Fecal coliform elevated-temperature test: a physiological basis. (1/14332)

The physiological basis of the Eijkman elevated-temperature test for differentiating fecal from nonfecal coliforms was investigated. Manometric studies indicated that the inhibitory effect upon growth and metabolism in a nonfecal coliform at 44.5 degrees C involved cellular components common to both aerobic and fermentative metabolism of lactose. Radioactive substrate incorporation experiments implicated cell membrane function as a principal focus for temperature sensitivity at 44.5 degrees C. A temperature increase from 35 to 44.5 degrees C drastically reduced the rates of [14C]glucose uptake in nonfecal coliforms, whereas those of fecal coliforms were essentially unchanged. In addition, relatively low levels of nonfecal coliform beta-galactosidase activity coupled with thermal inactivation of this enzyme at a comparatively low temperature may also inhibit growth and metabolism of nonfecal coliforms at the elevated temperature.  (+info)

Sympathetic nerve alterations assessed with 123I-MIBG in the failing human heart. (2/14332)

Norepinephrine (NE) reuptake function is impaired in heart failure and this may participate in myocyte hyperstimulation by the neurotransmitter. This alteration can be assessed by 123I-metaiodobenzylguanidine (MIBG) scintigraphy. METHODS: To determine whether the impairment of neuronal NE reuptake was reversible after metoprolol therapy, we studied 18 patients (43+/-7 y) with idiopathic dilated cardiomyopathy who were stabilized at least for 3 mo with captopril and diuretics. Patients underwent, before and after 6 mo of therapy with metoprolol, measurements of radionuclide left ventricular ejection fraction (LVEF), maximal oxygen consumption and plasma NE concentration. The cardiac adrenergic innervation function was scintigraphically assessed with MIBG uptake and release measurements on the planar images obtained 20 min and 4 h after tracer injection. To evaluate whether metoprolol had a direct interaction with cardiac MIBG uptake and release, six normal subjects were studied before and after a 1-mo metoprolol intake. RESULTS: In controls, neither cardiac MIBG uptake and release nor circulating NE concentration changed after the 1-mo metoprolol intake. Conversely, after a 6-mo therapy with metoprolol, patients showed increased cardiac MIBG uptake (129%+/-10% versus 138%+/-17%; P = 0.009), unchanged cardiac MIBG release and decreased plasma NE concentration (0.930+/-412 versus 0.721+/-0.370 ng/mL; P = 0.02). In parallel, patients showed improved New York Heart Association class (2.44+/-0.51 versus 2.05+/-0.23; P = 0.004) and increased LVEF (20%+/-8% versus 27%+/-8%; P = 0.0005), whereas maximal oxygen uptake remained unchanged. CONCLUSION: Thus, a parallel improvement of myocardial NE reuptake and of hemodynamics was observed after a 6-mo metoprolol therapy, suggesting that such agents may be beneficial in heart failure by directly protecting the myocardium against excessive NE stimulation.  (+info)

Effect of tumor necrosis factor alpha on vascular resistance, nitric oxide production, and glucose and oxygen consumption in perfused tissue-isolated human melanoma xenografts. (3/14332)

The effect of tumor necrosis factor alpha (TNF-alpha) on vascular resistance, nitric oxide production, and consumption of oxygen and glucose was examined in a perfused tissue-isolated tumor model in nude mice. One experimental group was perfused with heparinized Krebs-Henseleit buffer, a second one was perfused with TNF-alpha (500 microgram/kg) 5 h before perfusion. The vascular resistance increased significantly 5 h after TNF-alpha injection. The increase in vascular resistance did not seem to be mediated by a decrease in tumor nitric oxide production, as determined by perfusate nitrate/nitrite concentrations, but may be due to aggregation of leukocytes, platelets, and erythrocytes and/or endothelial consumption among the three experimental groups. The oxygen consumption was linearly dependent on the amount of available oxygen in the perfusate, whereas the glucose consumption was constant and independent of the glucose delivery rate. The present experiments provide new insights into physiological and metabolic mechanisms of action of TNF- alpha for optimization of future treatment schedules involving TNF-alpha.  (+info)

Endogenous plasma endothelin concentrations and coronary circulation in patients with mild dilated cardiomyopathy. (4/14332)

OBJECTIVE: To determine whether increased plasma concentrations of endothelin-1 (ET-1) and big endothelin (BET) play a role in the regulation of coronary circulation in patients with idiopathic dilated cardiomyopathy (IDCM). SETTING: Tertiary referral centre for cardiac diseases. PATIENTS: Fourteen patients (eight male/six female; mean (SD) age 59 (9) years) with IDCM (ejection fraction 36 (9)%) and five normotensive subjects (two male/three female; age 52 (7) years) serving as controls were studied. METHODS: Functional status was classified according to New York Heart Association (NYHA) class. Endogenous ET-1 and BET plasma concentrations from the aorta and the coronary sinus were determined by radioimmunoassay. Coronary blood flow, using the inert chromatographic argon method, myocardial oxygen consumption, and coronary sinus oxygen content under basal conditions were determined. RESULTS: In the aorta, mean (SD) concentrations of ET-1 (IDCM 0.76 (0.25) v controls 0.31 (0.06) fmol/ml; p = 0.002) and BET (IDCM 3.58 (1.06) v controls 2.11 (0.58) fmol/ml; p = 0.014) were increased in patients with IDCM. Aortic ET-1 concentrations correlated positively with NYHA class (r = 0. 731; p < 0.001), myocardial oxygen consumption (r = 0.749; p < 0. 001), and coronary blood flow (r = 0.645; p = 0.003), but inversely with coronary sinus oxygen content (r = -0.633; p = 0.004), which was significantly decreased in IDCM patients (IDCM 4.68 (1.05) v controls 6.70 (1.06) vol%; p = 0.003). CONCLUSIONS: The coronary circulation in patients with IDCM is exposed to an increased endothelin load. ET-1 concentrations correlate with functional deterioration. A decrease of the coronary sinus content of oxygen suggests a mismatch between coronary blood flow and metabolic demand. Thus, ET-1 might be a marker of a disequilibrium between myocardial oxygen demand and coronary blood flow in IDCM.  (+info)

Energy cost of sport rock climbing in elite performers. (5/14332)

OBJECTIVES: To assess oxygen uptake (VO2), blood lactate concentration ([La(b)]), and heart rate (HR) response during indoor and outdoor sport climbing. METHODS: Seven climbers aged 25 (SE 1) years, with a personal best ascent without preview or fall (on sight) ranging from 6b to 7a were assessed using an indoor vertical treadmill with artificial rock hand/foot holds and a discontinuous protocol with climbing velocity incremented until voluntary fatigue. On a separate occasion the subjects performed a 23.4 m outdoor rock climb graded 5c and taking 7 min 36 s (SE 33 s) to complete. Cardiorespiratory parameters were measured using a telemetry system and [La(b)] collected at rest and after climbing. RESULTS: Indoor climbing elicited a peak oxygen uptake (VO2climb-peak) and peak HR (HRpeak) of 43.8 (SE 2.2) ml/kg/min and 190 (SE 4) bpm, respectively and increased blood lactate concentration [La(b)] from 1.4 (0.1) to 10.2 (0.6) mmol/l (p < 0.05). During outdoor climbing VO2 and HR increased to about 75% and 83% of VO2climb-peak and HRpeak, respectively. [La(b)] increased from 1.3 (0.1) at rest to 4.5 mmol/l (p < 0.05) at 2 min 32 s (8 s) after completion of the climb. CONCLUSIONS: The results suggest that for elite climbers outdoor sport rock climbs of five to 10 minutes' duration and moderate difficulty require a significant portion of the VO2climb-peak. The higher HR and VO2 for outdoor climbing and the increased [La(b)] could be the result of repeated isometric contractions, particularly from the arm and forearm muscles.  (+info)

Myocardial oxygenation during high work states in hearts with postinfarction remodeling. (6/14332)

BACKGROUND: Postinfarction left ventricular remodeling (LVR) is associated with reductions in myocardial high-energy phosphate (HEP) levels, which are more severe in animals that develop overt congestive heart failure (CHF). During high work states, further HEP loss occurs, which suggests demand-induced ischemia. This study tested the hypothesis that inadequate myocyte oxygen availability is the basis for these HEP abnormalities. METHODS AND RESULTS: Myocardial infarction was produced by left circumflex coronary artery ligation in swine. Studies were performed in 20 normal animals, 14 animals with compensated LVR, and 9 animals with CHF. Phosphocreatine (PCr)/ATP was determined with 31P NMR and deoxymyoglobin (Mb-delta) with 1H NMR in myocardium remote from the infarct. Basal PCr/ATP tended to be decreased in postinfarct hearts, and this was significant in animals with CHF. Infusion of dobutamine (20 microg x kg-1 x min-1 IV) caused doubling of the rate-pressure product in both normal and LVR hearts and resulted in comparable significant decreases of PCr/ATP in both groups. This decrease in PCr/ATP was not associated with detectable Mb-delta. In CHF hearts, rate-pressure product increased only 40% in response to dobutamine; this attenuated response also was not associated with detectable Mb-delta. CONCLUSIONS: Thus, the decrease of PCr/ATP during dobutamine infusion is not the result of insufficient myocardial oxygen availability. Furthermore, in CHF hearts, the low basal PCr/ATP and the attenuated response to dobutamine occurred in the absence of myocardial hypoxia, indicating that the HEP and contractile abnormalities were not the result of insufficient oxygen availability.  (+info)

Energy cost of propulsion in standard and ultralight wheelchairs in people with spinal cord injuries. (7/14332)

BACKGROUND AND PURPOSE: Wheelchair- and subject-related factors influence the efficiency of wheelchair propulsion. The purpose of this study was to compare wheelchair propulsion in ultralight and standard wheelchairs in people with different levels of spinal cord injury. SUBJECTS: Seventy-four subjects (mean age=26.2 years, SD=7.14, range=17-50) with spinal cord injury resulting in motor loss (30 with tetraplegia and 44 with paraplegia) were studied. METHOD: Each subject propelled standard and ultralight wheelchairs around an outdoor track at self-selected speeds, while data were collected at 4 predetermined intervals. Speed, distance traveled, and oxygen cost (VO2 mL/kg/m) were compared by wheelchair, group, and over time, using a Bonferroni correction. RESULTS: In the ultralight wheelchair, speed and distance traveled were greater for both subjects with paraplegia and subjects with tetraplegia, whereas VO2 was less only for subjects with paraplegia. Subjects with paraplegia propelled faster and farther than did subjects with tetraplegia. CONCLUSION AND DISCUSSION: The ultralight wheelchair improved the efficiency of propulsion in the tested subjects. Subjects with tetraplegia, especially at the C6 level, are limited in their ability to propel a wheelchair.  (+info)

The respiratory responses of Carcinus maenas to declining oxygen tension. (8/14332)

The degree of respiratory independence shown by Carcinus under conditions of declining oxygen tension is dependent on the animal's level of activity. Inactive Carcinus are capable of maintaining respiratory independence down to a Po2 of 60-80 mmHg. This is achieved primarily by an increase in ventilation volume such that the amount of oxygen made available at the respiratory surfaces remains constant over a wide range of oxygen tension. The Po2 at which this can no longer be maintained corresponds closely to the Po2 at which respiratory independence is lost. Under normoxic conditions the Po2 of the post- and prebranchial blood was 97 and 18 mmHg respectively. At the high oxygen tensions prevailing in the postbranchial blood the respiratory pigment is fully saturated. Under conditions of declining oxygen tension the heart rate remains more or less constant until the Po2 reaches 60-80 mmHg, the onset of bradycardia coinciding with the loss of saturation of the haemocyanin. Although cardiac output falls during hypoxia, the capacity rate ratio remains approximately constant, which enables the effectiveness of oxygen uptake by the blood to remain at a high level.  (+info)