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Plasma free amino acid level in subjects during maximal workload.

Ten healthy young males were subjected to one-time physical exercise on cycle ergometer up to exhaustion. For the investigations blood samples were obtained twice from a vein before and after exercise. In the venous blood the levels of lactic acid and pyruvic acid were determined by enzymatic methods. In heparized blood plasma the composition of free amino acids was determined using an autoanalyzer Beckmann-Multichrom. The following amino acids were determined: lys, his, arg, asp, tre, ser, glu, pro, gli, ala, cys, val, met, leu, ileu, tyr, phen. The obtained results were subjected to statistical analysis by the paired test of Student. The observed rise in the concentration after exercise concerned alanine, glutamate and phenylalanine. The concentrations of the remaining amino acids were not statistically significantly changed after the exercise.

Adult↗

Mechanical performance and coronary flow adjustments to changes in workload are not affected by inhibiting nitric oxide production in isolated working rat heart.

The importance of NO-induced vasodilator tone in maintaining adequate coronary flow to sustain hemodynamic function in aerobic heart and the role of endothelial release of NO in reactive hyperemia was studied in isolated working and Langendorff perfused rat heart, respectively. Raising the preload from 0 to 20 cm H2O caused a linear increase in coronary flow, myocardial oxygen consumption (MVO2) and cardiac output in the untreated working hearts and in the hearts in which basal release of NO has been inhibited by NG-monomethyl L-arginine (L-NMMA, 200 microM). L-NMMA, but not L-arginine, reduced coronary flow by 48% and 21.5% at preload levels of 0 and 20 cm H2O, respectively. A steeper coronary flow/preload relation and an increased O2 extraction in L-NMMA treated hearts allowed for the fact that their MVO2, lactate release and cardiac output were not significantly different from those in the untreated hearts at any of the preload level tested. SIN-1, 10 microM, augmented coronary flow to 136% and 107% at preload levels of 0 and 20 cm H2O, respectively, indicating that coronary vascular reserve was preserved at all preloads tested. L-NMMA-treatment greatly reduced reactive hyperemia following 30 s occlusion period and it significantly increased hyperemia following 10 min occlusion period. These findings provide evidence that while the inhibition of NO synthesis reduces coronary flow it does not induce a state of ischemia in isolated rat heart.

Animals↗

The workload of a commercial deputizing service.

The analysis of 1,098 calls to a commercial deputizing service during a period of four weeks is described. Approximately 20 per cent of the calls were for illnesses considered potentially life-threatening while in 22 per cent telephone advice was given and the patient was not visited by the deputy on call.

Adolescent↗

[Clinical workload at the outpatient neuropediatric clinic].

OBJECTIVE: To obtain rapidly the basic clinical information from individual patients and about the total practice in a hospital based neuropediatric out patient clinic. MATERIAL AND METHODS: A database file was designed, performed by the medical staff during or immediately after the patients visit. A descriptive study of data obtained through 1995 is reported. RESULTS: 1,226 patients visited the clinic during the whole year, generating 2,315 visits. The percentage of new patients is larger than that of other pediatric specialties, except for pediatric cardiology, but it is similar to that reported by adult neurological patients. Age distribution show a bimodal curve with a peak during the first year of age and a second one at 11 years. Geographic distribution is similar to that of other outpatient clinics of our center. The most frequent motive, annually, to consult was headache followed by suspected epilepsy. The most frequent diagnoses in new patients were epilepsy, migraine and tension type headaches. Prevalence of diagnosis in the total number of patients visited showed the highest frequency of epilepsy, followed by mental retardation and cerebral palsy. EEG was study most often performed, and 46% of total number of patients had neuroimaging studies. The pharmacological agent used in the largest number of patients was sodium valproate while phenobarbital was the product most often discontinued. Non antiepileptic drugs were used in a comparative small number of cases. The percentage of patients discharged for chronic and severe diseases was 20% annually, while it amounted to 40% in new patients. CONCLUSIONS: This type of information allows doctors to plan resources needed at the clinic and by the patients, but it is not appropriate for other tasks belonging to the management area, since it would require a larger infrastructure than the one usually provided at the outpatient clinic.

Adolescent↗

Peripheral blood progenitor cell transplantation: impact on the pharmacy workload and budget.

Due to reduced engraftment times and significantly shortened hospitalizations, peripheral blood progenitor cell (PBPC) transplantation has reduced the costs associated with autologous transplantation. Several institutions reported a reduction of 20-50% in transplantation cost using PBPCs and an aggressive outpatient program. These savings could be offset by hospital readmissions, but improvements in supportive care such as administration of colony-stimulating factors and broad-spectrum oral antibiotics, and assigning a 24-hour caregiver as a prerequisite for transplantation enable safe performance of outpatient transplantation and limit readmission rates to about 20-40%. At this institution, the effect of this program on the pharmacy has been a shift in staff and drug costs to outpatient cost centers. The transition from inpatient to outpatient care did not necessitate a greater investment in pharmacy staffing, but did require cross-training for inpatient and outpatient pharmacists. Future management of outpatient transplantation will apply a cooperative care philosophy that will rely to a large extent on patient care by family members and on a multidisciplinary model of seamless care.

Ambulatory Care↗

Brain death-induced alterations in myocardial workload and high-energy phosphates: a phosphorus 31 magnetic resonance spectroscopy study in the cat.

BACKGROUND: Hemodynamic deterioration resulting from brain death-induced myocardial left ventricular dysfunction may preclude heart donation. A reduced myocardial high-energy phosphate content, assessed by biopsy specimens, has been suggested to be responsible for this phenomenon. By applying phosphorus 31 magnetic resonance spectroscopy, in vivo myocardial high-energy phosphate metabolism can be studied continuously. METHODS: Twelve cats were sedated, intubated, ventilated, and studied for 240 minutes. Heart rate, arterial blood pressure, and arterial blood gases were monitored. Central venous pressure was kept constant. Myocardial work was expressed as rate-pressure product (RPP=heart rate x systolic arterial blood pressure). After sternotomy a radio frequency surface coil was positioned onto the left ventricle. A parietal trephine hole was drilled, and an inflatable balloon was inserted. The animal was placed into a 4.7 T horizontal 40 cm bore magnet interfaced to a spectrometer. Brain death (n=6) was induced by rapid inflation of the balloon; the six other cats served as a sham-operated control group. 31P spectra were obtained in 30 seconds, with ventilation and arterial blood pressure curve triggering. The phosphocreatine/to/adenosine triphosphate ratio, as an estimator of energy metabolism, was calculated. RESULTS: Brain death was established within 30 seconds after inflation of the balloon. Changes in RPP were characterized by a triphasic profile with a maximum increase from 19.3+/-1.4 x 10(3) to 87.5+/-8.1 x 10(3) mm Hg x min(-1) (p < .0001 vs control group) at 2 minutes after inflation of the balloon. Subsequently, RPP decreased and was normalized at 15 minutes after inflation. The third phase was characterized by hemodynamic deterioration, which became significant at 180 minutes and resulted in mean arterial pressure of 71+/-12 mm Hg (p < .05 vs control group) at the end of the experimental period. RPP deteriorated to 14.6+/-2.0 x 10(3) mm Hg x min(-1) (p < .05 vs control group) at 240 minutes. Because the heart rate remained constant during the third phase, the decrease in RPP was caused by a decrease in systolic arterial blood pressure. The initial phosphocreatine/adenosine triphosphate ratio of 1.65+/-0.16 varied to 1.52+/-0.06 at 2 minutes, and to 1.73 +/-0.17 (all values NS vs control group and vs initial ratio) at 240 minutes. CONCLUSIONS: The energy status of the heart is not affected by brain death. Therefore brain death-induced hemodynamic deterioration is not caused by impaired myocardial high-energy phosphate metabolism.

Adenosine Triphosphate↗