Histamine-3 receptor antagonists reduce superoxide anion generation and lipid peroxidation in rat brain homogenates

Using a cyanide model to induce neurotoxic effects in rat brain homogenates, we examined the neuroprotective properties of three H3 antagonists, namely clobenpropit, thioperamide and impentamine, and compared them to aspirin, a known neuroprotective agent. Superoxide anion levels and malondialdehyde concentration were assessed using the nitroblue tetrazolium and lipid peroxidation assays. Clobenpropit and thioperamide significantly reduced superoxide anion generation and lipid peroxidation. Impentamine reduced lipid peroxidation at all concentrations used, but only reduced superoxide anion generation at a concentration of 1 mM. In the lipid peroxidation assay, all the drugs compared favourably to aspirin. This study demonstrates the potential of these agents to be neuroprotective by exerting antioxidant effects.     

Effect of various propofol plasma concentrations on regional myocardial contractility and left ventricular afterload

The cardiovascular effects of propofol infusions, designed to maintain constant plasma concentrations, were examined in an open-chested pig model. Regional myocardial contractility was measured with the end-systolic pressure-length relationship (Ees) and left ventricular afterload quantified by the effective arterial elastance (Ea). The propofol plasma concentrations in this study varied between 0 and 7.73 (SEM 0.96) micrograms/mL. A significant correlation for the increasing propofol plasma concentration and a decrease in myocardial contractility (P = 0.0056) was demonstrated, and the Ea remained constant. This gave rise to a reduction in stroke volume (P = 0.002) and, combined with a decrease in the heart rate (P = 0.0001), led to a reduction in the cardiac output (P = 0.0001). When the propofol infusion was stopped, myocardial contractility did not recover in parallel with the decrease in plasma propofol concentration.     

Sudden cardiac death during ambulatory ECG monitoring. A report of 2 cases

Two cases of sudden cardiac death during ambulatory ECG monitoring, each with an episode of torsade de pointes as part of the terminal dysrhythmia, are reported. In the first case, pause-dependent changes of the TU waves favour early after-depolarisations and triggered activity as the initiating mechanism of torsade. Quinidine therapy was probably an aggravating factor. Torsade was not initiated in a pause-dependent fashion in the second patient, who had ECG evidence of an episode of ischaemia as trigger for the terminal dysrhythmia. Both patients had impaired left ventricular function and underlying coronary artery disease.     

Oxygen balance in the normal dog myocardium with increased concentrations of inhaled anesthetics

Myocardial oxygen supply and demand in the normal dog were evaluated as the concentration of halothane, enflurane or isoflurane was increased. Although coronary blood flow decreased as the anaesthetic gas concentration increased, the O2 supply-to-demand ratio remained stable owing to a decrease in the myocardial O2 consumption.     

Distal dystrophy--unusual presentations. A report of 2 cases

Two men suffering from progressive muscle wasting and weakness are described. The first patient presented with a rapidly progressive myopathy of the right lower leg characterised on histological examination of muscle biopsy specimens by extensive ringed fibre formation. The second patient exhibited severe muscle weakness and wasting of the lower legs characterised by the accumulation of amorphous sarcoplasmic material and vacuolation seen on histochemical evaluation and confirmed by electron microscopy. There was no clinical or electrophysiological evidence of myotonia in either case.     

Kinetics and in vivo distribution of in-111-labelled platelets and platelet function in familial hypercholesterolaemia

The kinetics, in vivo distribution and sites of sequestration of autologous In-111-labelled platelets and other platelet function parameters were studied in ten patients with type IIa or IIb familial hypercholesterolaemia and thrombotic complications of atherosclerosis. The in vitro platelet aggregation response to ADP (P = 0.50) and collagen (P = 0.46); binding of fibrinogen to platelets (P = 0.61); and plasma beta-thromboglobulin levels (P = 0.42) of the patients and normal reference subjects did not differ significantly. The in vivo distribution of In-111-labelled platelets at equilibrium was within normal limits, and at the end of platelet life-span the sequestration pattern of labelled platelets in the reticuloendothelial system was also normal (spleen P = 0.31; liver P = 0.54). There was minimal evidence of in vivo platelet activation: only mean platelet lifespan (MPLS), 195 +/- 57 hours (difference between mean MPLS of patients and controls was 25 hours, with a 95% confidence interval from 23 to 31 hours; P = 0.02); mean platelet platelet turnover, 2298 +/- 824 platelets/microliter/hour (P = 0.005); plasma platelet factor 4 (P = 0.02); and the mean circulating platelet aggregate ratio, 0.8 +/- 0.1 (P = 0.02); differed significantly from normal. These results suggest that abnormalities of platelet function and kinetics observed in type II hyperlipoproteinaemia cannot be ascribed wholly to the hyperlipidaemia, but may be induced by the associated atherosclerosis.