Enhancement of P50 by inositol hexa phosphate entrapped in resealed erythrocytes in piglets.
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Biomedical subjects
Publications and source records attributed to B Teisseire.
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Nd-NAG laser carried by optical fibres 0.2 mm diameter was used in experimental studies to recanalize obstructed human cadaver arteries. Successful perforation of atheromatous plaques was obtained in all cases with a power of 12 W and a duration of exposure of 30-50 s provided that blood and not saline was used. The arterial wall was protected from injury by coaxial position of the optical fibre that was inserted into an inflated balloon catheter, and by circulating blood that cooled the system. The feasibility of guiding these devices in man was demonstrated in femoral and coronary arteries.
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To establish the optimal conditions for recanalisation of obstructed arteries without damage to vessel walls, a Nd-YAG laser coupled to a 0.2 mm diameter optic fibre was used on obstructed human cadaver coronary and peripheral arteries and on popliteal arteries in amputated limbs. Vaporization of atheromatous plaques was consistently obtained with an energy of 360-600 J and a diluted blood perfusate (3 g/100 ml haemoglobin) at a rate of 20 ml/min. The arterial wall was protected from thermal injury by inserting the optic fibre into an inflated balloon catheter and by cooling the system with the perfusate. Since recanalisation of occluded arteries was consistently obtained without damage to the arterial wall or debris and thin and flexible optic fibres were easy to guide in the arteries, percutaneous transluminal Nd-YAG laser angioplasty was used in obstructed femoral and popliteal arteries in three patients. The first European trials in man showed the method to be feasible, effective, and harmless, although further studies are required to improve penetration of the obstruction and increase the diameter of tunnel.
The mechanism by which mechanical ventilation (MV) with positive end-expiratory pressure (PEEP) improves hypoxemia in patients with acute respiratory failure (ARF) is unclear, and may be attributed in part to a decrease in cardiac output inducing by itself a reduction of the shunt. Using the multiple inert gas elimination technique we evaluated the effects of PEEP on ventilation-perfusion (VA/Q) distribution in 8 patients while cardiac output was maintained at control value by means of a dopamine infusion. In each patient, evaluation was performed during MV without PEEP (control) then with PEEP (17 +/- 2 cm H2O) and dopamine. After application of PEEP, PaO2, PvO2, and oxygen transport (TO2) increased significantly, whereas venous admixture decreased from 37.5 +/- 5 to 17 +/- 2% (p less than 0.01). Comparison of VA/Q distribution during PEEP and zero end-expiratory pressure documented a redistribution of pulmonary blood flow; the shunt decreased markedly from 30 +/- 4 to 13 +/- 2% (p less than 0.001), whereas the fraction of cardiac output distributed to "normal" VA/Q ratio units (0.1 to 10) increased from 62 to 78.5% (p less than 0.001). Dead space increased slightly with PEEP, from 44 to 49% (p less than 0.01) of total ventilation. The pattern of ventilation distribution was essentially unaltered; specifically, no additional high VA/Q mode was observed during PEEP. It is concluded that cardiac output maintenance with dopamine infusion during PEEP does not suppress the beneficial effects of PEEP on gas exchange, but induces a redistribution of pulmonary blood toward the main VA/Q ratio.
The energetic costs of post-extrasystolic potentiation (PEP) were assessed by evaluating left ventricular function and coronary blood flow in 16 patients with different forms of cardiac disease during cardiac catheterisation under basal conditions and sustained coupled right ventricular pacing. The coronary blood flow was measured by thermodilution techniques with sampling in the aorta and coronary sinus to measure O2 concentration, glucose, and plasma lactate and catecholamine levels. Parameters of LV function were calculated from data obtained from biplane left cineventriculography. During PEP, the ejection fraction increased from 0.48 +/- 0.8 to 0.62 +/- 0.22, the mean velocity of circumferential fibre shortening from 0.79 +/- 0.37 to 1.12 +/- 0.45 circ/s (p less than 0.001) and systolic work from 97 +/- 46 to 139 +/- 67 g/m2 (p less than 0.05). Coronary blood flow increased from 176 +/- 60 to 305 +/- 155 ml/min; myocardial oxygen consumption per potentialized beat rose from 0.15 +/- 0.07 to 0.50 +/- 0.33 ml/beat (p less than 0.001) whilst cardiac efficiency fell from 19.1 +/- 8 to 9.2 +/- 4% (p less than 0.001). PEP was associated with increased myocardial noradrenaline secretion (-3.1 +/- 31.5 ng/min under basal conditions to 30.2 +/- 42.8 ng/min, p less than 0.05). Therefore, the inotropic effect of PEP imposes a high metabolic demand and is associated with increased myocardial noradrenaline secretion.
The influence of increased enteral caloric intakes on respiratory gas exchanges was evaluated in 6 patients (5 men, 1 woman; mean-age: 54 years) in steady state and requiring continuous ventilatory support. Oxygen consumption (VO2), carbon dioxide production (VCO2), respiratory quotient (R), determined using an open circuit indirect calorimetric method, and arterial blood gases were measured on two consecutive days while ventilation conditions were unchanged. On the first day, the patients received a water diet only and on the following day an enteral caloric load (1491 +/- 65 Kcal/m2/24 h). The results showed a significant increase in VO2 (p less than 0.05) and R (p less than 0.001) and a rise in VCO2 from 106 +/- 4 to 139 +/- 9 ml/mn/m2 (p less than 0.01). The rise in VCO2 induced an increase of arterial carbon dioxide tension (PaCO2) from 26.3 +/- 1.6 to 34.4 +/- 2.4 mmHg (p less than 0.001). This study showed that because of the constancy of alveolar ventilation, the enteral nutrition-related increase of VCO2 is responsible for a PaCO2 increase and emphasized the need for adjusting artificial ventilation to any change in caloric intake in patients supported with mechanical ventilation.
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Increased blood viscosity has frequently been related to ischemic heart diseases. Since blood viscosity depends mainly on hematocrit (HTC), the effects of hemodilution have been studied on the isolated working rabbit heart perfused initially with 50% HCT, submitted to global ischemia for 10 min and reperfused with two different amounts of HCT: 50 and 30%. When the reperfusion was carried out with 50% HCT (N = 10) aortic flow failed to be restored in 4 hearts. When the reperfusion was performed with 30% HCT, all hearts recovered rapidly, reaching the preischemic cardiac output 20 min later. The ratio between cardiac output (C.O.) 20 min after reperfusion and C.O. before ischemia was 0.30 for the high hematocrit group (H.H.) as compared to 0.89 for the low hematocrit group (L.H.). The ratio of the coronary flow (C.F.) 20 min after reperfusion and that of C.F. before ischemia was 0.83 for the H.H. group as compared to 1.30 for the L.H. group. After reperfusion the myocardial oxygen consumption was not significantly different between both groups. The better recovery of heart performance after ischemia when the hearts were reperfused with a 30% HCT suggests that hemodilution results in a better oxygen distribution.
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Positive end expiratory pressure (PEEP) produces cardiopulmonary effects whether administered by controlled positive pressure ventilation (CPPV) or continuous positive airway pressure (CPAP). In eight patients with acute respiratory failure, the effects of 20 cm PEEP administered via CPPV and CPAP were compared. An esophageal balloon was used to calculate the transmural vascular pressures. The control values under mechanical ventilation with no PEEP (IPPV) for PaO2 and QS/QT (FiO2 being 1.0) were respectively 132 +/- 15 mmHg and 31 +/- 3%; CPPV gave a PaO2 of 369 +/- 27 mmHg and QS/QT fo 14 +/- 1.6%, CPAP 365 +/- 18 mmHg and 18 +/- 1.3% respectively. The two different modes of ventilation (CPPV and CPAP) gave identical blood gas improvement through the same level of end expiratory transpulmonary pressure despite marked differences between absolute mean airway and esophageal pressures. Conversely, hemodynamic tolerance was very different from one technique to the other: CPPV depressed cardiac index from 3.4 +/- 0.3 to 2.4 +/- 0.2 1/min/m2 as well as decreasing transmural filling pressures, suggesting a reduction in venous return. Conversely, filling pressures maintained at control values during CPAP and cardiac indexes were unchanged.
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Information provided by computation of shunt and alveolar arterial oxygen differences have been compared in 58 episodes of acute respiratory failure. In order to demonstrate the role of hemodynamic factors on pulmonary gas exchange, we compared blood gas measurements made in 29 patients with a high cardiac output and a reduced arteriovenous oxygen difference [C(a--v-)O2 less than 3.5 ml], with 33 measurements corresponding to a low cardiac output and a widened C(a--v-)O2 (greater than 6.5 ml). When the data was pooled together, the same P(A--a)O2 corresponded to many different shunt values, depending on the level of mixed venous oxygenation (PV-O2). QS/Qtot and P(A--a)O2 were quasi linearly correlated only when they corresponded to patients with the same C(a--v-)O2. For the same value of shunt, the PaO2 was always raised when the PV-O2 was raised. As far as pulmonary gas exchange is concerned, shunt calculation in acute respiratory failure is preferable to P(A--a)O2, especially when some hemodynamic disturbance is present.
Conditions of oxygen extraction by the myocardium have been studied in 12 subjects (44 +/- 9 years old) with pure mitral stenosis without clinical, metabolic or electrical sign of coronary insufficiency. Oxygen-hemoglobin equilibrium curves (OHEC) have been determined on arterial, mixed venous and coronary sinus blood, at rest and during a moderate (60 W, 10 min) exercise performed on a bicycle ergometer in supine position. Physiological values, at rest and during exercise, of the following functional parameters of the OHEC were determined in the in-vivo conditions of pH and PCO2 : P50, nHill, DS max = maximal value of OHEC slope (DS = delta SO2/delta PO2), PDSmax, SDS max. The concentration of plasma electrolytes capable to modify one of these parameters was controlled in each blood sample. In coronary sinus blood, P50 rises from 27.5 +/- 1.7 to 28.9 +/- 1.6 Torr during exercise (p less than 0.01). At rest, Hill's n in myocardial venous blood (2.67 +/- 0.09) is significantly higher than in arterial blood (2.61 +/- 0.08, p less than 0.01). A decrease in DS max (2.67 +/- 0.20 to 2.53 +/- 0.12%. Torr -1; p less than 0.01) and an increase in PDSmax (20.9 +/- 1.9 to 22.6 +/- 2.1 Torr, p less than 0.01) are observed. At rest, the myocardial "venous point" (PCSO2, SCSO2) is not significantly distinct from the maximal slope point (PDSmax, SDS max). After 1 min of exercise, a small gap appears which becomes significant at the end of the exercise (PDS max-PCSO2 = 0.2 Torr at rest, 2.7 Torr after exercise; SDS max-ScsO2 = 4.1% at rest, 7.9% after exercise). DS value at the myocardial venous point is only 2% at rest and 6% after exercise, lower than its maximal value. The gap between venous point and DS max point could constitute an error signal in the regulation loop of the coronary circulation. The existence of a physiological receptor, sensitive to instant variations in myocardial tissue PO2 and able to maintain venous point near DS max point could be considered.
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In the case of the clinical use of hemoglobin solution, the possibility of storing this preparation in the lyophilized state will be very useful. Freeze-dried preparations containing glucose alone or associated with albumin (25. 50. 75. 100 g/1) have been stored under air in darkness at room temperature or + 4 degrees C. At room temperature, the study has been stopped after one year in consideration of the important oxidation and denaturation of hemoglobin. The samples stored at low temperature have been studied after two years. With glucose alone, freeze-dried hemoglobin has generally a better stability than the four albumin containing preparations in the different assays (methemoglobin and oxyhemoglobin levels, Hill number, shape of the Barcroft's curve). The p 50 and the oxyphoric capacity are always low. Our hypothesis of an enhancement of hemoglobin stability by albumin in presence of glucose is not confirmed; the denaturation is in correspondence with the albumin concentration.