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Mannitol has previously been shown to reduce skeletal muscle reperfusion injury and postischaemic compartment pressure. The present study was designed to evaluate whether these effects result from hyperosmolarity or free radical scavenging. A rabbit hindlimb perfusion model was used to compare the effects of mannitol (n = 6), glucose (n = 6)--an isomer of mannitol without scavenging effect--and fasciotomy (n = 6) on oedema, compartment pressure, energy charge, and muscle injury after 4 hours of ischaemia and 2 hours of reperfusion. One limb from each animal received treatment, while the other limb served as an untreated control. Mannitol and glucose reduced (p < 0.05) muscle water content and decreased (p < 0.01) the compartment pressure. Fasciotomy had no effect on muscle water content but normalised compartment pressure. The increase in energy charge following reperfusion was improved (p < 0.05) and uptake of [Tc99]methylenediphosphonate--an indicator of muscle injury--was reduced (p < 0.05) by mannitol only. In conclusion, mannitol reduces postischaemic oedema mainly by its hyperosmolar property whereas restitution of energy production and reduction of muscle necrosis seem to be an effect of free radical scavenging. The compartment pressure is reduced by hyperosmolarity and free radical scavenging.

Cardiac monitoring and the selective use of initial non-operative management is reported to reduce the high mortality rate in patients with acute lower limb ischaemia. Early estimation, prior to selection of initial therapy, of the risk for intraoperative or postoperative cardiac death following thrombo-embolectomy is therefore important. The aim of this prospective multi-centre study was to develop a simple and clinically useful index for assessment of the risk of post-operative cardiac death. Patients judged to need thrombo-embolectomy for acute lower limb ischaemia were evaluated on admission for routine clinical, cardiac and limb ischaemia parameters that could be related to cardiac function and these parameters compared to postoperative cardiac outcome. Sixteen per cent of the 117 patients died from intraoperative or postoperative cardiac complications. Analysis revealed five admission parameters that significantly and independently predicted a high risk for cardiac death: mean arterial blood pressure below 90 mmHg, clinical sign(s) of cardiac decompensation, ischaemia affecting the thigh, haemoglobin concentration exceeding 140 gl-1, and a history of a myocardial infarction in the previous 4 weeks. Definition of risk points for each risk factor allowed a simple classification of each patient into one of three significantly different cardiac risk classes with cardiac death rates of 6 +/- 3%, 27 +/- 8% and 75 +/- 16%, respectively. More than two thirds of the patients belonged to the low risk group. The described risk index provides a tool for preoperative assessment of the cardiac death risk associated with early thrombo-embolectomy in patients with acute lower limb ischaemia.

Reperfusion of ischaemic skeletal muscle may lead to increased vascular permeability, oedema and ultimately muscle necrosis. Oxygen-derived free radicals have been suggested as aetiological factors in reperfusion injury. Amputated rabbit hindlimbs were subjected to 4 h of ischaemia followed by 2 h or reperfusion with Krebs' buffer. One limb from each animal was reperfused with oxygen-saturated buffer (reoxygenated limb) while the other limb was reperfused with nitrogen-saturated buffer (non-reoxygenated limb). Six animals received allopurinol orally 2 days prior to the experiment and ten animals received no treatment. The energy charge dropped from 0.90 to 0.54 during ischaemia and increased to 0.82 after reperfusion with oxygenated perfusate. Oedema was determined by limb weight and water content in muscle biopsies and muscle injury was assessed by uptake of [Tc99]methylenediphosphonate ([Tc99]MDP). The results were expressed in ratios, between the reoxygenated and nonreoxygenated limb. Without allopurinol treatment, the increase in water content and limb weight in reoxygenated limbs exceeded (p less than 0.05) non-reoxygenated limbs (ratios = 1.73 and 1.89, respectively). Allopurinol treatment significantly reduced (p less than 0.05 and p less than 0.02, respectively) the increase in water content and limb weight (ratios = 0.54 and 1.01, respectively). Without treatment, [Tc99]MDP-uptake was greater (p less than 0.05) in reoxygenated limbs than in non-reoxygenated limbs (ratio = 1.60). Allopurinol treatment significantly reduced (p less than 0.002) [Tc99]MDP-uptake in reoxygenated limbs (ratio = 0.80). These results demonstrate that additional injury to ischaemic skeletal muscle occurs during reperfusion with oxygen.(ABSTRACT TRUNCATED AT 250 WORDS)

Forty-one patients with acute iliofemoral venous thrombosis were randomised to conventional anticoagulation or acute thrombectomy combined with a temporary arterio-venous fistula (AVF) and anti-coagulation. Follow-up after 5 years in 22 medical and 19 surgical patients revealed slightly more asymptomatic patients (37 vs. 18%) and less frequent severe post-thrombotic sequelae (16 vs. 27%) in the surgical group (N.S.). The iliac vein was more frequently (P less than 0.05) normal following thrombectomy (71 vs. 30%) as demonstrated by radionuclide angiography, but occlusion plethysmography showed an outflow capacity (61 vs. 45 ml/min/100 ml) that was not significantly better. There was no obvious difference in muscle pump function (EVrel) and reflux (Q/EVrel) assessed by foot volumetry. Still, the ambulatory venous pressure was significantly (P less than 0.05) lower in the surgical group. There was a tendency towards better results following thrombectomy in patients with fresh thrombosis and a successful initial procedure. Although the numbers of observations in many cases were too small to provide statistical evidence of benefit with venous thrombectomy + AVF, this procedure seems to improve the long-term outcome following acute iliofemoral venous thrombosis. Since the difference in outcome is not very striking, anticoagulation treatment is still an acceptable alternative.

To determine the chronological changes of venous physiology following major thromboses, 20 patients were repeatedly examined for over 5 years after an acute ilio-femoral thrombosis which was treated with conventional anticoagulation. Radionuclide angiography showed that 70% of the patients had obstructive lesions of the iliac vein with only minor changes occurring from 6 months to 5 years. In spite of this, the plethysmographic maximum venous outflow increased from 31 to 45 ml/min/100 ml (P less than 0.001). The foot volumetric reflux did not change with time and about half of the patients had abnormal values. Venous reflux assessed by the refill time of foot vein pressure, deteriorated with time (P less than 0.05), and at 5 years all but one patient had a refill time less than 20 s. The muscle pump function, examined by foot volumetry, was abnormally low in about half of the patients throughout the study. The ambulatory foot vein pressure was constantly pathological (greater than 60 mmHg) in half of the patients and only two of 18 patients had normal values (less than 45 mmHg) at 5 years. Five patients with thromboses involving only the proximal veins had better physiological results than 15 patients with thromboses that extended to the peripheral veins. Three patients who developed venous claudication had iliac vein obstruction and an impaired venous outflow and three patients who developed venous ulcers had venous reflux and severe venous hypertension. Although venous outflow continuously improves following ilio-femoral thromboses, valvular competence and muscle pump function are constantly pathological, creating severe venous hypertension with a risk of post-thrombotic sequelae.

Experimental atherosclerosis was induced in a rabbit model by intimal damage of the infrarenal aorta followed by two months cholesterol feeding. The influence of four different antiplatelet drug regimens on acute platelet and fibrin deposition after transluminal angioplasty of the atherosclerotic abdominal aorta was then evaluated. The study group consisted of 32 New Zealand rabbits: 7 controls, 7 treated with prostacyclin (10 mg/kg/min i.v.), 5 treated with low-dose acetylsalicylic acid (2 mg/kg i.v.), 7 treated with acetyl-salicylic acid (5 mg/kg i.v.) and dipyridamole (2 mg/kg i.v.), and 6 treated with low molecular dextran (5 ml/kg). By 2 hours after angioplasty, there was a significant increase of the deposition of platelets (P less than 0.001) as well as fibrin (P less than 0.01) when comparing dilated to non-dilated segments in the control animals. There was no significant difference in the amount of platelets and fibrin deposition among the control and drug treated groups. Thus, in this animal model there appears to be no immediate benefit in using antiplatelet drugs during transluminal angioplasty. Although, this study did not address the potential long-term effects of antiplatelet drug therapy, future evaluation of the clinical benefits of these drugs in conjunction with transluminal angioplasty seems warranted.