Diagnosis of limb compartment syndrome is based on clinical vigilance and repeated examination. Many techniques exist for tissue pressure measurement but they are indicated only in doubtful cases, the unconscious or obtunded patient, and children. However, monitoring of pressure has no harmful effect and may allow early fasciotomy, although the intracompartmental pressure threshold for such an undertaking is still unclear. Abdominal compartment syndrome requires measurement of intra-abdominal pressure because clinical diagnosis is difficult. Treatment is by abdominal decompression and secondary closure. Both types of compartment syndrome require prompt treatment to avoid significant sequelae.

Reperfusion of the ischemic myocardium results in the generation of oxygen-derived free radicals, NO, and presumably peroxynitrite. These, in turn, may cause strand breaks in DNA, which activate the nuclear enzyme poly(ADP ribose) synthetase (PARS). This results in a rapid depletion of intracellular NAD and ATP. When this reaction is excessive, there is ultimately cell death. Here we demonstrate that 3-aminobenzamide (and several other, chemically distinct, inhibitors of PARS activity) reduces the infarct size caused by ischemia and reperfusion of the heart or skeletal muscle of the rabbit. Inhibition of PARS activity also attenuates the myocardial dysfunction caused by global ischemia and reperfusion in the isolated, perfused heart of the rabbit. In skeletal muscle, inhibition of the activity of neuronal NO synthase reduces infarct size, indicating that the formation of NO contributes to the activation of PARS there. There is no significant neuronal NO synthase activity in the heart, and hence NO synthase inhibitors did not reduce myocardial infarct size. Thus, activation of PARS contributes to the cell death caused by ischemia-reperfusion, and PARS inhibitors may constitute a novel therapy for ischemia-reperfusion injury.Poly(ADP ribose) synthetase (PARS; EC 2.4.2.30) is a chromatin-bound enzyme, which plays a physiological role in the repair of strand breaks in DNA (1). PARS is located in the nuclei of cells of various tissues, including the heart and skeletal muscle (2). When activated by strand breaks in DNA, PARS catalyzes the transfer of ADP ribose moieties from NAD with the concomitant formation of nicotinamide. This results in a substantial depletion of NAD. Nicotinamide, which inhibits PARS activity by negative feedback, can be recycled to NAD in a reaction that consumes ATP. As NAD is essential to mitochondrial electron transport, depletion of NAD rapidly leads to a fall in ATP, and ultimately cell death (3-5). Radicals including superoxide anions, hydrogen peroxide or hydroxyl radicals (3-5), and NO or peroxynitrite (6-8) cause the breakage of DNA strands and activation of PARS. Inhibitors of PARS activity attenuate the fall in NAD and ATP and improve survival of cultured cells (e.g., fibroblasts, endothelial cells, and smooth muscle cells) exposed to oxygen-derived free radicals (3-5, 9), NO (6-8), or peroxynitrite (8). The formation of radicals contributes to the ''reperfusion injury'' of previously ischemic organs, including the heart (10) and the skeletal muscle (11). Here we demonstrate that several inhibitors of PARS activity reduce the infarct size caused by ischemia-reperfusion of the heart and skeletal muscle. MATERIALS AND METHODS Determination of Myocardial Infarct Size (in Vivo).Male New Zealand white rabbits were premedicated [Hypnorm (Janssen, Saunderton, U.K.), 0.1 ml⅐kg Ϫ1 i.m.; containing 0.315 mg⅐ml Ϫ1 fentanyl citrate and 10 mg⅐mlϪ1 fluanisone] and anesthetized (pentobarbitone, 20 mg⅐kg Ϫ1 i.v.). Following tracheotomy and ventilation (36-40 strokes⅐min Ϫ1 , tidal volume: 18...

NAC (i.v. at 1 g) precontrast and postcontrast does not confer any benefit in preventing RCM-induced nephropathy in vascular patients. Patients with pre-existing raised SC have an increased risk of renal impairment as defined by a fall in CrCl and a rise in SC post-RCM when compared with patients with normal SC who appear to benefit from hydration.

cholesterol-lowering with atorvastatin 20 mg/day leads to a decrease in CCA-IMT and CFA-IMT. This difference achieved significance after 8 weeks of treatment, but a trend was visible at 4 weeks. These rapid changes in IMT may be attributable to an anti-inflammatory effect. IMT measurement may be a useful tool to rapidly assess the effect of drug treatment on the atherosclerotic process.

The objective of this study was to investigate the effects of lipid-lowering treatment on renal function in patients with peripheral arterial disease (PAD). This was a retrospective study of hyperlipidemic claudicants referred to a vascular surgery and risk modification clinic. Serum creatinine and urate concentrations and the fasting lipid profile were measured pretreatment and after 3-4 months of treatment with 20 mg/day simvastatin. In 103 consecutive patients with PAD (57 men; 46 women), median age 67 years (range: 51 to 83) there was a significant decrease in serum creatinine from a mean (SD) of 87 (12) micromol/L pretreatment to 84 (12) micromol/L post-treatment (p<0.0001). This difference was more marked in the tertile of patients with the highest baseline creatinine levels. There was also a significant reduction in serum urate from 0.37 (0.07) mmol/L to 0.35 (0.07) mmol/L (p<0.0001). Both these effects were independent of the degree of total cholesterol (TC) or low-density lipoprotein (LDL) cholesterol reduction. There was a significant reduction in TC from 6.6 (1.0) to 5.2 (0.8) mmol/L and LDL cholesterol from 4.3 (1.0) to 2.8 (0.7) mmol/L; both p<0.0001. Significant improvement also occurred in the high-density lipoprotein cholesterol and triglyceride levels. Cholesterol lowering with simvastatin 20 mg/day improved indices of renal function after 3-4 months of treatment in hyperlipidemic patients with PAD. Further studies are needed to establish and define the clinical relevance of these findings, especially in patients with different degrees of renal failure.

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Fewer patients are diagnosed with ACS in district general hospitals compared with teaching hospitals. The threshold for the diagnosis of ACS is variable in the UK, as were the numbers of patients who were decompressed, suggesting that many doctors are still reluctant to accept this condition. This study would suggest that there is a need for standardisation of diagnostic threshold and protocols regarding decompression in ACS.

In the UK the majority of vascular consultants see less than 10 patients annually with lymphoedema. Very few patients undergo confirmation of this diagnosis with non-invasive investigation and very few consultants perform surgery. Management of this condition is perceived by the consultants to be poor, with a lack of resources and particular shortage of lymphoedema physiotherapists. Centralisation of these services may be a way of improving this condition.