptor agonists in anaesthetized dogs

“…Potential advantages of Ado receptor agonists in this role include inhibition of atrial and ventricular automaticity (Szentmiklosi et al, 1980;Wainwright & Parratt, 1988), antirenin activity (Lagerkranser et al, 1989) and protection of cardiac muscle from ischaemic damage (Olafsson et al, 1987;Babbitt et al, 1989;Pitarys et al, 1991) in addition to their potent vascular smooth muscle relaxant properties (Collis, 1989).…”

Effects of adenosine–induced hypotension on cerebral blood flow and metabolism in the pig

“…The endogenous vasodilator adenosine has recently been introduced as a hypotensive agent in humans (1)(2)(3). Because of its extremely short plasma half-life (4), adenosine allows for rapid adjustments of the hemodynamic effects, which may be particularly advantageous during controlled hypotension.…”

“…Because of its extremely short plasma half-life (4), adenosine allows for rapid adjustments of the hemodynamic effects, which may be particularly advantageous during controlled hypotension. In humans, adenosine hypotension induces a hyperkinetic circulatory pattern, comprising increased cardiac output (1-3) and slightly reduced whole body oxygen consumption (\jo2) (1,3). Cerebral blood flow (CBF) is maintained while cerebral metabolic rate of oxygen (CMRo,) may be reduced (3).…”