| 1. |
- Ingemansson, Richard, et al.
(författare)
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Effect of temperature in long-term preservation of vascular endothelial and smooth muscle function
- 1996
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Ingår i: Annals of Thoracic Surgery. - : Elsevier BV. - 1552-6259 .- 0003-4975. ; 61:5, s. 1413-1417
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND. In clinical transplantation the donor organ is perfused with a cold preservation solution to obtain quick core cooling and a suitable environment for the tissue cells. Without good preservation of the vasculature, progressive deterioration of the blood flow during reperfusion may ultimately lead to the no-reflow phenomenon, even though the function of the other cells in the organ may be adequately preserved. The aim of this study was to find the optimal storage temperature for preservation of the vasculature. METHODS. The infrarenal aorta of 126 Sprague-Dawley rats were studied in organ baths: as fresh controls, after 36 hours of storage at 0.5 degrees C, 4 degrees C, 8.5 degrees C, and 22 degrees C in University of Wisconsin solution, and after 36-hour storage followed by transplantation and a lapse of 2 hours, 24 hours, and 7 days. The thromboxane analogue U-46619 was used to test contractility. Acetylcholine was used to elicit endothelium-dependent relaxation (EDR), and papaverine to elicit endothelium-independent relaxation. RESULTS. Storing the vessels at 0.5 degree C proved best regarding preservation of contractility, with a nonsignificant decrease, whereas storage at 4 degrees C and 8.5 degrees C resulted in a significant decrease after 36 hours. The contractility did not recover within 24 hours of in vivo reperfusion, but full recovery was seen after 7 days. Regardless of the preservation temperature used, a significant impairment in EDR was seen after 36 hours of storage. Two hours after transplantation, vessels stored at 4 degrees C and 8.5 degrees C showed no significant impairment in EDR, whereas those stored at 0.5 degrees C demonstrated a significant loss of EDR. After 24 hours and after 7 days, EDR was normal in all groups. CONCLUSIONS. Endothelium-dependent relaxing factor function is best preserved at 4 degrees C and 8.5 degrees C, whereas preservation of vascular smooth muscle function is best preserved at 0.5 degrees C.
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| 2. |
- Ingemansson, Richard, et al.
(författare)
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Importance of calcium in long-term preservation of the vasculature
- 1996
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Ingår i: Annals of Thoracic Surgery. - 1552-6259. ; 61:4, s. 1158-1162
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The aim was to investigate the effect of calcium in organ preservation solutions with respect to 36-hour preservation of vascular smooth muscle function and endothelium-dependent relaxation. METHODS: The infrarenal aortas of 60 Sprague-Dawley rats were studied in organ baths as fresh controls and after 36 hours of cold (4 degrees C) storage in different preservation solutions with and without calcium. The thromboxane A2 analogue U-46619 was used to study contractility. Endothelium-dependent relaxation was tested by the cumulative addition of acetylcholine. Papaverine hydrochloride was used to elicit endothelium-independent relaxation. RESULTS: Krebs solution was the only solution able to fully preserve contractility. Krebs solution without calcium gave poor preservation. After the addition of 1.5 mmol/L of calcium to University of Wisconsin solution and to Perfadex, both these solutions became fully able to preserve contractility. None of the solutions (with or without calcium) were fully able to preserve endothelium-dependent relaxation, although University of Wisconsin solution gave good preservation and Perfadex, fair preservation. Euro-Collins solution and K+ (124 mmol/L)-enriched Krebs solution were not able to preserve smooth muscle function or endothelium-dependent relaxation. CONCLUSIONS: Calcium is essential for long-term preservation of vascular smooth muscle function but not for long-term preservation of endothelium-dependent relaxation.
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| 3. |
- Lindberg, Lars, et al.
(författare)
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Inhalation of nitric oxide after lung transplantation
- 1996
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Ingår i: Annals of Thoracic Surgery. - : Elsevier BV. - 1552-6259 .- 0003-4975. ; 61:3, s. 956-962
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Pulmonary hypertension is a postoperative complication that may adversely affect the outcome of lung transplantation. The effect of nitric oxide (NO) inhalation on pulmonary hemodynamic indices after lung transplantation was studied and compared with findings in control pigs. METHODS: Varying concentrations of NO were inhaled by 5 pigs after left lung transplantation and right pneumonectomy and by 5 controls after right pneumonectomy at an inspired oxygen fraction of 0.21 and 0.5. Hemodynamic data were recorded continuously, and fast circulatory courses were analyzed. RESULTS: Inhalation of NO reduced pulmonary vascular resistance and mean pulmonary arterial pressure in all pigs, but the decrease was pronounced and dose dependent only at an inspired oxygen fraction of 0.21 in the pigs that had transplantation. These were the only pigs that became hypoxic. With the termination of NO, there was a dose-independent rebound pulmonary vasoconstriction in the controls, especially at an inspired oxygen fraction of 0.21, but not in the pigs that had transplantation. This response was transient and could be blunted with a higher inspired oxygen fraction. CONCLUSION: Inhalation of NO reduced pulmonary vascular resistance in the transplanted lung and may be useful in the treatment of pulmonary hypertension after lung transplantation. The rebound pulmonary vasoconstriction with the termination of NO inhalation stresses the need to be aware of this effect and to wean NO carefully in clinical situations. This study showed oxygen dependency, which has to be taken into consideration in dose-response studies involving NO inhalation.
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| 4. |
- Lindberg, Lars, et al.
(författare)
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Inhaled nitric oxide reveals and attenuates endothelial dysfunction after lung transplantation
- 1996
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Ingår i: Annals of Thoracic Surgery. - 1552-6259. ; 62:6, s. 1639-1643
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Maintaining endothelial function within transplanted organs may be critical to successful preservation. In this study we have evaluated the relationship between the effect of inhalation of nitric oxide and the degree of endothelial dysfunction after lung transplantation. METHODS: A left lung, which had been preserved for 24 hours, was transplanted and a right pneumonectomy was performed in 5 pigs. After a 24-hour observation period the pigs inhaled 5, 20, and 80 ppm nitric oxide, and pulmonary vascular resistance was recorded continuously. From the same donors preserved pulmonary arteries from the contralateral lung were studied simultaneously in organ baths. Acetylcholine chloride was used to elicit endothelium-dependent relaxation in vessel segments contracted with the thromboxane A2 analogue U-46619. RESULTS: Maximal endothelium-dependent relaxation decreased in the preserved lungs and correlated to the pulmonary vascular resistance in the simultaneously transplanted lungs. Inhalation of nitric oxide in the pigs that had received transplants caused the pulmonary vessels to dilate in proportion to the endothelial dysfunction. CONCLUSIONS: Preservation of lung for transplantation induces an endothelial dysfunction, and the degree of the decrease in pulmonary vascular resistance caused by nitric oxide inhalation may be an indication of the degree of this endothelial damage. The vasodilation caused by inhaled nitric oxide increases as the endothelial function deteriorates.
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| 5. |
- Kimblad, P O, et al.
(författare)
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Prostanoid release after lung transplantation
- 1996
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Ingår i: The Journal of Heart and Lung Transplantation. - 1557-3117. ; 15:10, s. 999-1004
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Increased pulmonary vascular resistance is frequently seen after lung transplantation. Thromboxane A2 is a potent vasoconstrictor of pulmonary arteries. Thromboxane-elicited vasoconstriction can ben counteracted by prostacyclin. The effects of lung transplantation on the biosynthesis of these substances were investigated. METHODS: Pulmonary artery flush perfusion with a low-potassium dextran glucose solution was performed in six donor pigs. After a 24-hour storage period, the left lung was transplanted into a recipient, followed by right pneumonectomy, making the recipient's survival entirely dependent on the transplanted lung. A sham operation (bilateral thoracotomy, right pneumonectomy) ws done in six pigs. the urine contents of the stable thromboxane A2 metabolite 2,3-dinor-thromboxane B2 and the stable prostacyclin metabolite 2,3-dinor-6-keto-protaglandin F1 alpha were measured with a gas chromatography-mass spectrometry method. RESULTS: One to four hours after reperfusion, thromboxane A2 production reached its maximum in both groups: it ws fivefold the basal value in the transplanted group, but only twofold in the sham-operated group, the difference being significant (p < 0.005). Twenty to twenty-four hours after reperfusion, thromboxane A2 production had stabilized at about twofold the basal value in both the transplanted and in the sham-operated group. Four to eight hours after reperfusion, prostacyclin production reached 15 times the basal value in the transplanted group and twofold in the sham-operated group, the difference being significant (p < 0.05). Twenty to twenty-four hours after reperfusion, prostacyclin production was 18-fold the basal value in the transplanted group and sevenfold in the sham-operated group. No correlation was found between the thromboxane or prostacyclin production and the pulmonary vascular resistance or the mean pulmonary arterial pressure. CONCLUSIONS: The thromboxane A2 production increased fivefold after lung transplantation, with a concomitant 15-fold increase in prostacyclin synthesis, which might have counteracted the vasoconstrictor effect of thromboxane.
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| 6. |
- Sjöberg, Trygve, et al.
(författare)
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Short-term preservation of vascular grafts
- 1996
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Ingår i: Compromised perfusion. 13th Bodensee Symposium on Microcirculation, Lindau, June 1995.. - : S. Karger AG. - 9783318040814 ; 22, s. 74-80
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Bokkapitel (refereegranskat)
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| 7. |
- Adner, Mikael, et al.
(författare)
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Contractile endothelin-B (ETB) receptors in human small bronchi
- 1996
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Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 1399-3003 .- 0903-1936. ; 9:2, s. 351-355
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Tidskriftsartikel (refereegranskat)abstract
- Endothelins (ETs) are a family of novel regulatory peptides and various lines of evidence suggest an important role for ETs in regulating pulmonary function. Two receptors for endothelin, ETA and ETB, have been found in the human lung, and according to recent studies a non-ETA receptor seems to mediate the contraction of large sized human bronchi. Several studies have emphasized the importance of small bronchi in the pathogenesis of airway disease. In the present paper, improved methodology was used which enables in vitro studies of small human bronchi down to a diameter of 0.5-1.0 mm. Using the new methodology we have tried to further characterize this receptor. Small bronchi from the distal parts of the bronchial tree were obtained from pulmonary tissue removed from 15 patients with lung cancer. They were dissected and cut into ring segments, in which isometric tension was recorded. ET-1, ET-2 and ET-3 elicited strong concentration-dependent contractions of the human small bronchus. Basically, the three peptides were equipotent with about the same maximal response. Upon reapplication, they all showed the same tachyphylaxis pattern, reaching half the initial contraction. Comparative analysis of IRL 1620, a selective ETB receptor agonist, revealed that the effect of the ETB agonist was, in all respects, similar to the responses induced by the ETs. PD 145065, a combined ETA/ETB receptor antagonist competitively inhibited the contractions induced by IRL 1620, whereas FR139317, a selective ETA receptor antagonist, was without effect. In conclusion, the present study shows that accurate measurements can be made in vitro on small human bronchi and all present data are in favour of an ETB receptor mediating endothelin-induced contraction of human bronchi smaller than 1.0 mm.
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