The satisfactory results obtained in the present study are probably due to two main factors. First, the three participating radiologist are highly skilled and experienced. Secondly, a conscientious surveillance was adhered to, so that restenoses could be diagnosed and treated early. SA is a relevant alternative to bypass surgery in patients with disabling IC due to long femoro-popliteal occlusions. It is far less traumatic than conventional vascular reconstructions, complications are few and not serious. Very importantly, SA never interfered with later successful vascular surgery. Therefore, we have adopted SA as the primary treatment for patients with IC when medical treatment alone has not been satisfactory.

Elevated plasma levels of vascular inflammatory markers have been reported in patients with peripheral arterial disease (PAD). We assessed the effect of supervised exercise training (ET) on vascular inflammation, hypothesizing that ET reduces plasma levels of the endothelial adhesion molecules E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-I (VCAM-I). Twenty-nine patients with PAD underwent a supervised ET program for 8 weeks. Before and after ET, walking distances (pain-free, PWD; maximal, MWD) were determined by a standard treadmill test. Plasma levels of E-selectin and ICAM-I were significantly reduced (E-selectin: 45.5-40.4 ng/mL, P = .013); ICAM-I: 342.0-298.0 ng/mL, P = .016). VCAM-1 levels were unchanged. Walking distances increased significantly (PWD: median 77-150 m, P < .001; MWD: median 306-535 m, P < .001). In conclusion, 8 weeks of ET in patients with PAD reduces plasma levels of the specific endothelium-derived inflammatory markers E-selectin and ICAM-I.

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In a porcine model of Gram-positive sepsis, 28 juvenile pigs were studied to evaluate the effect of a continuous infusion of live serogroup A streptococci (GAS) on the activation of coagulation and fibrinolysis. Plasma levels of thrombin-antithrombin (TAT) complexes, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) activities were measured using commercially available kits. The continuous infusion of GAS [(3-5) x 10(8) colony-forming units/kg per h] caused early signs of severe septicaemia in the pigs, with pulmonary hypertension, systemic hypotension, reduced cardiac output and liver hypoperfusion, ultimately leading to shock with a high mortality. There was a sequential and ordered activation of the coagulation, fibrinolytic and antifibrinolytic systems. GAS infusion induced a gradual, maximally 2.5-fold increase in plasma TAT levels. Plasma t-PA activity levels peaked at 2 h (nine-fold increase), whereas the peak of PAI-1 activity was delayed (eight-fold increase at 4 h). These findings are similar to changes observed during endotoxin infusion. This procoagulant state favours disseminated intravascular coagulation and microthrombus formation, ultimately threatening tissue viability.

To elucidate the pathophysiology of acute shock caused by serogroup A streptococci (GAS), GAS were given intravenously to 25 pigs. Short-time infusions of GAS (n=11) caused variable and unpredictable responses. A continuous infusion of 5x108 cfu/kg/h (n=8) caused pulmonary hypertension, arterial hypotension, and reduced cardiac output and liver perfusion, progressing to circulatory shock within 2-4 h. Halving the infusion rate (n=6) induced a more gradual development of shock and doubled the mean survival time from 2.1 to 4.0 h. Mean tumor necrosis factor-alpha levels (+/-SE) increased from 25+/-1 to 40+/-3 pg/mL. Only slight signs of organ dysfunction were observed, which indicates that this is primarily a model of acute septic shock. Light microscopy revealed moderate inflammatory reactions in lung, liver, and gut biopsy samples, although high numbers of viable, M-typeable GAS were recovered from tissues. The present model may be useful to study mechanisms involved in acute septic shock as well as therapeutic interventions.

In a double-blind study, methyldopa was shown to be significantly more effective than placebo in reducing menopausal hot flushes. The median reduction in the number of hot flushes was 38% with placebo and 65% with methyldopa. The active metabolite of methyldopa, alpha-methylnoradrenaline, is an alpha 2-adrenoceptor agonist. Since the alpha 2-adrenoceptor agonist clonidine also reduces hot flushes, while the alpha 2-adrenoceptor antagonist yohimbine produces flushes, it is speculated that menopausal hot flushes might result from a reduced stimulation of alpha 2-adrenoceptors, probably in the CNS.

In this model of porcine GAS-induced septic shock, which was not associated with enhanced NO production, infusion of the NOS inhibitor AE-ITU prolonged survival, prevented hypotension, and improved cardiac contractility, organ perfusion, and tissue oxygenation. These beneficial effects of AE-ITU might be a result of the combined effect of ROS scavenging and modulation of local NO production, thus improving the balance of vasodilator and vasoconstrictor forces and reducing oxidative stress.