Biomedical subjects
Publications and source records attributed to M Nannan.
A case of Streptococcus suis meningitis is observed in a 39-year-old and previously healthy meat factory worker. Neurological recovery was incomplete despite adequate and sustained antimicrobial therapy. Early deafness was demonstrated by brainstem auditory evoked potentials. Death due to aspiration pneumonia, cardiac arrest and subsequent cerebral anoxia occurred late in the course of the illness.
The effects of xamoterol 0.2 mg kg-1 i.v. on haemodynamics at rest and on exercise were tested in eight patients, before and after 60 days regular treatment with 200 mg b.d. Left ventricular function improved equally with xamoterol on both occasions. Tachyphylaxis and beta-receptor down-regulation do not occur during xamoterol therapy.
The respective roles of peripheral and myocardial determinants of exercise ventricular performance were studied in 10 normal volunteers and in 9 mildly hypertensive patients without evidence of coronary disease. Hemodynamic measurements and equilibrium blood pool scintigraphy were simultaneously performed at rest and during maximal upright exercise. In hypertensive patients, mean systolic and diastolic blood pressure were, respectively, 199 +/- 23 and 102 +/- 12 mm Hg at rest, and 271 +/- 28 and 113 +/- 8 mm Hg at peak exercise. Ejection fraction response to exercise was normal (increase by more than 5%) in 4 hypertensive patients (normal hypertensive group: 63 +/- 4 to 77 +/- 6%) and in volunteers (65 +/- 3 to 78 +/- 4%) and abnormal in 5 hypertensive patients (abnormal hypertensive group: 66 +/- 6 to 58 +/- 10% at peak exercise). The abnormal response in the abnormal hypertensive group was not due to an inadequate decrease in systemic vascular resistance during exercise. By contrast, the ratio systolic blood pressure/end-systolic volume, an index of contractility, decreased by 2.3 +/- 4.9 in the abnormal hypertensive group, whereas it increased by 9.8 +/- 9.1 in the normal hypertensive group and by 7.3 +/- 2 in volunteers. Thus, abnormal exercise ejection fraction response in mild hypertension was not related to increased afterload but rather to intrinsic myocardial factors.
The ideal sympathomimetic derivative should possess the positive inotropic and relaxing effects of catecholamines whilst remaining free of their side-effects. Theoretically, such properties could be present in beta 1-adrenoceptor partial agonists. Xamoterol (ICI 118,587, Corwin; ISA 43 p. 100) seems to be the most promising beta 1 partial agonist. The aim of the study was to determine if the beneficial effects of Xamoterol were maintained during long term administration. Xamoterol (200 mg twice dialy) was administered to 14 patients with anterior myocardial infarction and moderate heart failure (class II-III NYHA). After 3 months' therapy, left ventricular function improved as indicated by reduction in left ventricular (LV) end-diastolic pressure (23 +/- 5 to 16 +/- 5 mm Hg; P less than 0.0005), LV end-diastolic volume (153 to 140 ml/m2; P less than 0.05) and in LV end-systolic volume especially in 11 patients with a control end-systolic volume less than 100 ml/m2 (- 15 p. 100; P less than 0.05). LV inotropic state was also enhanced as indicated by 21 p. 100 increases in EMax, the maximal LV pressure/volume ratio (P less than 0.02) and 20 p. 100 increases in the ratio end-systolic stress/ end-systolic volume (P less than 0.02). Myocardial oxygen consumption was unchanged, global lactate extraction fraction increased from 20 +/- 18 to 33 +/- 14 p. 100 (P less than 0.05) and LV alanine release was reduced (-1.7 to -0.2 muMol/min; P less than 0.05). The rate of LV pressure fall accelerated from 57 to 52 ms (P less than 0.05) and the mean diastolic wall stress was reduced by 35 p. 100 (P less than 0.05), reflecting the improvement in LV relaxation and diastolic function. Thus, the beneficial effects of Xamoterol were maintained after prolonged therapy particularly in patients with class II-III heart failure; patients in class IV benefited less from this therapy. No tachyphylaxis or side-effects were observed.
A nongeometric radionuclide technique with correction for attenuation was used for the determination of cardiac output and stroke volume during exercise in nine normal subjects and in ten hypertensive patients. Simultaneous reference stroke volume (range 48-159 ml) and cardiac output (range 3.6-23.8 l/min) measurements were obtained by the Fick method. Data were collected at rest and during 60 degrees upright exercise, at two or three levels of increasing severity. Three statistical measurements were used for the comparison of both methods: correlation, precision, and accuracy. Radionuclide and Fick cardiac output measurements (n = 67, rest and exercise data) correlated well (r = 0.90). For stroke volume, the correlation was less (r = 0.64); however, the precision or random variability of both methods was similar for stroke volume (radionuclide: 8 ml or 9%; Fick: 16 ml or 16%). The accuracy or systematic error was defined as the mean difference between radionuclide and Fick measurements. The radionuclide method underestimated the Fick measurements. The systematic error was 18 +/- 18 ml for stroke volume and 2.4 +/- 2.4 l/m for cardiac output. A similar comparison of both methods was made on the absolute changes of stroke volume (r = 0.61; range -19 + 70 ml) and cardiac output (r = 0.82; range +1.6 + 16.4 l/m) between rest and exercise. The precision of the two methods was similar; the systematic error was 1.9 +/- 2.2 l/m for cardiac output and 6 +/- 17 ml for stroke volume. Thus, in these two groups of patients, although radionuclide and Fick cardiac output measurements at rest and during exercise correlated well, the radionuclide values were systematically and significantly lower.
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