Acute ischaemic stroke is characterised by reductions in local cerebral blood flow (CBF) and activation of circulating platelets and leucocytes. Nitric oxide is a vasodilator and can inhibit these circulating cells. The aim of this study was to assess the effect of nitric oxide on platelet function and regional CBF in patients with acute ischaemic stroke. Sodium nitroprusside (SNP), a spontaneous nitric oxide donor, was administered at a dose which caused a 10 mm Hg fall in mean arterial blood pressure (MABP) in a pathophysiological study to 22 patients with acute ischaemic stroke and 12 matched control subjects. Platelet function (whole blood aggregation and flow cytometry) was assessed before and during SNP administration. Changes in regional CBF were measured using single photon emission computerised tomography (SPECT) scanning. SNP significantly reduced platelet aggregation in both the patient and control subject groups. Equally, the expression of platelet adhesion molecules P-selectin (CD62) and glycoprotein (GP) GP IIIa (CD61) were significantly reduced in both groups. GP Ia (CDw49b) expression was significantly attenuated in the patient but not in the control group. Four patients underwent SPECT scanning and improvements in local CBF corresponding to the penumbral area of the clinical stroke site were seen in 3 of these patients. A total of 24 regions of asymmetrical perfusion were examined, pre-SNP (median (SQR)), 0.68 (0.14) vs. peri-SNP 0.78 (0.17), 2p = 0.065. SNP, given at a dose which reduced MABP by 10 mm Hg, significantly inhibited platelet aggregation and adhesion molecule expression. Improved regional CBF was seen in some patients. SNP is a candidate therapeutic agent for patients with acute ischaemic stroke and warrants further study.

Blood Coagulation↗

PubMedDate not supplied

Acetate fails to reverse myocardial depression in dogs anesthetized with halothane.

Sodium acetate has been shown to reverse the myocardial depression induced by halothane in vitro. The biochemical basis for this restoration of contractility has been located in the glycolytic pathway. The present study was designed to determine whether this antagonistic property of acetate also occurs in vivo. Dogs autonomically blocked with guanethidine, phenoxybenzamine, and atropine were sequentially anesthetized with halothane in O2 and N2O-O2-succinylcholine in a random pattern. All animals were given sodium acetate IV in amounts adequate to produce pharmacologically active levels. Myocardial performance was measured by LVdP/dtmax, LVPDP/dt/KPmax, and Vmax. Halothane effected a significant depression of these myocardial parameters. Acetate did not reverse this depressant effect of halothane. Acetate, a well-established peripheral vascular vasodilator, did decrease left ventricular and aortic pressures.

Acetates↗

PubMedDate not supplied

Do not resuscitate in the operating room: more than rights and wrongs.

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Anesthesiology↗