Biomedical subjects

M Wayne

Publications and source records attributed to M Wayne.

7 recordsLinked to original sources

PubMed2001

Endoscopic subfascial surgery for incompetent perforator veins in patients with active venous ulceration.

BACKGROUND: Previously, subfascial ligation of perforator veins to treat venous ulceration in the lower extremities required long skin incisions through diseased skin and subcutaneous tissue. This was known as "the Linton operation." In 1985, Hauer described an endoscopic technique for ligating incompetent perforator veins; this seminal contribution marked the advent of subfascial endoscopic perforator surgery (SEPS). METHODS: From 1996 to 1998, we prospectively collected data on 41 patients with chronic venous insufficiency (CVI) who underwent a SEPS procedure at our institution. Preoperative assessment consisted of color-flow duplex ultrasound scanning, as well as ascending and descending phlebography. RESULTS: Some 45 SEPS procedures were performed on the 41 patients. Ages ranged from 42 to 84 years (mean, 60). Active venous ulcers were present in 37 legs; healing occurred within 9 weeks in 33 of them. No new ulcers developed in the follow-up period, a mean of 44 weeks. CONCLUSION: The results suggest that the SEPS procedure incorporated into the overall treatment plan for patients with CVI produces active healing with a minimum of postoperative complications. The study demonstrates the safety and efficiency of this procedure; it also underscores the important role incompetent perforator veins have in the formation of venous ulcers.

Adult↗

PubMed2000

Iliac vein compression syndrome: a new method of treatment.

Iliac vein compression syndrome (May-Thurner syndrome) is caused by compression of the left iliac vein against the pelvic rim by the right iliac artery. Serious vascular sequelae to the leg can result if this is not recognized and corrected in a timely fashion. The condition, often underdiagnosed, is thought to be present in approximately 20 per cent of the adult population. Previously, a major vascular operation with a significant hospital stay was required to correct this compression. As a nonsurgical option, we elected balloon dilation of the stenosed iliac vein, with insertion of a venous stent to maintain the restored lumen. Two patients who had this procedure have been followed for 12 months; venograms show continued patency of the iliac vein with no pressure gradient present. This procedure is safe and cost effective, and it requires a minimal hospital stay.

Adolescent↗

PubMed1999

Bilateral iliac vein filter deployment in a patient with megacava.

An 85-year-old-woman presenting with low back pain developed shortness of breath and right-sided chest pain. She was found to have perfusion defects indicative of pulmonary embolus (PE). Heparin was at first employed, but had to be discontinued because of gastrointestinal bleeding. Caval filtration was the obvious course, but it was found on computed tomography (CT) scan that the suprarenal portion of the inferior vena cava was 55 mm in diameter, and the infrarenal portion 44 mm. These measurements were too large for insertion of a Greenfield filter, for which the maximum diameter should be 28 mm. The right common iliac vein was 28 mm in diameter, and the left external iliac vein 25 mm. Two filters were inserted percutaneously in these vessels. The patient was followed for 9 months. No clinical evidence of recurrent PE or venous insufficiency occurred.

Aged↗

PubMed1993

Redirection of arachidonic acid metabolism by ICI D1542: effects on thrombus formation in the coronary artery of the anaesthetized dog.

1. The effects of simultaneous redirection of arachidonic acid metabolism, by inhibition of thromboxane A2 (TXA2) synthase and blockade of the platelet thromboxane A2 receptor (TP-receptor), was examined on the rate of thrombus formation in a stenosed coronary artery with damaged endothelium in an anaesthetized dog. 2. Redirection of arachidonic acid metabolism was achieved by intravenous doses of ICI D1542, a selective and potent inhibitor of TXA2 synthase and the TP-receptor. 3. Redirection of arachidonic acid metabolism was demonstrated in whole blood, stimulated ex vivo by collagen. The ED50 for inhibition of TXB2 production was 7.1 micrograms kg-1, i.v.; there were corresponding increases in the production of the eicosanoids prostaglandin D2 (PGD2), PGE2 and PGF2 alpha. 4. Thrombus formation was inhibited by D1542 (ED50 0.55 micrograms kg-1, i.v.), but could be restarted by an intravenous infusion of adrenaline (0.2-38 micrograms kg-1 min-1, i.v.). In the presence of the maximum effective dose of D1542 (1 mg kg-1, i.v.) a 190 fold increase in the infusion rate of adrenaline was required to restore thrombus formation. 5. In the presence of D1542, removal of endoperoxide metabolites by inhibition of cyclo-oxygenase with aspirin (5 mg kg-1, i.v.) caused thrombus formation to restart, indicating the ability of the endoperoxide metabolites to inhibit thrombus formation in vivo. 6. These results indicate that, in the stenosed and damaged coronary artery of the dog, redirection of arachidonic acid metabolism by D1542 is more effective at preventing thrombus formation than inhibition of cyclo-oxygenase by aspirin.

Anesthesia↗

PubMed1989

Chest trauma.

Chest trauma will continue to be a significant cause of acute respiratory distress. It is a major source of morbidity and mortality in otherwise healthy young people. Airway control, oxygenation, drainage of pneumothoraces and hemothoraces and fluid resuscitation are the cornerstones of therapy. With these basic maneuvers, most chest trauma patients can be treated successfully.

Emergencies↗

PubMed1988

Studies in the guinea-pig with ICI 185,282: a thromboxane A2 receptor antagonist.

The effects of ICI 185,282 (5(Z)-7-([ 2,4,5-cis]-4-O-hydroxyphenyl-2-trifluoromethyl-1, 3-dioxan-5-yl)heptenoic acid) have been studied on guinea-pig platelets and pulmonary smooth muscle in-vitro and in-vivo. When tested on guinea-pig lung parenchyma in-vitro. ICI 185,282 (1 x 10(-7) M) produced a significant shift in U-46619 response curves (concentration ratio of 13:3); the antagonist (1 x 10(-5) M) did not modify histamine responses. When tested on guinea-pig trachea in-vitro ICI 185,282 (1 x 10(-7) M) caused significant inhibition of U-46619 and PGD2 responses (concentration ratios of 8.3 and 14.1, respectively); the antagonist (1 x 10(-5) M proved less effective against contractions of PGF2 alpha, LTD4 and histamine (concentration ratios of 7.0, 1.5 and 1.6). When added to guinea-pig platelet rich plasma in-vitro, ICI 185,282 (x 10(-6), 1 x 10(-5) M) caused concentration-dependent parallel shifts to the right of U-46619 aggregation curves, yielding concentration ratios of 13.6 and 141.9, respectively. In-vitro, addition of ICI 185,282 (x 10(-5) M) to indomethacin-treated pulmonary smooth muscle did not modify resting tone, neither did it induce aggregation or swelling in platelet-rich plasma preparations. When administered orally to guinea-pigs ICI 185,282 (0.1, 0.5 mg kg-1) caused a significant inhibition of U-46619-induced platelet aggregation ex-vivo which persisted greater than or equal to 8 h. In-vivo, a single oral dose of ICI 185,282 (1 mg kg-1) inhibited bronchospasm induced by U-46619, PGD2, PGF2 alpha, arachidonic acid, LTD4 and PAF; responses to histamine were unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Pharmacological actions of ICI 180080, a novel thromboxane receptor antagonist.

ICI 180080 (5(Z)-7-[2,2-dimethyl-4-(2-hydroxyphenyl)-1,3-dioxan-cis-5-yl] heptenoic acid) potently inhibited contractions of rat and rabbit aortae and guinea-pig trachea elicited by 11,9-epoxymethano PGH2 (U-46619). This antagonism was selective because contractions of aortae to noradrenaline and 5-hydroxytryptamine and trachea to histamine were not antagonized by ICI 180080. Schild analysis of data obtained from experiments on rabbit aortae indicated that this thromboxane receptor antagonism was competitive (pA2 = 7.50, slope = 1.07). Addition of ICI 180080 to human platelet-rich plasma caused dose-related inhibition of U-46619-induced platelet aggregation. This modification of platelet aggregation was not associated with inhibition of thromboxane synthetase, cyclo-oxygenase or lipoxygenase. ICI 180080 did not modify the primary phase of ADP-induced aggregation of human platelets neither did it affect the platelet inhibitory activity of prostacyclin. When dosed orally to anaesthetized guinea-pigs, ICI 180080 (5-50 mg kg-1) caused dose-related inhibition of U-46619-evoked bronchoconstriction. We conclude that ICI 180080 is a potent, selective, competitive, orally active thromboxane antagonist.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗