Mediation of bradykinin-induced contraction in canine veins via thromboxane/prostaglandin endoperoxide receptor activation

1. Canine jugular and femoral veins were studied to determine the possible importance of thromboxane (TXA2) and prostaglandin endoperoxides (prostaglandin H2, PGH2) in mediating bradykinin(BK)-induced contraction. 2. Isolated vein rings incubated in modified Krebs solution contracted to TXA2/PGH2 analogs SQ26655 and U44069 with potency of contraction exceeding that for BK. The potency ranking for both veins was SQ26655 greater than U44069 greater than BK greater than PGF2 alpha greater than TXB2 much greater than PGD2. 3. The cyclo-oxygenase inhibitors indomethacin (3 x 10(-7) M) and flufenamic acid (10(-5) M) reduced BK contractions without affecting those induced by noradrenaline (NA). 4. TXA2/PGH2 receptor antagonists SQ29548 (10(-8) M) and BM13177 (10(-6) M) strongly inhibited BK-induced tension. The action of antagonists was reversible with negligible influence on NA-elicited contraction. Selective removal of endothelium had no effect on BK-induced contraction or the action of the antagonists. 5. The thromboxane synthase inhibitors dazoxiben (10(-4) M) and CGS 12970 (10(-5) M) had no significant inhibitory effect on BK-induced tension. 6. These results suggest that in canine jugular and femoral vein, the action of BK is largely dependent upon stimulation of the cyclo-oxygenase pathway to produce PGH2 and possibly TXA2, which can activate a smooth muscle TXA2/PGH2 receptor to elicit vasoconstriction.     

Fractured talar beaks

The talar beak is a well-described secondary sign of talocalcaneal coalition but is not pathognomonic of the condition and may be seen in other causes of restricted or abnormal subtalar motion. We present an unusual complication of talar beaks in two patients who sustained fractures through their beaks. One of the patients described did not have a talocalcaneal coalition but had developed a beak following a compound fracture dislocation of the ankle joint complicated by infection, a previously undescribed predisposing cause.     

Preventive care for patients following myocardial infarction. The Wessex Research Network (WReN)

OBJECTIVE: We aimed to assess general practice care for patients following a myocardial infarction (MI). METHOD: A structured review was carried out of general practice records of patients identified from hospital administration data. A total of 266 survivors following MI were identified from the discharge data of 13 hospitals in Southern England and registered with 71 GPs belonging to the Wessex Research Network. Median time since hospital discharge was 2.1 years. The main outcome measures were the provision of appropriate preventive care, including cardiac rehabilitation, drug therapy, and lifestyle advice for modifiable risk factors. RESULTS: Basic care was provided to nearly all patients; 253 (95.1%, 95% Cl 91.8-97.4) had blood pressure documented after their MI, 216 of 234 patients eligible for aspirin (92.3%; 88.1-95.4) had been recommended treatment, and the provision of advice on smoking cessation was documented for 27 of 33 continuing smokers (81.8%; 64.5-93.0). However, only 73 of 236 patients eligible to attend a structured rehabilitation programme (30.9%; 25.0-36.8) were documented as having received rehabilitation. Of 89 patients with heart failure following MI, 33 (37.1%; 27.1-48.0) had no record of having been offered treatment with an ACE inhibitor. Total cholesterol measurement was documented for only 144 patients (54.1%; 48.1-60.1). We estimate that there is still the potential to prevent between 4 and 9 deaths in this group of 266 surviving patients in the next 2 years by further improving the quality of follow-up care. CONCLUSIONS: Preventive care in patients with proven ischaemic heart disease in general practice remains haphazard, even among doctors enthusiastic to participate in research and to audit their quality of care. As general practitioners we should ensure that we are providing high quality preventive care to patients with clinical disease before we focus on the even more demanding task of primary prevention.      

Symptomatic and Clinical Improvement in Morbidly Obese Patients with Gastroesophageal Reflux Disease Following Roux-en-Y Gastric Bypass

Background: Patients who suffer with gastroesophageal reflux Disease (GERD) endure a worsening of symptoms as their weight increases. When medical treatment of this condition in the morbidly obese patients fails, surgical intervention may be indicated. Choosing a procedure which not only helps achieve weight control but which also relieves symptoms and complications of GERD is the goal. We present a review of patients who have undergone Roux-en-Y Gastric Bypass (RYGBP) and related procedures for this disease. Methods: One hundred eighty-eight patients undergoing surgery for morbid obesity and for GERD in 1992-1996 were contacted by mail or phone. All of these patients had undergone preoperative esophagogastroduodenoscopy to grade the severity of their disease. Their preoperative symptoms were compared to those experienced postoperatively. Results: One hundred thirty patients underwent a RYGBP with modified Hill fundopexy, 22 patients underwent a distal gastrectomy with modified Hill fundopexy, 8 patients underwent distal gastrectomy alone and 28 patients underwent RYGBP alone. There have been no deaths. There were nine surgical complications, eight early and one at 2.5 years postoperation. Follow-up is 4-48 months. The average BMI dropped from 43 to 30.2 kg/m². Whereas all patients were on some form of medical therapy before surgery, only 14 reported the need for medication postoperatively. Conclusions: Surgical intervention for weight control and treatment of GERD has been highly successful in our experience both with respect to weight control and to the reduction of reflux symptoms. Depending upon endoscopic and operative findings a RYGBP with or without an antireflux procedure can provide dramatic improvement. Gastrectomy with antireflux modifications is appropriate in selected cases.     

Cobb's collar--a forgotten entity

Cobb's collar or Moormann's ring is a stricture of the bulbar urethra which is largely unrecognised but has considerable relevance urologically as the site of congenital or post-instrumental strictures. The history, anatomy, embryology and surgical importance are reported.     

Beta carotene uptake into atherosclerotic plaque: Enhanced staining and preferential ablation with the pulsed dye laser

The yellow color of atherosclerotic plaque is due to the presence of carotenoids, which absorb light between 430–530 nm and account for the preferential ablation of plaque by the pulsed dye laser operating at 480 nm. This study was designed to examine tissue uptake of β-carotene and the effect of uptake on arterial plaque ablation. Forty-two atherosclerotic NZW rabbits were given intravenous β-carotene at a dose of 40 mg/kg, twice weekly and killed between 1 hour and 28 days after the initial injection. β-carotene was not detected in control specimens but was significantly greater in plaque than in normal wall at all time points following β-carotene injection (P < 0.04 Mann Whitney U test). The ablation threshold was significantly lower in β-carotene treated plaque than in untreated plaque or normal arterial wall (P < 0.01, Fisher's exact test). In this model β-carotene is preferentially taken up into arterial plaque, resulting in increased absorption of laser radiation at 480 nm and enhanced tissue ablation. © 1993 Wiley-Liss, Inc.     

Relation between toxicity and carcinogenesis in the kidney: an heuristic hypothesis

Cellular toxicity and cellular carcinogenesis are closely linked. In the kidney, this relationship has been emphasized by the recent discovery of a number of putatively non-mutagenic chemicals that result in acute and chronic toxicity and ultimately in carcinogenesis, especially in the male rat. Many, but not all such compounds, result in renal PTE phagolysosomal overload. At the same time, known metabolites of other carcinogens, e.g., HCBD and FBPA, result in acute renal injury and/or necrosis, followed by chronic tubular disease, interstitial nephritis, and ultimately carcinogenesis. A series of cell mechanisms have been suggested that lead from acute cell injury to altered control of cell division. These mechanisms appear to involve ion deregulation, (especially [Ca2+]i) resulting from a variety of continued injuries, (e.g., oxidative stress from inflammatory cells) and ultimately leading to altered gene expression.     

Endoscopic cleaning and disinfection procedures for preventing iatrogenic spread of human immunodeficiency virus

With estimates as high as 1.8 million individuals infected with human immunodeficiency virus (HIV) in the United States, the majority asymptomatic, it is crucial that all physicians routinely use adequate disinfection procedures for medical instruments. The protosigmoidoscopic disinfection procedures used by US family physicians were evaluated for adequacy in inactivating HIV. Sixty-seven percent of 1,585 randomly selected American Academy of Family Physicians members completed a mail survey regarding these procedures. Comparing procedures used with those recommended by the Centers for Disease Control or documented to inactivate HIV, 32.4 percent were judged to be appropriate procedures; 54.4 percent of the procedures were not tested or recommended; and 13.2 percent used appropriate solutions but at inadequate concentrations or exposure times. Therefore, a substantial proportion of US family physicians performing endoscopic procedures use disinfection procedures that may not inactivate HIV. The ever-increasing prevalence of HIV demands that standardized adequate disinfection procedures be implemented by all physicians to prevent the potential nosocomial spread of HIV.     

Carbon Monoxide Mass Exposure in a Pediatric Population

Abstract. Objectives:To describe the outcomes of a mass carbon monoxide (CO) intoxication, and to calculate the CO half-life in a pediatric school-aged population.
Methods:A retrospective chart review was performed based on Regional Poison Center database information, hospital laboratory data, and medical records of the pediatric patients who sought care at one of 3 St. Louis area hospitals, after exposure to high levels of CO. Exposures occurred on January 5, 1996, after evidence of a CO leak was discovered at an area elementary school. Charts were reviewed for major demographics, symptoms reported, carboxyhemoglobin (COHb) levels and times, and level of effect.
Results:Information about 177 (35%) of the 504 children in attendance at school that day was available. Mean age was 8.7 ± 1.8 years (range 4–12 years). Symptoms were present in 155 (88%) of the 177 children for whom data were available. Initial COHb levels were obtained for 147 (83.1%) of the 177 children. First mean COHb level was 7.0% (95% CI = 6.6–7.5%). Second COHb level was obtained for 26 children with a mean of 2.7% (95% CI = 2.2–3.2%). Calculated half-life of COHb, on 100% 0₂ at 1 atm, was 44.0 minutes (95% CI = 39.6–48.2 minutes).
Conclusion:Some children had symptoms at COHb levels that traditionally have been considered nontoxic. The elimination of COHb was found to be more rapid in this population of children than reported in other studies.     

The role of extracellular calcium in ischemia/reperfusion injury in skeletal muscle

Ischemia-reperfusion injury to skeletal muscle, following an acute arterial occlusion is a significant cause of morbidity and mortality. The purpose of this study is to examine the role of extracellular calcium in the production of cellular necrosis following a prolonged period of normothermic ischemia. Bilateral canine gracilis muscles were made ischemic for 4.5 to 5 hr. The control muscle had normal blood reperfusion (ionized Ca2+ 1.2 mM). The treated muscle was perfused for 30 min with an oxygenated solution (ionized Ca2+ 0.11 mM) containing free radical scavengers followed by normal blood perfusion. Necrosis was determined by nitroblue tetrazolium staining after 48 hr of reperfusion. Total muscle Ca2+ was measured by atomic absorption spectrometry. Pre- and postischemic muscle Ca2+ levels were similar (2.8 +/- 0.4 vs 3.2 +/- 0.8 nmole/mg protein, n = 13, P greater than 0.1). After 30 min of reperfusion the treated muscle Ca2+ was 2.4 +/- 0.4 compared to control levels of 8.6 +/- 0.8 nmole/mg protein (P less than 0.001). Total tissue calcium returned to normal at 60 min in viable muscle, but continued to accumulate in necrotic tissue. However, the delay in initial muscle Ca2+ influx was not associated with increased overall salvage of muscle 78 +/- 9% vs 77 +/- 8% necrosis, (P greater than 0.1). In conclusion we could not demonstrate a protective effect of reduced extracellular Ca2+ during early reperfusion, and it negated our previously demonstrated beneficial effects of free radical scavengers. It was shown however that the early ability to extrude intracellular calcium was associated with significant salvage of muscle tissue.