| 1. |
- Kimblad, Per Ola, et al.
(författare)
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Endothelium-dependent relaxation in pulmonary arteries after lung preservation and transplantation
- 1993
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Ingår i: Annals of Thoracic Surgery. - 1552-6259. ; 56:6, s. 1329-1333
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Tidskriftsartikel (refereegranskat)abstract
- Pulmonary hypertension is frequently seen after lung transplantation. To study how the release of the endothelium-dependent relaxing factor is affected by lung preservation and transplantation, porcine pulmonary arteries were investigated in organ baths. The arteries (1 mm in diameter) were taken from fresh nonperfused lungs (group I), lungs immediately after flush-perfusion with a low-potassium-dextran solution (group II), non-perfused lungs stored for 12 hours in low-potassium-dextran solution (group III), flush-perfused lungs stored for 12 hours in low-potassium-dextran solution (group IV), and group IV lungs after left lung transplantation and right pneumonectomy followed by 24 hours of reperfusion (group V). Stable contractions were induced with the thromboxane A2 analogue U-46619. Acetylcholine was used to stimulate the release of endothelium-dependent relaxing factor. In vessel segments where the endothelium had been removed, acetylcholine elicited no response. In segments with intact endothelium, acetylcholine induced concentration-dependent relaxation; the maximum relaxation obtained was 91% +/- 3% (I), 86% +/- 3% (II), 85% +/- 3% (III), 69% +/- 5% (IV), and 69% +/- 9% (V). Relaxation was significantly reduced in groups IV (p < 0.01) and V (p < 0.05) as compared with group I. Stable moderate pulmonary hypertension was present in all the transplanted lungs throughout the 24-hour observation period. It is concluded that the endothelium-mediated relaxation is significantly reduced after flush perfusion combined with 12 hours of storage in low-potassium-dextran solution. Lung transplantation, followed by 24 hours of reperfusion did not further impair the endothelium-dependent relaxation.
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| 2. |
- Steen, Stig, et al.
(författare)
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Safe pulmonary preservation for 12 hours with low-potassium-dextran solution
- 1993
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Ingår i: Annals of Thoracic Surgery. - 1552-6259. ; 55:2, s. 434-440
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Tidskriftsartikel (refereegranskat)abstract
- The function of porcine left lung allografts was studied after perfusion with (150 mL/kg) and storage for 12 hours in a 4 degrees to 6 degrees C low-potassium-dextran solution (Perfadex; Kabi Pharmacia AB, Uppsala, Sweden). After a left lung transplantation, an artificial lung in the form of venoarterial extracorporeal membrane oxygenation was established. The artificial lung has a "biological" heparin-coated surface (Carmeda AB, Stockholm, Sweden), and there is no need for systemic anticoagulation. Immediately thereafter, pneumonectomy of the normal right lung was done. All the animals were weaned from the artificial lung within 1 hour after the pneumonectomy. Six animals were followed up for 24 hours. They were in good condition throughout the 24-hour observation period with arterial oxygen tensions around 200 mm Hg (inspired oxygen fraction = 0.4) and arterial carbon dioxide tensions around 40 mm Hg. This study demonstrates a reliable method for continuous evaluation of the function of a transplanted lung immediately after transplantation and over the ensuing postoperative period. Safe 12-hour lung preservation can be obtained with the low-potassium-dextran solution Perfadex.
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| 3. |
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| 4. |
- Wetterberg, T, et al.
(författare)
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Effects of buffering in hypercapnia and hypercapnic hypoxemia
- 1993
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Ingår i: Acta Anaesthesiologica Scandinavica. - 0001-5172. ; 37:4, s. 343-349
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Tidskriftsartikel (refereegranskat)abstract
- Anesthetized, paralyzed and mechanically ventilated pigs were exposed to extreme hypercapnia (PaCO2 approximately 20 kPa) at FiO2 0.4 for 480 min, with (n = 6) or without (n = 6) continuous infusion of isotonic buffers (bicarbonate and trometamol). Arterial pH was higher in buffered animals than controls, 7.21 +/- 0.01 vs 7.01 +/- 0.01 (mean +/- s.e.mean, P < 0.01). Serum osmolality and PaCO2 did not differ between groups throughout the experiment. The hemodynamic response to hypercapnia was attenuated in the buffered group, who had lower heart rate, 133 +/- 6 vs 189 +/- 12 min-1 (P < 0.01), mean arterial pressure (MAP) 109 +/- 4 vs 124 +/- 4 mmHg (14.5 +/- 0.5 vs 16.5 +/- 0.5 kPa) (P < 0.05), mean pulmonary arterial pressure 16 +/- 1 vs 23 +/- 1 mmHg (2.1 +/- 0.1 vs 3.1 +/- 0.1 kPa) (P < 0.01), and pulmonary vascular resistance (PVR) 249 +/- 21 vs 343 +/- 20 dyn s.cm-5 (2490 +/- 210 vs 3430 +/- 200 microN.s.cm-5) (P < 0.01), compared with the control group. Subsequently, both groups were exposed to hypercapnic hypoxemia by stepwise increases in FiO2 (0.15, 0.10, 0.05) at 30-min intervals, while FiCO2 was kept at 0.2. PVR increased in both groups (P < 0.05) but, except for heart rate, all hemodynamic differences between the groups disappeared during hypoxia. At FiO2 0.15, buffered animals had higher arterial oxygen saturation (73 +/- 5%) than the controls (55 +/- 5%), (P < 0.05).
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| 5. |
- Wetterberg, T, et al.
(författare)
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Effects of hypothermia in hypercapnia and hypercapnic hypoxemia
- 1993
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Ingår i: Acta Anaesthesiologica Scandinavica. - 0001-5172. ; 37:3, s. 296-302
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Tidskriftsartikel (refereegranskat)abstract
- Anesthetized, paralyzed and mechanically ventilated pigs were hypoventilated to extreme hypercapnia (PaCO2 approximately 20 kPa) at FiO2 0.5, and allotted to a hypothermic group (31.5 +/- 0.1 degrees C, n = 6) or a control group (39.6 +/- 0.2 degrees C, n = 6). Compared with the controls, the hypothermic animals had higher PaO2 (19.2 vs 15.6 kPa, P < 0.05), SaO2 (97.2 vs 89.3%), SvO2 (78.7 vs 68.2%), end-tidal O2 (34.5 vs 24.8 kPa) and arterial pH (7.01 vs 6.91), (P < 0.01), but lower PvO2 (7.0 vs 10.2 kPa) and PaCO2 (13.2 vs 23.5 kPa), (P < 0.01). Hypothermia reduced O2 delivery (DO2), O2 consumption (VO2) and CO2 production by 40-45% (P < 0.05), but O2 extraction ratio, i.e. VO2.DO(2)-1 x 100(%), did not differ between groups. Hypothermic animals had lower heart rate (127 vs 223 beats.min-1, P < 0.05) and cardiac output (2.5 vs 3.9 l.min-1, P < 0.01). Subsequently, the inspired oxygen fraction (FiO2) was decreased stepwise (0.3, 0.25, 0.21, 0.15, 0.10) at 30-min intervals. At FiO2 0.3, the hypothermic group had higher PaO2 (10.0 vs 5.7 kPa), SaO2 (91.3 vs 28.5%), PvO2 (5.8 vs 3.4 kPa), SvO2 (70.7 vs 10.3%), end-tidal O2 (16.7 vs 8.5 kPa), O2 delivery (344 vs 155 ml.min-1), arterial pH (7.02 vs 6.94) and systemic vascular resistance (3850 vs 1652 dyn.s.cm-5 (38,500 vs 16,520 microN.s.cm-5)) compared with the controls (P < 0.01), while PaCO2 was lower (12.4 vs 22.7 kPa), as well as O2 extraction ratio (23 vs 63%) and O2 half saturation tension (4.3 vs 8.0 kPa) (P < 0.01).
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