Oxygen uptake and cardiac output during progressive and constant load work in patients after acute myocardial infarction

PURPOSE: Simultaneously measured oxygen uptake (VO2) and Doppler echocardiography could verify if an alteration in the VO2 response to progressive and constant load work is due to reduced cardiac output. METHODS: The study group consisted of nine patients after acute myocardial infarction (MI), five age-matched healthy subjects (HE), and five young well-trained subjects (WT). Each subject performed a progressive exercise test and two bouts of constant load work at power outputs equated to 10% below (W1) and 10% above (W2) their ventilatory thresholds. VO2 and cardiac output were measured continuously and simultaneously during the tests. RESULTS: VO2 was significantly reduced for the MI group during the initial stages of the progressive exercise test (P < .02) and remained lower throughout the entire test. During the first 60 seconds of constant load work (W2), VO2 was lower for MI (P < .05). At steady state exercise during W2, cardiac output was significantly less for MI (P < .05). VO2 for the MI group was more reliant on cardiac output during lower power outputs and differences in the arterial and venous O2 content (a-VO2 difference) during greater power outputs. CONCLUSIONS: Cardiac rehabilitation programs must be aware of this delayed VO2 and cardiac output response when setting training workloads or selecting the magnitude of the workload increments during progressive exercise tests.     

A reappraisal of mouth-to-mouth ventilation during bystander-initiated cardiopulmonary resuscitation: a statement for Healthcare Professionals from the Ventilation Working Group of the Basic Life Support and Pediatric Life Support Subcommittees, American Heart Association

There is growing recognition that race and socioeconomic variables in health research demand greater attention. The investigators compared racial differences in health definition, health value, and health-promoting behavior of 62 pairs (N = 124) of Black and White college women matched on age, body mass index, and socioeconomic status. Both groups of women had similar definitions of health, valued health to the same extent, and reported similar levels of self-actualization, health responsibility, exercise, and stress management. Black women, relative to White women, practiced fewer nutrition behaviors and had less interpersonal support. Interventions to reduce health risk associated with nutrition practices of Black women are warranted and further research is needed to explore the influence of the social structure of educational institutions on interpersonal relationships and other health behaviors. When socioeconomic status is taken into consideration, Black and White college women demonstrated more commonalities in health behavior than differences.     

Identification of a new inborn error in bile acid synthesis: mutation of the oxysterol 7alpha-hydroxylase gene causes severe neonatal liver disease

We describe a metabolic defect in bile acid synthesis involving a deficiency in 7alpha-hydroxylation due to a mutation in the gene for the microsomal oxysterol 7alpha-hydroxylase enzyme, active in the acidic pathway for bile acid synthesis. The defect, identified in a 10-wk-old boy presenting with severe cholestasis, cirrhosis, and liver synthetic failure, was established by fast atom bombardment ionization-mass spectrometry, which revealed elevated urinary bile acid excretion, a mass spectrum with intense ions at m/z 453 and m/z 510 corresponding to sulfate and glycosulfate conjugates of unsaturated monohydroxy-cholenoic acids, and an absence of primary bile acids. Gas chromatography-mass spectrometric analysis confirmed the major products of hepatic synthesis to be 3beta-hydroxy-5-cholenoic and 3beta-hydroxy-5-cholestenoic acids, which accounted for 96% of the total serum bile acids. Levels of 27-hydroxycholesterol were > 4,500 times normal. The biochemical findings were consistent with a deficiency in 7alpha-hydroxylation, leading to the accumulation of hepatotoxic unsaturated monohydroxy bile acids. Hepatic microsomal oxysterol 7alpha-hydroxylase activity was undetectable in the patient. Gene analysis revealed a cytosine to thymidine transition mutation in exon 5 that converts an arginine codon at position 388 to a stop codon. The truncated protein was inactive when expressed in 293 cells. These findings indicate the quantitative importance of the acidic pathway in early life in humans and define a further inborn error in bile acid synthesis as a metabolic cause of severe cholestatic liver disease.     

Multiple pulmonary aneurysms secondary to Hughes-Stovin syndrome: demonstration by MR angiography

We report a case of a 41-year-old patient with multiple pulmonary aneurysms secondary to Hughes-Stovin syndrome. Conventional pulmonary angiography could not be performed, because thrombus in both the inferior and superior vena cavae prevented catheter passage. Contrast-enhanced three-dimensional (3D) MR angiography (MRA) showed two segmental pulmonary aneurysms in the right lung. The affected segments of the lung were resected successfully, predicated on the MRA findings.     

The addition of tenoxicam to prilocaine for intravenous regional anaesthesia

The analgesic effects of tenoxicam 20 mg added to prilocaine in a standard Bier's block (group 2) was studied in 45 patients who had their Colles' fractures reduced under intravenous regional anaesthesia, and compared both to a control group (group 1), and to a group who received a standard Bier's block combined with the same dose of tenoxicam given intravenously into the contralateral arm (group 3). Patients in group 2 obtained significantly better analgesia than group 1, as judged by a longer time before first additional analgesia was required (p < 0.05), less total analgesic consumption (p < 0.01), and lower pain scores (p < 0.01). These benefits were not obtained by patients in group 3.     

Can clinical response to cyclosporin in chronic severe asthma be predicted by an in vitro T-lymphocyte proliferation assay?

This study tests the hypothesis that the clinical response to cyclosporin therapy of patients with chronic severe asthma is related to the sensitivity of their T-lymphocytes to the antiproliferative effects of cyclosporin in vitro. In a previous study, we observed such a relationship with glucocorticoids and the same lectin-driven proliferation assay was used in the present study. Peripheral blood mononuclear cells were obtained from 33 patients participating in a cross-over trial of oral cyclosporin therapy during both cyclosporin and placebo treatment periods, and cultured in the presence of phytohaemagglutinin and serial dilutions of cyclosporin and dexamethasone. Proliferation was measured by tritiated thymidine uptake. Both cyclosporin and dexamethasone inhibited T-lymphocyte proliferation in a concentration-dependent manner in vitro at concentrations encompassing those achieved in peripheral blood during therapy in vivo. T-lymphocytes from the asthmatic patients showed a range of sensitivity to the antiproliferative effects of cyclosporin, but this could not be correlated with improvements in peak expiratory flow rate (PEFR) or forced expiratory volume in one second (FEV1) during cyclosporin therapy as compared with placebo. In contrast to previous observations with glucocorticoids, this in vitro T-lymphocyte proliferation assay is not predictive of clinical response to cyclosporin therapy in chronic severe asthmatics.     

Improving vision: neural compensation for optical defocus

Anecdotal reports abound of vision improving in myopia after a period of time without refractive correction. We explored whether this effect is due to an increased tolerance of blur or whether it reflects a genuine improvement in vision. Our results clearly demonstrated a marked improvement in the ability to detect and recognize letters following prolonged exposure to optical defocus. We ensured that ophthalmic change did not occur, and thus the phenomenon must be due to a neural compensation for the defocus condition. A second set of experiments measured contrast sensitivity and found a decrease in sensitivity to mid-range (5-25 cycles deg-1) spatial frequencies following exposure to optical defocus. The results of the two experiments may be explained by the unmasking of low contrast, high spatial frequency information via a two-stage process: (1) the pattern of relative channel outputs is maintained during optical defocus by the depression of mid-range spatial frequency channels; (2) channel outputs are pooled prior to the production of the final percept. The second set of experiments also provided some evidence of inter-ocular transfer, indicating that the adaptation process is occurring at binocular sites in the cortex.