Early diagnosis of abdominal trauma.
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Biomedical subjects
Publications and source records attributed to R McLeod.
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A clear benefit of increased hospital procedure volume or teaching hospital status on outcomes of rectal cancer surgery has yet to be shown. Few have examined treatment differences that may lead to varying outcomes. This study assessed the impact of hospital procedure volume and teaching status on both treatment and outcome measures of rectal cancer surgery in a large general population. Data were obtained for 1072 incident cases of rectal adenocarcinoma diagnosed in 1990 from Ontario, Canada, and treated with a major resection. Hospitals were classified by teaching status and procedure volume. Pathology reports were examined for 418 procedures. Abdominoperineal resections accounted for 31.0% of all procedures. There were no clinically significant differences in treatment measures, operative mortality, and long-term survival among the hospital groups according to both univariate and multivariate analyses. In conclusion, the absence of a hospital volume or teaching status effect on treatment and outcome measures suggests that for rectal cancer surgery in Ontario, centralization of procedures into high-volume or teaching centers is unlikely to improve surgical quality.
The effect of total parenteral nutrition (TPN) containing approximately 800 ml Nutralipid daily on plasma cholesterol and lecithin:cholesterol acyl transferase (LCAT) activity was studied in 11 adult hospital patients. LCAT was assayed using an endogenous (S/N) and an artificial (ASA) substrate to differentiate between altered plasma substrate composition (which would influence the S/N method) and enzyme quantity (measured by the exogenous ASA method). Total cholesterol levels increased significantly during TPN, but generally remained within normal range. In comparison to laboratory reference values, free cholesterol was elevated and high-density lipoprotein cholesterol and ASA LCAT activity was reduced in patients before the start of TPN and remained unaltered by the TPN regime. S/N LCAT activity was normal and not altered by TPN. Since changes in plasma high-density lipoprotein and free cholesterol and ASA LCAT were present in patients before TPN, it must be concluded that they resulted from the underlying disease rather than the TPN per se. Longitudinal analyses showed that during the first 21 days of TPN nine patients showed a further fall in ASA LCAT and a rise in free cholesterol, thereafter ASA LCAT activity rose and free cholesterol fell despite continuation of TPN. It is suggested that ASA is a more reliable indicator of cholesterol esterification than S/N and that change in LCAT activity, although not caused by TPN, was related to the altered plasma lipid profile in the patients studied.
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Dilevalol (SCH 19927) is a potent, long-acting, nonselective beta-blocker with marked vasodilator actions. Unlike classical beta-blockers, dilevalol promptly lowers blood pressure and vascular resistance in animal models of hypertension. The present studies address the peripheral vascular effects of dilevalol and explore the role of beta-receptor agonism in the acute vasodilator and antihypertensive effects of the compound. In the denervated dog hindlimb preparation, dilevalol (0.1, 0.3, 1.0 and 3.0 micrograms, i.a.) significantly increased femoral blood flow by 12 +/- 6, 27 +/- 6, 84 +/- 31 and 132 +/- 41 ml/min, respectively. In contrast, celiprolol, a beta-blocker with purported vasodilator activity, caused a significant increase in flow of 31 +/- 9 ml/min at a dose of 30 micrograms i.a. Systematic pretreatment with the selective beta 2-antagonist ICI 118,551 virtually abolished dilevalol's vasodilator effect in the dog hindlimb. In conscious spontaneously hypertensive rats, 3 mg/kg i.v. dilevalol reduced blood pressure by 58 +/- 8 mmHg (P less than 0.05) and vascular resistance by 171 +/- 27 dyne.sec.cm-5/100 g (P less than 0.05) but did not change cardiac output significantly. Pretreatment of spontaneously hypertensive rats with ICI 118,551 significantly reduced both dilevalol's antihypertensive and resistance-lowering effects. Oral doses of 10 and 25 mg/kg dilevalol lowered blood pressure by 19 +/- 3 (P less than 0.05) and 37 +/- 5 mmHg (P less than 0.05) in spontaneously hypertensive rats with chronically implanted Doppler flow probes. The lower dilevalol dose reduced mesenteric vascular resistance 38 +/- 6% (P less than 0.05) while the higher dose significantly lowered vascular resistance in the hindlimb, mesenteric and renal vascular beds of spontaneously hypertensive rats by 18 +/- 8, 33 +/- 2 and 43 +/- 4%, respectively. Propranolol lowered neither blood pressure nor regional vascular resistances at the above doses in spontaneously hypertensive rats. Thus, dilevalol promotes a generalized fall in vascular resistance. Furthermore, the present studies illustrate that beta 2-receptor stimulation plays an obligatory role in both the vasodilatory and antihypertensive actions of dilevalol.
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