123rc/medical_text huggingface dataset:
Overestimation of myocardial infarct size by histologic measurement in a model of occlusion followed by reperfusion. We studied 32 transverse left ventricular slices of myocardium from 16 pigs after 45 to 100 minutes of coronary artery occlusion followed by 180 minutes of reperfusion. Infarct area for each slice was determined as follows: (1) grossly, by triphenyl tetrazolium chloride staining of each slice, and (2) microscopically, by complete histologic sectioning of the triphenyl tetrazolium chloride-stained surface of each slice. Planimetry of necrotic and nonnecrotic areas was performed from tracings and photographs of triphenyl tetrazolium chloride-stained slices and from actual histologic sections. When triphenyl tetrazolium chloride and histologic measurements were compared, necrotic tissue area had decreased 11.4% +/- 15.0% (2.59 +/- 1.04 vs 2.09 +/- 0.86 cm2). Nonnecrotic tissue area decreased 20.6% +/- 24.0% (8.31 +/- 3.79 vs 5.16 +/- 2.73 cm2). In this model of ischemia followed by reperfusion, with fixation and processing, viable tissue shrank almost twice as much as necrotic tissue. This differential shrinkage introduces an error resulting in overestimation of infarct size by histologic quantitation.
Evidence of an antiplatelet aggregation action of doxazosin in patients with hypertension: an ex vivo study. Eighteen patients with a mean age of 54.7 years were included in the study. All patients had a diagnosis of mild or moderate essential hypertension (sitting diastolic blood pressure of 96 to 114 mm Hg). The study design was single blind and in two phases: phase I, placebo (4 weeks), and phase II, the active treatment (8 weeks) with increasing doses, if needed, of doxazosin every 2 weeks (1, 2, 4, and 8 mg/day). Results show that doxazosin has an antihypertensive effect that is dose dependent. Systolic, diastolic, and mean blood pressures were decreased significantly, and no effect on heart rate was observed. Doxazosin significantly inhibited the platelet aggregation induced by epinephrine, adenosine diphosphate, and collagen in a dose-dependent manner. In addition, treatment with doxazosin lowered total serum cholesterol and triglyceride levels, without changing other standard biochemical parameters. This indicates that doxazosin could offer a distinct therapeutic advantage in the modulation of atherogenic and thromboembolic factors associated with coronary heart disease.
Adenine nucleotide changes in kidney, liver, and small intestine during different forms of ischemic injury. The purpose of this study was to better characterize renal adenine nucleotide pool responses to different forms of shock, contrast the changes to those found in other intra-abdominal organs (the liver and small intestine), and assess whether these changes are closely mimicked by those produced by renal arterial occlusion, the usual method used to study ischemic acute renal failure. Rats were subjected to hemorrhagic shock, septic shock, or cardiopulmonary shock of varying severities and durations. The liver consistently had the greatest energy depletion, followed by the kidney, and then the small intestine. However, only the kidney developed clear morphological damage (S3 brush border sloughing). Kidney adenylate pools were better preserved during septic shock and cardiopulmonary shock than during hemorrhagic shock despite comparable blood pressures. Only profound hemorrhagic shock (35-40 mm Hg for 25 minutes) decreased total adenylate pools (ATP + ADP + AMP). However, the degree of renal catabolite (nucleosides plus purine base) accumulation did not correlate with the amount of renal total adenine nucleotide depletion, partially because circulating catabolites contributed to intrarenal catabolite pools. Purine base/uric acid ratios differed among shocked organs, consistent with different degrees of xanthine oxidase activity (small intestine greater than liver greater than kidney). Renal morphological damage decreased during the immediate (0-30 minutes) postshock period, and the extent of this improvement was not altered by xanthine oxidase inhibition (oxypurinol), suggesting that the immediate postshock period is not one of serious oxidative injury. Shock, in comparison with renal arterial occlusion, caused only modest ATP loss/catabolite accumulation, very low purine base/uric acid ratios, and no immediate-reperfusion (0-30 minutes) resynthesis of the total adenylate pool. Thus, ischemia-induced renal adenylate changes may differ considerably, depending on the nature of the ischemic event.
Responses of intercostal muscle biopsies from normal subjects and patients with myasthenia gravis. In order to evaluate the mechanisms of weakness in muscles of patients with myasthenia gravis (MG), intercostal muscle biopsies were obtained from 9 normal subjects and 6 MG patients, and the compound muscle action potential (AP) and tension responses to nerve and muscle stimulation, and contracture responses on exposure to caffeine, were monitored in vitro. In normal muscle, on stimulation of the nerve or muscle at 30 to 100 Hz, the AP responses showed decrement in amplitude, one-third of which was attributable to failure of neuromuscular transmission and two-thirds to failure of muscle membrane excitation. On stimulation at 1 to 5 Hz, the AP responses showed very little decrement, while the contractile responses showed significant fade in tension, due to failure of E-C coupling or contractility. In muscle from patients with generalized MG, stimulation of the nerve at all frequencies (1 to 100 Hz) caused much greater decrement in APs and fade in tension responses than in normal muscle, due mainly to failure of neuromuscular transmission. However, at 100 Hz, 40% of the decrement in APs was due to failure of muscle membrane excitation, and at 1 to 5 Hz, 40% of the fade in tension was due to failure of E-C coupling or contractility, as in normal muscle. On direct stimulation the contraction and half-relaxation times were slower and the tetanic tension was smaller than in normal muscle, especially in the MG patient with thymoma. Caffeine-induced contractures were smaller in MG muscle than in normal muscle. These results indicate that while the weakness of MG muscle is due mainly to failure of neuromuscular transmission, it is also partly due to reduced E-C coupling or contractility.
Mechanism of intermittent preexcitation in the Wolff-Parkinson-White syndrome. The concept of electronically mediated conduction across an inexcitable gap. A man with intermittent preexcitation in the Wolff-Parkinson-White syndrome is reported. Once a sinus impulse was blocked in the accessory pathway, the block (ie, loss of preexcitation) was continued for a while until a PP interval reached or exceeded a critical period inducing sudden reappearance of preexcitation. This critical period was considerably longer than the effective refractory period of the accessory pathway. These findings are explained by the use of the concept of electronically mediated conduction across an inexcitable gap in the accessory pathway. It seems that when loss of protection was maintained, the sinus impulse was blocked at the site proximal to the gap, but the impulse passing through the atrioventricular node always reached retrogradely the site distal to the gap, and therefore, the next sinus impulse was blocked again.
Iatrogenic injuries of peripheral nerves. In this study, we discuss 68 cases in which peripheral nerve trunks were inadvertently divided by surgeons. Most of these accidents occurred in the course of planned operations. Delay in diagnosis and in effecting repair was common. We list the nerves particularly at risk and the operations in which special care is needed. We recommend steps to secure prompt diagnosis and early treatment.
Evidence for motor neuropathy and reduced filling of the rectum in chronic intractable constipation. Subtotal colectomy with ileorectal anastomosis is now frequently offered to patients with slow transit constipation who have severe symptoms and no response to more conventional medical treatment. If this operation is to be successful, the underlying problem should be delay in the progress of contents through the colon but no mechanical or functional obstruction in the small bowel or rectum. We have used a recently described technique of prolonged ambulant manometry and electromyography to investigate anorectal function in these patients. Pressure data were collected using a 2 mm diameter intrarectal probe carrying microtransducers, and external anal sphincter activity was assessed by a pair of silver-silver chloride surface electrodes. Fourteen control subjects and eight patients with colonic inertia were studied. Sampling reflexes, indicative of rectal filling, occurred at mean (SEM) rates of 7.4 (2.0)/hour in controls but were significantly reduced in patients (2.4 (0.3)/hour (p less than 0.01]. Recurrent rectal motor complexes were seen to occur in both groups at intervals of 76 (1.8) minutes in controls and 64.9 (7.2) minutes in patients (p less than 0.1), and with amplitudes of 42.4 (2.1) mmHg and 9.2 (0.7) mmHg (p less than 0.001), respectively. External sphincter electromyographic spike activity did not differ between groups. Our results support the concept of reduced transit of faeces to the rectum from the colon over a 24 hour period in slow transit constipation and suggest that a motor neuropathy may also be present in the rectum.
Surgical therapy in Barrett's esophagus. Seventy-six patients with Barrett's esophagus were cared for during a 10-year period. Fifty-six patients (74%) presented with complications of the disease. There were 20 strictures, 7 giant ulcers, 11 cases of dysplasia, and 29 patients with carcinoma. In patients with benign disease, 93% had mechanically defective sphincters and 83% had peristaltic failure of the lower esophageal body. Esophageal pH monitoring showed excessive esophageal exposure to pH less than 4 in 93% and excessive exposure to pH more than 7 in 34% of the patients tested. Ninety-three per cent of patients with excessive alkaline exposure had complications, compared to only 44% with normal alkaline exposure (p less than 0.01). Gastric pH monitoring, serum gastrin levels, and gastric acid analysis supported a duodenal source for the alkaline exposure. Antireflux surgery was performed using Nissen fundoplication in 30, Belsey partial fundoplication in 3, and Collis-Belsey gastroplasty in 2. Six required resection with colon interposition. Good symptomatic control was achieved in 77% after antireflux surgery. Four patients had symptoms and signs of duodenogastric reflux; three required a bile diversion procedure. Fifteen patients had an en bloc curative resection with colon interposition. One patient with high-grade dysplasia on biopsy was found to have intramucosal carcinoma after simple esophagectomy. Five tumors were intramucosal, seven were intramural, and four were transmural. Lymph node involvement occurred only in the latter two. Actuarial survival 5 years after curative resection was 53%. Median survival time for patients after palliative resection or no resection was 12 months. Study of en bloc specimens indicated that extent of resection should be adapted to extent of disease: esophagectomy for intramucosal disease, en bloc esophagectomy with splenic preservation for intramural and transmural disease. Serum CEA was useful in detecting recurrent disease after surgery when the primary tumor stained positively for CEA.
Correction of subclavian artery stenosis by percutaneous angioplasty. Subclavian artery stenosis is an infrequently recognized cause of left-sided chest and arm pain that can mimic the signs and symptoms of angina pectoris. In addition, more proximal subclavian artery stenoses can be associated with cerebrovascular symptoms in the "subclavian steal syndrome." This article reviews the clinical experience in four patients who presented with different manifestations of subclavian artery stenosis and who were all successfully treated by percutaneous angioplasty. Their clinical presentation, angiographic findings, and post-angioplasty results are documented. In conclusion, it is felt that nonsurgical correction of critical subclavian artery stenosis, using current angioplasty techniques, is the preferred method of treatment.
Radiographic manifestations of anomalies of the brain. Congenital brain anomalies are classified as developmental anomalies, effects of teratogens, errors of histogenesis, or sequelae of infections. The imaging options for delineation of these anomalies are many; a basic understanding of the disorder is central to the effective choice of imaging modality. This review begins with a brief overview of embryogenesis then reviews the common congenital brain anomalies encountered in infants.
Absent or minimal cerebrospinal fluid abnormalities in Haemophilus influenzae meningitis. A case of Haemophilus influenzae type b (Hib) meningitis in which the diagnosis and treatment were delayed because of normal cerebrospinal fluid analysis is presented. A retrospective review was conducted at two children's hospitals to determine the frequency and clinical characteristics of patients with Hib meningitis whose spinal fluid had a normal total white blood cell count, normal chemistries, and negative Gram stain, but subsequent growth of Hib in culture. Of 379 cases of Hib meningitis, two had completely normal CSF, and two had CSF containing small numbers of polymorphonuclear cells as the sole abnormality. In three of the four cases, the duration of symptoms was less than 24 hours, and appropriate therapy was significantly delayed because of benign-appearing CSF. Normal CSF cell counts, chemistries, and Gram stain do not exclude the possibility of bacterial meningitis, and one should remain suspicious when a child has clinical findings suggesting meningitis.
Orbital complications secondary to endoscopic sinus surgery. Eight cases of significant orbital complications associated with endoscopic sinus surgery are described. The anatomic problems generally fall into four categories: nasolacrimal sac or duct injury, extraocular muscle injury, intraorbital hemorrhage/emphysema, or optic nerve injury. The successful management of each complication depends on a thorough knowledge of the anatomy and pathophysiology of the orbital injury. Return to normal function of the traumatized orbital structures after medical and/or surgical intervention is anticipated. However, direct optic nerve injury with immediate visual field and/or acuity deficit is usually irreversible.
Systemic and renal production of thromboxane A2 and prostacyclin in decompensated liver disease and hepatorenal syndrome. To assess the role of altered renal and systemic production of thromboxane A2 and prostacyclin in the hepatorenal syndrome, urinary excretion of their major renal and extrarenal metabolites was measured in patients with compensated and decompensated liver disease, chronic renal failure, and hepatorenal syndrome. Urinary excretion rates of all prostanoids (renal and extrarenal) were increased in subjects with liver disease compared with normal controls. Moreover, they were considerably higher in subjects with severe hepatic decompensation but good renal function compared with those with hepatorenal syndrome. In contrast, the excretion rate of all metabolites was reduced in patients with chronic renal failure. The excretion rate of all metabolites was markedly elevated during the early stages of hepatorenal syndrome and decreased in parallel with creatinine clearance. When corrected for creatinine clearance, there was a strong correlation between prostanoid excretion and serum bilirubin in subjects with liver disease; there was no difference, however, in the excretion of renal and extrarenal prostanoids between hepatorenal syndrome and severe hepatic decompensation. It is concluded that hepatic decompensation is associated with a progressive increase in prostanoid excretion but that changes in production of prostacyclin or thromboxane A2 are unlikely to be major factors in the pathogenesis of the hepatorenal syndrome.
Healing or amelioration of esophagitis does not result in increased lower esophageal sphincter or esophageal contractile pressure [published erratum appears in Am J Gastroenterol 1991 Feb;86(2):253] There is conflicting evidence regarding whether lower esophageal sphincter and esophageal contractile pressures are affected by changes in the severity of gastroesophageal reflux disease. We compared the manometric and endoscopic findings from 30 patients before and after treatment for esophagitis. Before treatment, the grade of esophagitis (I-III) was significantly correlated (r = -0.37; p less than 0.05) with lower esophageal sphincter pressure, but not with esophageal contractile pressure. After treatment, the grade of esophagitis did not change or became worse in 15 patients, and became better in 15 patients. Of these, seven healed. The group that showed no endoscopic improvement demonstrated no change in lower esophageal sphincter or esophageal contractile pressures. The group that did show endoscopic improvement also demonstrated no increase in lower esophageal sphincter or esophageal contractile pressures, and this was particularly evident in those whose esophagitis healed. These data suggest that healing of esophagitis does not result in improvement of esophageal motor function.
Prevalence of Raynaud phenomenon in the adult population of South Carolina. A prevalence estimate for Raynaud phenomenon among adult residents of South Carolina was based on data obtained from respondents in a statewide health survey, followed by face-to-face interviews and clinical screening for Raynaud phenomenon, using a screening procedure developed by the authors. The survey obtained 5246 personal interviews from a probability sample of over 3000 households, and 494 survey subjects participated in the clinical screening. The prevalence estimates and their standard errors were computed using survey case weights, design-based estimation, and logistic modelling techniques. The prevalence of Raynaud phenomenon among adult residents of South Carolina was determined to be 3.5%, with a standard error of 0.6%. Prevalence was higher for females (4.3%, SE = 0.7%) than for males (2.7%, SE = 0.6%). These figures are much lower than most estimates in the existing literature on Raynaud phenomenon.
Stasis syndromes following gastric surgery: clinical and motility features of 60 symptomatic patients. We retrospectively reviewed the records of 60 patients who had been referred for gastrointestinal manometry because of stasis after gastric surgery. Nausea, vomiting, bloating, abdominal pain, and weight loss were the most common symptoms. Two thirds of these patients had a well-documented history of peptic ulcer before their initial operations; in others, surgery was performed for other reasons, such as obesity (5%) or reflux esophagitis (8%). Twelve patients had undergone truncal vagotomy and a "drainage operation" and 48 had received a partial gastrectomy with a gastroenterostomy: Billroth I (n = 8), Billroth II (n = 11), Roux-en-Y (n = 29). All patients had recordings of gastrointestinal manometry; 16 also had a scintigraphic measurement of gastric emptying. Measurements were compared with data from healthy controls. Gastric manometry, which could be assessed only in the group with an intact antrum, was characterized by antral hypomotility (p less than 0.05). Gastric emptying studies showed rapid early emptying of liquids and delayed emptying of solids (both p less than 0.05). In the whole group, fasting jejunal motility was characterized by absence of phase II in 13, presence of bursts of phasic activity in 18, and abnormal propagation of phase III in 8. A significantly increased frequency of phase III of MMC was noted in the patients after Billroth II and Roux-en-Y operations. Postprandially, 19 patients failed to develop a "fed pattern.".
Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B BACKGROUND AND METHODS. The effect of intensive lipid-lowering therapy on coronary atherosclerosis among men at high risk for cardiovascular events was assessed by quantitative arteriography. Of 146 men no more than 62 years of age who had apolipoprotein B levels greater than or equal to 125 mg per deciliter, documented coronary artery disease, and a family history of vascular disease, 120 completed the 2 1/2-year double-blind study, which included arteriography at base line and after treatment. Patients were given dietary counseling and were randomly assigned to one of three treatments: lovastatin (20 mg twice a day) and colestipol (10 g three times a day); niacin (1 g four times a day) and colestipol (10 g three times a day); or conventional therapy with placebo (or colestipol if the low-density lipoprotein [LDL] cholesterol level was elevated). RESULTS. The levels of LDL and high-density lipoprotein (HDL) cholesterol changed only slightly in the conventional-therapy group (mean changes, -7 and +5 percent, respectively), but more substantially among patients treated with lovastatin and colestipol (-46 and +15 percent) or niacin and colestipol (-32 and +43 percent). In the conventional-therapy group, 46 percent of the patients had definite lesion progression (and no regression) in at least one of nine proximal coronary segments; regression was the only change in 11 percent. By comparison, progression (as the only change) was less frequent among patients who received lovastatin and colestipol (21 percent) and those who received niacin and colestipol (25 percent), and regression was more frequent (lovastatin and colestipol, 32 percent; niacin and colestipol, 39 percent; P less than 0.005). Multivariate analysis indicated that a reduction in the level of apolipoprotein B (or LDL cholesterol) and in systolic blood pressure, and an increase in HDL cholesterol correlated independently with regression of coronary lesions. Clinical events (death, myocardial infarction, or revascularization for worsening symptoms) occurred in 10 of 52 patients assigned to conventional therapy, as compared with 3 of 46 assigned to receive lovastatin and colestipol and 2 of 48 assigned to receive niacin and colestipol (relative risk of an event during intensive treatment, 0.27; 95 percent confidence interval, 0.10 to 0.77). CONCLUSIONS. In men with coronary artery disease who were at high risk for cardiovascular events, intensive lipid-lowering therapy reduced the frequency of progression of coronary lesions, increased the frequency of regression, and reduced the incidence of cardiovascular events.
Sudden cervical pain: spontaneous cervical epidural hematoma. Three cases of cervical epidural hematoma are reported. Acute neck pain usually associated with a mild effort, closely followed by radicular pain and a neurologic deficit below the lesion is the typical presentation of this extremely rare and difficult diagnosis. As prognosis depends on preoperative neurologic state, the authors emphasize the importance of prompt identification of this lesion. The diagnosis is confirmed by computed tomography, and emergency neurosurgical laminectomy is mandatory.
Endometrioma of the liver. Hepatic endometriosis is extremely rare. We describe a patient sent to us with epigastric pain as the only symptom and who was found to have associated endometrioma of the liver and left ovary. We suggest a gynecologic evaluation before surgery for hepatic cyst of unknown cause.