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S A Loer

Publications and source records attributed to S A Loer.

22 records · Page 2Linked to original sources
PubMed1997

Interaction between haematocrit and pulmonary blood volume on pulmonary vascular flow resistance and pressure flow relationships.

OBJECTIVE: Pulmonary vascular flow resistance depends on blood viscosity, mainly due to haematocrit, and on vessel dimensions determining blood volume in this highly compliant vascular bed. We, therefore, evaluated the interaction between haematocrit, blood flow, and transpulmonary vascular pressure gradient under conditions of controlled pulmonary blood volume. DESIGN: Experimental study in isolated zone-III rabbit lungs perfused with autologous blood. SETTING: Laboratory for experimental studies. INTERVENTIONS: Stepwise and independent variation of flow (50, 100, and 200 ml/min), pulmonary blood volume (increments of 2.5 ml and 5 ml imposed by changes of left atrial pressure), and haematocrit (0-50%) varied by haemodilution (Krebs-Henseleit/albumin) or haemoconcentration (centrifugation). MEASUREMENTS: Pulmonary arterial, left atrial, and airway pressures as well as reservoir volume (reflecting reciprocal changes of lung blood volume) and lung weight. RESULTS: Haemodilution from the normal haematocrit (32%) to 10% at constant pulmonary blood volume and flow decreased flow resistance only slightly, whereas haemoconcentration (50%) increased flow resistance up to 130%. At the same time increments of in pulmonary blood volume of 2.5 and 5 ml (approx. 15 and 30% of normal pulmonary blood volume) at constant haematocrit significantly shifted downwards pressure-flow relationships for all investigated haematocrits (0-50%). CONCLUSIONS: Because of the multiple interrelationships between haematocrit, blood flow and pulmonary blood volume, haematocrit effects on pulmonary flow resistance and pressure-flow relationships in the pulmonary vasculature should be studied at controlled blood volume. While haemodilution only has minor effects, haemoconcentration changes pressure-flow relationships markedly. Pulmonary blood volume has a major impact on slope and position of pressure-flow relationships for all haematocrits investigated.

Animals↗
PubMed1997

How much oxygen does the human lung consume?

BACKGROUND: The amount of oxygen consumed by the lung itself is difficult to measure because it is included in whole-body gas exchange. It may be increased markedly under pathological conditions such as lung infection or adult respiratory distress syndrome. To estimate normal oxygen consumption of the human lung as a basis for further studies, respiratory gas analysis during total cardiopulmonary bypass may be a simple approach because the pulmonary circulation is separated from systemic blood flow during this period. METHODS: Lung oxygen consumption was determined in 16 patients undergoing cardiac surgery. During total cardiopulmonary bypass their lungs were ventilated with low minute volumes (tidal volume, 150 ml; rate, 6 min-1; inspiratory oxygen fraction, 0.5; positive end-expiratory pressure, 3 mmHg). All expiratory gas was collected and analyzed by indirect calorimetry. As a reference value also, whole-body oxygen consumption of these patients was determined before total cardiopulmonary bypass. In a pilot study of eight additional patients (same ventilatory pattern), the contribution of systemic (bronchial) blood flow to pulmonary gas exchange during cardiopulmonary bypass was assessed. For this purpose, the amount of enflurance diffusing from the systemic blood into the bronchial system was measured. RESULTS: The human lung consumes about 5-6 ml oxygen per minute at an esophageal temperature of 28 degrees C. Prebypass whole-body oxygen consumption measured at nearly normothermic conditions was 198 +/- 28 ml/min. Mean lung and whole-body respiratory quotients were similar (0.84 and 0.77, respectively). Extrapolating lung oxygen consumption to 36 degrees C suggests that the lung consumes about 11 ml/min or about 5% of total body oxygen consumption. Because the amount of enflurane diffused from the systemic circulation into the bronchial system during cardiopulmonary bypass was less than 0.1%, the contribution of bronchial blood flow to lung gas exchange can be assumed to be negligible. CONCLUSIONS: The lung consumes about 5% of whole-body oxygen uptake.

Aged↗
PubMed1995

Desflurane inhibits hypoxic pulmonary vasoconstriction in isolated rabbit lungs.

BACKGROUND: Inhalational anesthetics inhibit hypoxic pulmonary vasoconstriction (HPV) in vivo and in vitro with a half-maximum inhibiting effect (ED50) within concentrations applied for general anesthesia. Because it is unknown whether desflurane acts likewise, we studied its effect on HPV in isolated blood-perfused rabbit lungs and compared its ED50 with that of halothane. METHODS: Isolated blood-perfused rabbit lungs were randomly allocated to treatment with either desflurane (n = 6) or halothane (n = 6). HPV, defined as an increase in pulmonary arterial pressure (PAP) at constant flow, was elicited by decreasing inspiratory oxygen concentration from 20% to 3% for 4 min. This effect was determined without (control HPV) and with increasing concentrations of the anesthetics (fraction of inspired carbon dioxide kept constant at 4.8 +/- 0.2%, perfusate temperature at 37 degrees C, and blood flow at 100 ml.min-1). RESULTS: Before exposure to the anesthetics, PAP increased by 8.6 +/- 1.9 cmH2O for all lungs within 4 min of hypoxia (control PAP for all lungs 19.6 +/- 2.5 cmH2O). Desflurane decreased this effect in a concentration-dependent fashion with an ED50 of 14.5%, compared with that of halothane, with an ED50 of 1.7%. CONCLUSIONS: Assuming that 1 minimum alveolar concentration (MAC) values of desflurane and halothane for rabbits are 8.9% and 1.39%, respectively, this study yields ED50 values for the inhibition of HPV of approximately 1.6 MAC for desflurane and 1.2 MAC for halothane (P not statistically significant).

Anesthetics, Inhalation↗