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OBJECTIVE: To analyze the quantity and distribution of intramuscular nerves within the striated urogenital sphincter and test the hypothesis that decreased nerve density is associated with decreased striated sphincter muscle and cadaver age. METHODS: Thirteen cadaveric urethras (mean age 47 years, range 15-78 years) were selected for study. A sagittal histologic section was stained with S100 stain to identify intramuscular nerves. The number of times that a nerve was seen within the striated urogenital sphincter (nerve number) was counted. The number of axons within each nerve fascicle was also counted. Regression analysis of nerve density against muscle cell number and age was performed. RESULTS: Remarkable variation was found in the quantity of intramuscular nerves in the striated urogenital sphincter of the 13 urethras studied. The number of nerves ranged from 72 to 543, a sevenfold variation (mean 247.1 +/- standard deviation 123.2), and the range of number of axons was 431 to 3523 (2201 +/- 1152.6). The larger nerve fascicles were seen predominantly in the distal (13.1 +/- 5.7 axons per nerve) compared with the proximal part of the striated urogenital sphincter (1.2 +/- 2). Reduced nerve density throughout the striated urogenital sphincter correlated with fewer muscle cells (P =.02). Nerve density also decreased with advancing age (P =.004). CONCLUSION: Remarkable variation in the quantity of intramuscular nerves was found. Women with sparse intramuscular nerves had fewer striated muscle cells. Intramuscular nerve density declined with age.

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The authors describe a 6-year-old girl in whom they found an embryonal rhabdomyosarcoma in a choledochal cyst; they found no previous reports of such an association. The patient presented with recurrent jaundice and loss of weight and appetite. A large abdominal mass was palpable. Ultrasonography and computed tomography revealed a large subhepatic mass, which contained multiple septations and mural masses delineating cystic areas. The common hepatic duct opened directly into the mass, and the intrahepatic radicles were dilated. Intraoperative cholangiography revealed that the cysts in the mass were continuous with the hepatic and intrahepatic radicles. The mass was completely excised, and a Roux-en-Y hepaticojejunostomy was performed. Postoperative adjunct chemotherapy and radiotherapy were instituted.

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The effect of repetitive brief periods of coronary occlusion on subsequent prolonged ischemic insult was studied using a swine heart model. Four 5-min episodes of left anterior descending coronary artery (LAD) occlusion, each separated by 10 min of reperfusion, did not affect any of the regional or global myocardial functions examined, except that the level of adenosine triphosphate (ATP) dropped to some extent. Sixty minutes of LAD occlusion following four repeated stunnings further reduced the ATP level, but this reduction was significantly lower compared to nonstunned control. Myocardial global functions were not affected significantly by prolonged ischemic insult. Segment shortening (SS) was reduced comparably in both control and stunned groups. However, SS improved significantly during subsequent reperfusion in the stunned group compared to control. The experimental group also demonstrated reduced infarct size and an area of risk compared to nonstunned control. These results indicate that repeated stunning prior to irreversible ischemic insult can attenuate ischemic injury and post-ischemic dysfunction.

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We report a fatal case of lipoid pneumonia in a two and one half month old Saudi female caused by aspiration of animal fat, ghee and complicated by Mycobacterium fortuitum infection. It highlights the need to look for M. fortuitum in lipoid pneumonia and suggests the prevention of the condition through health education.

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Intracellular Ca2+ accumulation is implicated in the pathogenesis of myocardial reperfusion injury. To study approaches designed to modify Ca2+ uptake during coronary revascularization after acute infarction, a pig heart surgical infarct model (left anterior descending artery occlusion for 60 min) was subjected to 60 min hypothermic potassium cardioplegic arrest, followed by 60 min of global reperfusion. Four groups of six hearts each were studied in a randomized manner, i.e., cardioplegia alone (control), cardioplegia + 10 microM diltiazem (Ca2+ slow channel blocker), cardioplegia + 10 microM trifluoperazine (TFP), (a Ca(2+)-calmodulin antagonist), and cardioplegia+diltiazem (10 microM) + TFP (10 microM). Left ventricular contractility (global and segmental), metabolism (coronary blood flow and O2 consumption), and creatine kinase generation were measured during reperfusion. Both the Ca2+ channel blocker, diltiazem, and the calmodulin antagonist, TFP, improved myocardial global and regional function as well as myocardial metabolism. While diltiazem better restored global and regional contractility, trifluoperazine had a greater effect on coronary blood flow and myocardial oxygen consumption. Enzyme release and lipid peroxidation were equally moderated by both drugs. From this study it can be concluded that Ca2+ influx does play a role in ischemic and reperfusion injury. The mechanisms of its effect are complex, but can be successfully antagonized by Ca2+ blockers as well as by calmodulin antagonists, with improved myocardial preservation.

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Repeated regional ischemia of short duration followed by reperfusion leads to preconditioning of the myocardium. Left anterior descending coronary artery (LAD) occlusion was applied for 5 minutes and then released for 10 minutes. This was repeated four times by using an intact pig model. LAD occlusion was then continuously applied for 1 hour. Myocardial function, high energy phosphates, and membrane phospholipids were compared with a control (nonstunned) group over a 6-hour reperfusion period. Stunning itself produced no significant change in regional function, total phospholipids, or free fatty acids (FFA). However, regional function, adenosine triphosphate, and creatine phosphate were significantly (p less than 0.05) reduced over control. After 60 minutes of ischemia, regional function was significantly improved by preconditioning that persisted throughout reperfusion (p less than 0.01). This was associated with an 11% mean decrease in infarct size (p less than 0.05). Adenosine triphosphate was significantly preserved during ischemia in the preconditioned hearts, and this preservation persisted throughout reperfusion (p less than 0.05). Total phospholipids were not affected by ischemia in either group. However, during reperfusion both groups demonstrated a 15-20% decrease in phospholipid levels at 1 hour, with only the stunned group showing a progressive increase at 3 and 6 hours (p less than 0.05). Examination of FFA during reperfusion demonstrated a profound increase in only the unstunned animals (p less than 0.05), correlating with the decreased level of membrane phospholipids noted in this group. In conclusion, repeated stunning predisposes the heart to recovery after regional ischemia. This results in improved mechanical function, increased high-energy phosphate stores, and decreased infarct size.(ABSTRACT TRUNCATED AT 250 WORDS)

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Captopril is an angiotensin-converting enzyme inhibitor that has been reported to be effective in salvaging post-ischemic reperfused myocardium by its ability to function as a free radical-scavenging agent. A study was performed in the isolated porcine-heart model evaluating the influence of pretreatment with captopril on salvage of myocardium after an induced myocardial infarction. Measurement was carried out of regional and global myocardial function, myocardial high-energy phosphate levels, creatine kinase release, malonaldehyde formation, and 6-keto-prostaglandin F1 alpha generation. In an in vitro preparation, the influence of captopril for scavenging various free radicals was evaluated. A dose-response curve was carried out using this free radical-generating system and differing levels of captopril. Results of the study demonstrate that pretreatment with captopril at a 45-mumol/L level reduced reperfusion injury in the pig heart model. This was manifested by improved cardiac performance, a reduction in creatine kinase release, and reduced malonaldehyde generation. In vitro evaluation of captopril and its free radical-scavenging ability indicated that it is a weak scavenger of superoxide anions (O2-) but behaves as a potent scavenger of hydroxyl radicals (-OH) as well as hypohalite radicals (OCl-). Based on the influence of captopril in reducing lipid peroxidation (decreased malonaldehyde formation) and its documented ability to scavenge -OH as well as OCl-, it is suggested that myocardial preservation in a postinfarction model is due primarily to its free radical-scavenging activity, primarily of the potent free radicals -OH and OCl-.

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The amino acids aspartate and glutamate, in combination, were evaluated as a means of reducing infarct size and improving cardiac function during reperfusion in an intact pig having an acute anteroseptal infarct. Three groups of 6 pigs each were randomly studied in a blinded manner: control (no amino acids), aspartate/glutamate 3 mmol/L, and aspartate/glutamate 13 mmol/L. The left anterior descending coronary artery was occluded distal to its first diagonal branch for 60 minutes followed by reperfusion for 6 hours. Aspartate and glutamate were administered systemically immediately before reperfusion. The following parameters were measured: infarct size and percent area at risk, global metabolic function, global and regional myocardial function, and tissue parameters of metabolic function. The results clearly showed a significant decrease in infarct size from 60% of the area at risk in control pigs to 37% in both 3 mmol/L and 13 mmol/L amino acid groups. Cardiac output, coronary blood flow, and global oxygen consumption were not significantly affected by the use of amino acids relative to the control group. Global left ventricular mechanical function was also not adversely affected by the infarct and was not altered by amino acid administration. Regional function, however, was significantly decreased by occlusion of the left anterior descending coronary artery in all groups to near 20% and only significantly recovered to 64% in the 13 mmol/L amino acid group. Adenosine triphosphate and acetyl coenzyme A measurements documented significant increases in the 13 mmol/L amino acid group relative to the control group. The conclusions of this study strongly support aspartate/glutamate supplementation for stunned, reperfused myocardium. It is apparent that the effect of amino acid supplementation on glycolysis is directly translated into improved regional function and reduced infarct size.

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A recent study from our laboratory indicated additional tissue injury during rewarming of a cooled rabbit leg. Oxygen-derived free radicals were believed to play a role in such "rewarming injury." Since free radicals may attack membrane phospholipids, we analyzed the phospholipid composition in the leg tissue during cooling and rewarming. Our results indicated significant breakdown of membrane phospholipids, particularly phosphatidylcholine and phosphatidylethanolamine, with a corresponding accumulation of lysophosphatidylcholine and nonesterified fatty acids. Quinacrine, a phospholipase inhibitor, was able to preserve membrane phospholipids during rewarming of the cooled leg. Rewarming of cooled tissue was also accompanied by additional tissue injury, as evidenced by the increased release of lactic acid dehydrogenase and creatine kinase, as well as enhanced lipid peroxidation, as evidenced by increased malonaldehyde formation. Quinacrine reduced the release of these intracellular enzymes and decreased lipid peroxidation, suggesting its efficacy as a therapeutic agent against hypothermic injury.

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We describe seven patients who suffered chronic gastric torsion, seen during a 28-month period. Four were children, of which three were infants. The infants had projectile vomiting and two also had failure to thrive. The adults presented with epigastric pain and vomiting. Upper gastrointestinal series clinched the diagnosis in all patients. The classic radiographic presentation of a stomach lying across the epigastrium with the cardia and fundus in a dependent position to the body of the stomach and pylorus may be overlooked in some cases. Choice of surgical procedure in its management has been discussed. There was no associated abnormality in four of the six operated cases. One infant had an atretic bowel, vascular anomalies, umbilical hernia, and previous meconium peritonitis; a second infant had jejunojejunal intussusception. A high index of suspicion is warranted in patients presenting with recurrent abdominal pain or in infants with unexplained vomiting and failure to thrive. Upper gastrointestinal series in adults should preferably be performed while the pain is present.

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The cardioprotective effects of a novel antiinflammatory drug, ONO-3144 (ONO), on ischemic-reperfused myocardium were investigated using an in situ pig heart model. Heart was subjected to 2 h of regional ischemia, with the final 1 h having superimposed global cardioplegic arrest followed by 1 h of reperfusion. ONO (20 microM) was administered after the arrest at the onset of reperfusion. Left ventricular developed pressure (LVDP), maximum rate of rise of left ventricular pressure (LV dp/dt), and left ventricular end-diastolic pressure (LVEDP) were measured under isovolumic conditions to assess cardiac contractility and compliance. ONO improved LVDP and LV dp/dt, and reduced LVEDP after 60 min of reperfusion compared to control. This drug also improved segment shortening and end-diastolic length significantly after 15 and 60 min of reperfusion. Slight improvements in oxygen consumption and creatine kinase (CK) release were also noted. In addition, ONO reduced lipid peroxidation and thromboxane formation but enhanced the production of prostaglandins. In vitro studied demonstrated ONO to be effective scavengers for both hydroxyl (OH.) and hypohalite (OCL.) radicals. The results suggest that myocardial reperfusion injury that developed after ischemic arrest was reduced significantly by ONO. This drug inhibited such injury, probably by directly scavenging potentially harmful radicals such as OH. and OCI., which are generated in ischemic-reperfused myocardium.

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Rewarming of a cooled rabbit leg was associated with the generation of oxygen-derived free radicals, shown to be instrumental for tissue injury occurring during rewarming. The present study used a compound that, by its ability to bind with free iron, can remove hydroxyl radical (OH.) from tissue. Deferoxamine reduced tissue injury during cooling and rewarming, as evidenced by its ability to decrease tissue release of lactic acid dehydrogenase and creatine kinase. Deferoxamine also reduced the formation of OH. and lipid peroxidation during the rewarming phase. This compound did not have any effect on the arterial blood flow pattern, which uniformly decreased during cooling and was restored during rewarming. The results of this study indicate the efficacy of deferoxamine in reducing cellular injury associated with cold and rewarming and further suggest a role for oxygen-derived free radicals in the pathophysiology of cold-rewarming injury.

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Four commercially available proteases were tested, in conjunction with a lipase, for efficacy in hydrolyzing 3 tissue substrates: cod fillet, chicken egg, and bovine liver. Enzymatic hydrolysis of tissues minimizes the formation of emulsions during liquid-liquid extraction and does not accelerate the decomposition of acid- or base-labile analytes. Recovery of hexane and benzene phases from the hydrolysates was also evaluated. Protease from Streptomyces griseus combined with lipase from Candida cylindracea (available commercially) produced the highest percent hydrolysis (relative to classical acid hydrolysis) in all 3 tested tissues (60-95%) and the greatest recovery of hexane (100%) and benzene (92-100%) solvent phases.

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Captopril, an angiotensin converting enzyme inhibitor, has been shown to increase prostaglandin production by an as yet unknown mechanism, which this study was designed to explore. Isolated rat heart was perfused by the Langendorff technique for 15 minutes in the presence or absence of captopril. Ischemia was then induced for 60 minutes by terminating the coronary flow, followed by 60 minutes of reperfusion. Our results indicate that captopril stimulated prostaglandin and thromboxane production, but it inhibited malonaldehyde formation. Coronary flow and high energy phosphate compounds were increased, but lactate dehydrogenase and creatine kinase release decreased, demonstrating cardioprotective effects. Captopril also inhibited the production of hydroxyl radical in the heart during reperfusion, suggesting that stimulated prostaglandin production may be linked with the generation of free radicals via the eicosanoid system.

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We studied 20 patients with advanced degrees of hypospadias and undescended testes for the presence of an intersex disorder. A comprehensive clinical, cytogenetic, endocrinological and surgical evaluation was performed. All patients were found to have an intersex disorder, including 10 with male pseudohermaphroditism and 10 with a gonadal/genetic intersex disorder. In the latter group 4 patients had mixed gonadal dysgenesis, 3 had dysgenetic male pseudohermaphroditism, 1 had the 46XX male syndrome, 1 had true hermaphroditism and 1 had Klinefelter's syndrome. Genetic and gonadal intersex disorders were more frequent in patients with a unilateral undescended testis and perineal hypospadias.

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