Further evidence associating hemolytic uremic syndrome with infection by Verotoxin-producing Escherichia coli O157:H7.
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Biomedical subjects
Publications and source records attributed to J E Carter.
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Hypoxia has been demonstrated to cause impairment of myocardial relaxation. This impairment of relaxation is particularly pronounced during early reoxygenation. This study was undertaken in 24 isometric cat papillary muscles at 38 degrees C to determine if nifedipine can influence the impairment of relaxation produced during reoxygenation following hypoxia. A dose of nifedipine was chosen that produced only a minimal depression of peak systolic tension and no change in the half time to relaxation (RT 1/2) under well-oxygenated conditions. Thirty minutes of hypoxia were produced in 12 muscles, and systolic tension decreased by the same amount in muscles treated or not treated with nifedipine. During early hypoxia in the absence of nifedipine, RT1/2 was significantly prolonged (P less than 0.01) from 104 +/- 7 to 126 +/- 9 ms. After pretreatment with nifedipine, the change in RT1/2 with hypoxia was not significant. More striking was the near abolition of the marked impairment of relaxation seen during early reoxygenation (238 +/- 33 ms without nifedipine and 128 +/- 8 ms with nifedipine, P less than 0.01). These data establish that, although nifedipine only minimally attenuates the relaxation impairment early during hypoxia, this agent can substantially reduce the impairment of relaxation produced by early reoxygenation.
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Three patients were found to have visual field defects which involved homonymous horizontal sectors of the visual fields, thus mimicking field defects associated with lesions of the lateral geniculate nucleus. Computed tomography provided anatomical evidence that the responsible lesion involved the optic radiations rather than the lateral geniculate nucleus.
Quantitative perimetric studies in two women, each 52 years of age, with involvement of the lateral geniculate nucleus (caused by a small arteriovenous malformation in one and by an astrocytoma in the other) disclosed a striking wedge-shaped horizontal sectoranopia that was perfectly congruous in one case and incongruous in the other. Selective interruption of the dual blood supply to the lateral geniculate nucleus (with the anterior choroidal artery supplying the anterior hilus, together with the anterior and lateral nucleus and the lateral choroidal artery supplying the remainder of the nucleus) may result in a congruous visual field defect with steeply sloping borders because such a lesion must respect the anatomic boundaries produced by this vascular supply. Partial infiltration or involvement of the lateral geniculate nucleus (where uncrossed retinal projections terminate in one group of laminae, while crossed retinal projections terminate in another) provides a logical explanation for the occurrence of incongruous visual field defects. This unusual horizontal wedge-shaped defect should suggest lateral geniculate nucleus involvement, especially in the absence of trauma.
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An Amerindian girl with Friedreich's ataxia presented at the age of 14 years with intermittent bifrontal headaches and abdominal aching, often associated with nausea and recurrent vomiting and an evanescent pink, blotchy rash on the upper trunk. In these attacks she also had hypertension up to 210/160 mm Hg. Renal function studies, including intravenous pyelogram and angiography, were normal. Plasma renin activity (2.5 ng/ml/hr) was also normal. Total body CT scan was negative for phaeochromocytoma, and repeated estimations of 24-hour excretion of urinary VMA were normal or borderline high. Levels of total catecholamines in 24-hour urine were normal twice, but two random specimens during the paroxysmal episodes contained abnormally high levels of norepinephrine and dopamine. Plasma catecholamine concentrations were increased but not as high as with phaeochromocytoma. Blood pressure monitoring demonstrated marked fluctuations with position and temperature. A clonidine suppression test showed a substantial fall of plasma catecholamine levels, consistent with dysautonomia and not with phaeochromocytoma. It is concluded that the patient has dysautonomia of central origin, probably as a manifestation of Friedreich's ataxia. These findings are discussed in relation to the recent demonstration of increased levels of plasma catecholamines in that disease.
The overdose shock strengths required to depress ventricular contraction were determined for damped sinusoidal current in 7 metabolically supported, isolated contracting canine hearts. Each heart was suspended in an isoresistive and isotonic solution-through which the defibrillating shocks were delivered. Defibrillation thresholds were determined with standard damped sine wave shocks of 4.4-5.5 msec duration. Then overdose shocks were delivered and the depressant effect on systolic left ventricular pressure was measured for shocks of 3-12 times threshold current. The minimum (threshold) current and energy densities required to defibrillate were 59.5 +/- 4.6 mA/cm2 (average) and 3.12 +/- 0.2 mJ/cm3. Increasing the shock strength above threshold produced a concomitant reduction of postshock left ventricular systolic pressure. The current and energy densities required to produce 50% depression (TD50) of left ventricular systolic pressure were 5.0 and 24.1 times the threshold current and energy densities respectively, indicating a wide safety margin using this criterion.
A patient had transient ischemic attacks and venous stasis retinopathy due to an occlusion of the common carotid artery. Medical therapy controlled the cerebral symptoms but the venous stasis retinopathy progressed over ten months until neovascularization of disc and iris were present. Panretinal photocoagulation resulted in resolution of ocular ischemic changes over six months. Panretinal photocoagulation may be an effective therapy in patients with ocular neovascularization secondary to carotid occlusive disease which is not amenable to endarterectomy or extracranial-intracranial arterial bypass.
The stability of nitroglycerin in concentrations of 200 and 400 micrograms/ml in eight common intravenous solutions was studied. Two containers of each solution at each concentration, one glass and one polyolefin, were stored under each of the following conditions: intense light (1400-2000 foot-candles) and ambient room temperature (18-27 degrees C), normal light and ambient room temperature, dark and 40 degrees C, and dark and 5 degrees C. All samples were tested at 0 and 24 hours. Room temperature and refrigerated samples were also tested at 48 hours, 7 days, and 1 month. Testing included measurement for optical density at 400 and 600 nm, pH, and nitroglycerin content as determined by HPLC. The admixtures remained clear and colorless, and no appreciable changes in pH were observed. HPLC assays showed no significant changes in nitroglycerin concentrations. There were no differences in the stability of the admixtures stored in the glass and polyolefin containers. Nitroglycerin is compatible with each of the common intravenous solutions tested under the storage conditions and in the containers used for this study.
A high-performance liquid chromatographic method for determining the concentration of mononitroglycerins and dinitroglycerins in the commonly used pharmaceutical raw material nitroglycerin (10% w/w) on lactose USP is presented. A coefficient of variation of less than 5% for the partially nitrated glycerins was achieved over the range examined (0-4.0 micrograms/mg). Thirteen lots of raw material were examined and found to contain a total of less than 0.13% w/w partially nitrated glycerins. A variable wavelength detector (lambda = 218 nm) and a microphenyl column were employed. The mobile phase was acetonitrile-water (36:64) pumped at 2 ml/min. The internal standard was isosorbide dinitrate. Total analysis time was 12 min.
Three cases of whiplash shaking injury of infants are presented. All children presented with seizures and had minimal signs of external injury. Examination of the retina revealed extensive retinal hemorrhages. These were missed on initial examination and were only discovered after pupillary dilatation. The presence of these palecentered retinal hemorrhages suggested the diagnosis of child abuse and skeletal surveys and thorough social histories confirmed the diagnosis. Despite extensive retinal hemorrhages, computerized axial tomography (C.T.) scan showed minimal inter-hemispheric bleeding. In contrast to the "Battered Child Syndrome," all the findings in whiplash shaking syndrome of infants are subtle and demand an awareness, an index of suspicion and a thorough examination which may include extensive retinal examination following dilatation of the pupils. This latter examination is frequently not performed by family physicians and residents so that the syndrome may be missed. A fourth case is also discussed where shaking is admitted on initial presentation but said to be done for resuscitation. This poses an immense diagnostic dilemma to the pediatrician since in this case the child presented later with all the signs of physical abuse.
The latency for saccadic eye movements to a visual stimulus was studied in 59 adults whose ages ranged from 20.7 to 79.5 years. All were free of neurologic disease and drug use. Horizontal eye movements were recorded by electrooculography and the latency from the onset of a peripheral visual stimulus to the onset of a saccadic refixation eye movement was determined. A linear regression analysis revealed a correlation between increasing age and increasing latency for saccadic refixation eye movements. The direct relationship between increasing age and increasing latency for saccadic eye movements is a factor that should be taken into account in eye-movement studies as well as other methodologies such as tachistoscopic studies in which saccadic eye movements play a role in study design.
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To determine the course of left ventricular ejection fraction (LVEF) in the early hours after aortocoronary bypass grafting, 24 patients underwent serial gated bloodpool scanning. Twenty-two had received propranolol until the day of surgery. ECGs showed no evidence of perioperative infarction. Preoperatively, the mean (+/- SD) LVEF was 0.56 +/- 0.13; after bypass, it was 0.38 +/- 0.11 at 4 hours, 0.42 +/- 0.12 at 5 hours, 0.43 +/- 0.11 at 6 hours, 0.48 +/- 0.13 at 7 hours, 0.52 +/- 0.15 at 8 hours, and 0.54 +/- 0.15 at 10 to 14 days. The LVEFs at 4, 5, and 6 hours postoperatively were significantly lower than preoperatively (p less than 0.05). Postoperative mean heart rate was higher at all times; mean temperature was depressed at 4 and 5 hours and elevated at 7 and 8 hours; and mean arterial blood pressure was depressed at 7 hours, 8 hours, and 10 to 14 days (p less than 0.05). The degree of the early postoperative LVEF depression correlated with the daily preoperative propranolol dose (p less than 0.05) and was unrelated to bypass time, aortic cross-clamp time, or changes in temperature, heart rate, and blood pressure. The LVEF at 10 to 14 days postoperatively was not significantly different from the preoperative value. The LVEF is depressed in the early hours after aortocoronary bypass grafting and approaches the preoperative value with time. The magnitude of the early depression appears to be related to the preoperative propranolol dose, but does not significantly correlate with factors related to surgical technique.
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