Effects of low-dose dopamine on gut ischemia in a porcine model of hemorrhagic shock.
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Biomedical subjects
Publications and source records attributed to W Hasibeder.
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Transcutaneous PO2 (PtcO2) is suggested to reflect tissue oxygenation in intensive care patients, whereas transcutaneous PCO2 (PtcCO2) is advocated as a noninvasive method for assessing PaCO2. In 24 critically ill adult patients (mean Apache II score 14.2, SD 4.7) we investigated the impact of variables that are commonly thought to determine PtcO2 and PtcCO2 measurements. A linear correlation was found between PtcO2 and PaO2 (r = 0.6; p less than or equal to 0.0001) and between PtcO2 and mean arterial blood pressure (MAP; r = 0.42; p less than or equal to 0.003). Cardiac index (CI) correlated with tc-index (PtcO2/PaO2; r = 0.31; p less than or equal to 0.03). There was no relationship between PtcO2 and hemoglobin concentration (Hb) and the position of the oxygen dissociation curve (ODC). Stepwise multiple regression analysis demonstrated a significant influence of PaO2 and MAP on PtcO2. The contribution of CI, Hb and the ODC was not significant. Only 40% of the variability of a single PtcO2 measurement could be explained by PaO2 and MAP. A significant linear correlation was demonstrated between PtcCO2 and PaCO2 (r = 0.76; p less than or equal to 0.0001) but not between PtcCO2 and CI, MAP and arterial base excess (BEa). Stepwise multiple regression analysis revealed an influence of PaCO2 and of CI on PtcCO2; 66% of the variability of a single PtcCO2-value could be explained by PaCO2 and CI. Our data demonstrate that transcutaneous derived gas tensions result from complex interaction between hemodynamic, respiratory and local factors, which can hardly be defined in ICU-patients.
Effects of endurance training on O2 transport and on iron status are well documented in the literature. Only a few data are available concerning the consequences of strenuous anaerobic muscular exercise on red cell function. This study was performed to test the influence of strength training alone on parameters of red cell O2 transport and iron status. Twelve healthy untrained males participated in a strength-training programme of 2-h sessions four times a week lasting 6 weeks. After 6 weeks a small but significant reduction of haemoglobin (Hb; -5.4 g.l-1) was found (p less than 0.05). Mean red cell volume did not change, but a pronounced decrease of mean cell Hb concentration (from 329.2 g.l-1, SE 2.5 to 309.8 g.l-1, SE 1.2; p less than 0.001) and mean corpuscular Hb (from 29.6 pg, SE 0.4 to 27.7 pg, SE 0.3; p less than 0.01) was observed. Serum ferritin decreased significantly by 35% (p less than 0.01); transferrin, serum iron and iron saturation of transferrin were unaltered. Serum haptoglobin concentration was diminished significantly by 30.5% (p less than 0.01). The reticulocyte count had already increased after 3 weeks of training (p less than 0.05) and remained elevated during the following weeks. Strength training had no significant influence on the O2 partial pressure at which Hb under standard conditions was 50% saturated, red cell 2,3-diphosphoglycerate and ATP concentration as well as on erythrocytic glutamate-oxalacetate transaminase activity. The data demonstrate that mechanical stress of red cells due to the activation of large muscle masses led to increased intravascular haemolysis, accompanied by a slightly elevated erythropoiesis, which had no detectable influence on Hb-O2 affinity. Training caused an initial depletion of body iron stores (prelatent iron deficiency). Although Hb had decreased by the end of the training phase a true "sports anaemia" could not be detected.
Reactive hyperemia (RH) in the forearm skin after an arterial occlusion of 5 min was investigated in 29 ICU patients and 17 age-matched healthy control subjects using a transcutaneous PO2/PCO2 electrode heated to 37 degrees C. There was no difference in preocclusive baseline PtCO2 between patients (8 +/- 5 torr) and control subjects (8 +/- 4 torr). Patients exhibited a significantly decreased RH (16 +/- 9 torr) in comparison with control subjects (26 +/- 8 torr) and a diminished CO2 elimination. There was no correlation between the RH response and the oxygen extraction ratio, Hgb concentration, and hemodynamic and blood gas variables in patients. In contrast with control subjects, there was a significant correlation between CO2 elimination from the skin and the amount of RH in patients. The finding of a diminished RH in the patients was not related to a specific disease but correlated with the degree of physiologic derangement as assessed by the APACHE II score.
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Oxygen transport by erythrocytes was studied in eight patients on maintenance hemodialysis before, during and after a 2-week stay at an altitude of 2000 m. Dialysis was continued at that altitude. In all tests, blood samples were collected one or two days following hemodialysis. Pre-altitude tests: The patients exhibited anemia (hemoglobin concentration, Hb = 97.4 +/- 17 g/l). Due to an elevated red cell 2,3-diphosphoglycerate concentration (2,3-DPG) and mild metabolic acidosis, elevated standard and in vivo P50 values (pO2 at 50% oxygen saturation of hemoglobin, sO2) were measured. Altitude: Upon ascent, arterial pO2 decreased from 82 +/- 4 torr to about 60 torr, sO2 was lowered by 5%. After 2 weeks sojourn, pO2 and sO2 increased towards normal values. In contrast to healthy subjects, dialysis patients developed respiratory alkalosis (blood pH: +0.074) upon ascent. This caused a significant shift to the left of the oxygen dissociation curve (ODC), indicated by lowered in vivo P50-values (P50,vv,-2 torr). Red cell 2,3-DPG, P50,st (P50 at a blood pH = 7.4 and pCO2 = 40 torr), hemoglobin concentration and hematocrit showed a high day-to-day variability and did not change because of the altitude exposure. We interpret the increase of the oxygen affinity of hemoglobin in patients with renal anemia as beneficial, as it favors oxygen loading of hemoglobin in the lung during exposure to a hypoxic environment.
The work capacity of patients on maintenance hemodialysis is impaired even at normal inspiratory oxygen pressure. A further restriction can be expected when these patients are exposed to hypoxia at altitude, since most of the usual compensatory mechanisms required to adjust to this environment are impaired or even missing. We tested the tolerance of hemodialysis patients to hypoxia and measured work capacity, hematological, and cardiovascular parameters at rest and during incremental bicycle ergometry during 3-hour exposure to altitudes of 2,000 m and 3,000 m, and during 2 weeks of exposure to an altitude of 2,000 m and compared these data with prealtitude values or with data evaluated in a control group, respectively. In control tests the patients reached work loads at exercise termination of about 66% of age and sex-matched healthy controls, the reduction correlated well with the degree of anemia. During short-term altitude exposure to 2,000 m peak work performance remained unchanged in comparison to prealtitude tests, whereas at 3,000 m it was reduced by about 12%. During the 2-week stay at 2,000 m peak work loads increased significantly by 17% accompanied by an increase in peak oxygen uptake (+15%), blood lactate, heart rates (+10 min-1), and systolic blood pressure (+20 mmHg), whereas the diastolic pressure was comparable to prealtitude values. In another group of hemodialysis patients studied at low altitude under similar experimental conditions none of these parameters was changed. Our data show that during acute exposure to altitudes up to 2,000 m maximal work of hemodialysis patients is not reduced, but is restricted at altitudes higher than that.(ABSTRACT TRUNCATED AT 250 WORDS)
We report a 1-year-old boy in hemorrhagic shock due to a large subgaleatic hematoma following severe head trauma (blood pressure (BP) 30/15 mmHg; heart rate (HR) 110; Hb 45 g/l; arterial pH 7.16; BE-20 mEq/l). The child was intubated and ventilated; initial FIO2 was 0.9. In an attempt to monitor the cardiovascular system noninvasively a transcutaneous oxygen/carbon dioxide combielectrode was placed on the chest. Initially we observed a large difference between arterial pO2 (paO2 = 166 mmHg) and transcutaneous pO2 (tcpO2 = 7 mmHg) and arterial pCO2 (paCO2 = 16 mmHg) and transcutaneous pCO2 (tcpCO2 = 55 mmHg), reflecting poor skin perfusion and severe tissue acidosis. Under aggressive volume replacement tcpO2 rose along with BP and tcpCO2 returned to near arterial values. Even after stabilization of gross hemodynamic parameters such as HR and BP and despite reductions in FIO2, tcpO2 continued to increase with further volume replacement, reflecting an existing volume deficit.
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Parameters of oxygen transport were determined in 12 national class swimmers of both sexes during a 6-week training phase. Training intensity was high at the beginning of the training period (60 km/week); at the end the intensity was reduced to 25 km/week. At the beginning, in the middle, and at the end of the training period maximal swim tests (3 X 50 m) were performed. At rest 2,3-diphosphoglycerate (2,3-DPG) concentration (+0.82 mmol/l RBC) and P50 values (+0.92 mmHg) were increased after the period of intensive training, but decreased during the following 3 weeks, remaining still higher than pre-training values. Hemoglobin (Hb), concentration (MCHC) decreased during the training phase in dependence on training intensity. On day 0 and day 25 no changes in 2,3-DPG were found during the swim tests, but at the end a significant reduction in red cell 2,3-DPG (-0.44 mmol/l RBC) occurred. This can be explained by the more pronounced lactacidosis in this last swim test. The degree of hemoconcentration during exercise was the same throughout the training period and consequently independent of the state of physical fitness. During the training period, a good correlation between training intensity, increase in red cell 2,3-DPG, and P50 value as well as in the degree of sports anemia could be found.
The effect of a ascent to moderate altitude (2,300 m) and altitude training on the O2-transport properties of Hb and their possible consequences on tissue oxygenation during exercise were studied on six control and six training subjects. A rapid increase in P-50 values (+2.4 mm Hg, 0.32 kPa) was measured within one day after ascent. At the end of the stay at altitude (13th day) P-50 values were higher in subjects performing training than in controls. At altitude a slow but constant increase in 2,3-DPG, pyruvate kinase activity and reticulocyte count was found, which was more pronounced in training subjects as compared to controls. Ascent to altitude resulted in a decreased maximal performance capacity (-9%), but both groups recovered during the stay. In training subjects maximal exercise performance was increased after descent. Exercise at altitude was performed at a lower heart rate (controls: -10/min; training: -18/min) and at a lower lactate concentration (-4 mmol/l). These data indicate a positive effect of adaptation to altitude on exercise performance. Training itself shifts the ODC to the right and adds this effect to the effects of passive altitude adaptation on the O2-binding properties of hemoglobin.
Reports from the literature and our own data on red cell 2,3-DPG and its importance for unloading O2 from Hb to the tissues during exhaustive exercise are contradictory. We investigated red cell metabolism during incremental bicycle ergometry of various durations. Furthermore changes in blood composition occurring during exercise were simulated under in vitro conditions. The effect of a moderate (11.2 mmol X l-1 lactate, pH = 7.127) and severe (18 mmol X l-1 lactate, pH = 6.943) lactacidosis on red cell 2,3-DPG concentration was compared with the effect of similar acidosis induced by HCl. Our data indicate that the concentration of 2,3-DPG in red cells depends on the degree of lactacidosis, but not on the duration of exercise. During moderate lactacidosis red cell 2,3-DPG remains unchanged. This can be explained by an interruption of red cell glycolysis on the PK and GAP-DH step caused by a lactate and pyruvate influx into the erythrocyte, as well as an intraerythrocytic acidosis and a drop in the NAD/NADH ratio. During severe lactacidosis and HCL-induced acidosis a decrease in 2,3-DPG due to an inhibition of 2,3-DPGmutase and other glycolytic enzymes can be found. Mathematical correction of the observed P-50 value for the decrease in 2,3-DPG occurring during severe lactacidosis showed that a decrease in Hb-O2-affinity during strenuous exercise depends on the degree of lactacidosis and temperature elevation.