PubMed Health⌕ Search

Biomedical subjects

T Sjöberg

Publications and source records attributed to T Sjöberg.

At least 37 records · Page 2Linked to original sources
PubMed1996

Prostanoid release after lung transplantation.

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.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Long-term preservation of vascular endothelium and smooth muscle.

This study was performed in organ baths on 400 ring segments of infrarenal aorta taken from 40 Sprague-Dawley rats that had been randomized into five groups. Contractility was tested with the thromboxane analogue U-46619. Acetylcholine was used to elicit endothelium-dependent relaxing factor (EDRF). The results obtained from vessels preserved at 4 degrees C for 6, 12, 24, and 36 hours were compared with those from autologous vessels studied immediately after harvesting. Vessels preserved in Euro-Collins solution showed a 46% (p < 0.01) decrease in contractility after 12 hours of storage; after 24 hours only weak contractions could be elicited, and after 36 hours they had lost their ability to contract. The EDRF function was slightly reduced after 12 hours and could not be investigated after 24 and 36 hours. With the University of Wisconsin solution (UW) and the low-potassium-dextran-glucose solution Perfadex no decrease in contractility was seen in the first 24 hours, but at 36 hours the vessels preserved in UW had lost 40% (p < 0.01) and those preserved in Perfadex 30% (p < 0.05) of their contractility. The EDRF function was significantly reduced by about 15% after 6, 12, and 24 hours in both the UW and the Perfadex groups. At 36 hours, vessels stored in Perfadex had lost 41% (p < 0.001) and those stored in UW 17% (p < 0.01) of their EDRF function.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1995

Perfadex is superior to Euro-Collins solution regarding 24-hour preservation of vascular function.

BACKGROUND: The aim of this study was to compare Perfadex with Euro-Collins solution regarding 24-hour preservation of endothelium-dependent relaxation and vascular smooth muscle function. METHODS: The infrarenal aorta of 72 isogenic rats was studied in organ baths as fresh controls, after 24 hours of cold (4 degrees C) storage, and after 24-hour storage followed by transplantation and examination after 7 or 30 days. The thromboxane A2 analogue U-46619 was used to test contractility. Acetylcholine chloride was used to elicit endothelium-dependent relaxation and papaverine hydrochloride, to elicit endothelium-independent relaxation. RESULTS: With both solutions, all grafts were patent after 7 and 30 days. Vessels preserved in Euro-Collins solution for 24 hours lost 95% (p < 0.001) of their contractility compared with fresh controls; 7 days after transplantation, they had regained 40% of initial contractility, and after 30 days, there was no significant decrease in contractility. Vessels preserved in Perfadex manifested no significant decrease in contractility at any time. Endothelium-dependent relaxation could not be evaluated in vessels stored for 24 hours in Euro-Collins solution because they had lost almost all contractility; 7 days after transplantation, endothelium-dependent relaxation was reduced by 65% (p < 0.001), but at 30 days after transplantation, there was no significant decrease in endothelium-dependent relaxation. Vessels preserved in Perfadex for 24 hours lost 17% (p < 0.05) of endothelium-dependent relaxation, but 7 and 30 days after transplantation, there was no significant decrease in endothelium-dependent relaxation. CONCLUSIONS: Perfadex, but not Euro-Collins solution, has the capacity to preserve vascular function after 24 hours of storage followed by in vivo reperfusion.

Animals↗
PubMed1994

Endothelium-dependent relaxation after short-term preservation of vascular grafts.

As the integrity of graft endothelium seems to be essential to successful long-term patency in coronary operations, its preservation demands the utmost care. The aim of the present study was to investigate the effects of currently used solutions on endothelium-dependent relaxation after short-term storage of vessels at room temperature or at 4 degrees C. The infrarenal rat aorta was selected for study because its use enabled standardization of the investigation, which was performed in organ baths on 672 vessel segments from 112 Sprague-Dawley rats. Stable vasoconstriction was obtained with the thromboxane analogue U-46619. Acetylcholine was used to elicit endothelium-dependent relaxation. The results obtained for vessels preserved for 2 hours were compared with those for autologous vessels studied immediately after harvesting. Vessel contractility was unaffected by the preservation solutions, except in the Ringer's acetate group, where it was reduced by 50% (p < 0.05). Endothelium-independent relaxation, tested with papaverine, was unaffected in all groups. Ringer's lactate, Krebs solution, and Perfadex (a low-potassium-dextran-glucose solution) did not significantly affect endothelium-dependent relaxation either at room temperature or at 4 degrees C, although a tendency to impaired relaxation was seen in these three groups after cold storage. Standard Ringer's solution and fresh heparinized blood each significantly reduced endothelium-dependent relaxation in vessels stored at room temperature (p < 0.05), but not in those stored at 4 degrees C. Endothelium-dependent relaxation was significantly reduced after storage in normal saline solution (p < 0.05) and in Ringer's acetate (p < 0.01), both at room temperature and at 4 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Safe lung preservation for twenty-four hours with Perfadex.

The function of six porcine left lung allografts was studied after pulmonary (140 mL/kg) and bronchial (50 mL/kg) artery perfusion with Perfadex (Kabi Pharmacia, Uppsala, Sweden) at room temperature, followed by 24-hour storage of the lungs in an atelectatic state in 6 degrees to 8 degrees C Perfadex, which is a low-potassium-dextran solution. Left lung transplantation was done followed by right pneumonectomy, thereby making all the animals 100% dependent for their survival on the transplanted lungs. The pigs (mean weight = 56 kg, range = 51 to 58 kg, n = 18; 6 donors, 6 recipients, and 6 sham operated) were ventilated with a volume-controlled ventilator (20 breaths/min, 500 mL tidal volume, 8 cm H2O positive end-expiratory pressure, inspired oxygen fraction = 0.5). All the transplanted animals were in good condition throughout the 24-hour observation period with arterial oxygen tensions around 25 kPa (188 mm Hg) and arterial carbon dioxide tensions around 5 kPa (38 mm Hg). The mean pulmonary arterial pressure was around 30 mm Hg, and the pulmonary vascular resistance around 500 dyn.s.cm-5; neither showed any tendency to change with time. After 24 hours the inspired oxygen fraction was increased to 1.0 and the arterial oxygen tension increased to 43.3 +/- 5 kPa (325 +/- 38 mm Hg) (mean +/- standard error of the mean; n = 6). A sham operation (bilateral thoracotomy, right pneumonectomy) was done in 6 pigs, which were followed up for 24 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Efficacy of topical cooling in lung preservation: is a reappraisal due?

The aim of the present study was to test the efficacy of topical cooling as the only viable lung preservation method using the most challenging evaluation method, namely single-lung transplantation followed by immediate contralateral pneumonectomy. Ten domestic pigs (5 donors and 5 recipients) with a mean body weight of 57 kg (range, 53 to 59 kg) were used. After we administered systemic heparin (4 mg/kg), the lungs were harvested and placed in an atelectatic state under cold (8 degrees to 9 degrees C) low-potassium-dextran solution for 12 hours. Left lung transplantation was then done in the recipient pig followed by right pneumonectomy, thus making the recipient 100% dependent on the transplanted donor lung. No operative mortality or morbidity occurred. All animals were in excellent condition throughout the 24-hour observation period. They had normal blood gases which did not differ significantly from the preoperative blood gases obtained from the 5 recipients before transplantation (ie, when they had their own two lungs). A moderate increase (p < 0.05) in pulmonary vascular resistance was seen as compared with sham-operated animals. To conclude, topical cooling to 8 degrees C provides excellent lung preservation for 12 hours in pigs. If similar results can be obtained with other species, the currently accepted 6-hour limit for safe clinical lung preservation may be extended to 12 hours. It seems also warranted to critically reconsider which factors, apart from cooling alone, actually contribute favorably to 12-hour lung preservation.

Animals↗
PubMed1994

Pulmonary vascular resistance related to endothelial function after lung transplantation.

In 8 donor pigs, flush perfusion was performed with a low-potassium-dextran solution. Ring segments were taken from a small intralobar pulmonary artery in the right lung immediately after perfusion and after 24 hours of cold storage for studies in organ baths. Stable vasoconstriction was induced with the thromboxane mimic U-46619, and acetylcholine was used to induce endothelium-dependent relaxation. The maximum relaxation was significantly reduced after flush perfusion compared with fresh nonperfused controls, and a significant additional reduction was seen after the 24-hour storage period. The left donor lung was transplanted into a recipient after 24 hours of cold storage. Contralateral pneumonectomy was then performed, making the recipient entirely dependent on the transplanted lung for survival. All 8 pigs were in good condition throughout the 24-hour observation period, with arterial oxygen tension of around 165 mm Hg (range, 80 to 275 mm Hg; inspired oxygen fraction, 0.5) and pulmonary vascular resistance of around 450 dyne.s.cm-5 (range, 260 to 730 dyne.s.cm-5). The maximum endothelium-dependent relaxation for each donor was checked for correlation to pulmonary vascular resistance and to systolic, mean, and diastolic pulmonary artery pressures as recorded at 4-hour intervals. Regression analyses showed arterial oxygen tension to be unrelated to pulmonary vascular resistance and endothelial dysfunction to be unrelated to pulmonary artery pressure but to correlate to pulmonary vascular resistance, this correlation being significant after reperfusion for 16 hours (p < 0.05) and highly significant after 24 hours (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1994

Effects of hypothermia with and without buffering in hypercapnia and hypercapnic hypoxemia.

Anesthetized, paralyzed and mechanically ventilated pigs were hypoventilated to extreme hypercapnia (PaCO2 approximately 20 kPa) at FiO2 0.5, and allotted to receive hypothermia (approximately 31.5 degrees C) and buffer infusion, (HB-group, n = 6) or to a hypothermic control group (H-group, n = 6). The HB-group had higher arterial pH (7.34 vs 7.09, P < 0.01) and plasma bicarbonate (58.8 vs 35.4 mmol.l-1, P < 0.01) than the controls, but lower mean pulmonary arterial pressure (MPAP), (16 vs 23 mmHg (2.1 vs 3.1 kPa), P < 0.01) and pulmonary vascular resistance (PVR), (512 vs 699 dyn.s.cm-5 (5120 vs 6990 microN.s.cm-5), P < 0.05). Mixed venous PO2 (PVO2) was lower in the HB-group (5.1 vs 6.8 kPa, P < 0.01), as well as serum potassium (2.8 vs 3.7 mmol.l-1, P < 0.01) and ionized calcium (1.01 vs 1.29 mmol.l-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 HB-group had lower PVO2 (6.6 vs 7.8 kPa, P < 0.01), O2 half saturation tension (3.6 vs 4.2 kPa, P < 0.01), MPAP (17 vs 25 mmHg (2.3 vs 3.3 kPa, P < 0.01) and PVR (598 vs 793 dyn.s.cm-5 (5980 vs 7930 microN.s.cm-5, P < 0.05) compared with the controls, but higher arterial O2 saturation (95.3 vs. 88.6%, P < 0.01) and O2 content (17.7 vs 15.7 ml.100 ml-1, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Endothelium-dependent relaxation in pulmonary arteries after lung preservation and transplantation.

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.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Safe pulmonary preservation for 12 hours with low-potassium-dextran solution.

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.

Animals↗
PubMed1993

Effects of hypothermia in hypercapnia and hypercapnic hypoxemia.

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).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effects of buffering in hypercapnia and hypercapnic hypoxemia.

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).(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Imbalance↗
PubMed1992

Endothelium-mediated relaxation in transplanted aorta.

This study compares the vasodilating effect of endothelium-derived relaxing factors (EDRFs) in free arterial grafts with that in their normal control vessels. The infrarenal aorta of Sprague-Dawley rats was transplanted into the same position in other inbred recipient rats. A Krebs buffer solution (4 degrees C) served as the preservation solution. The ischemic time for the grafts (n = 8) was 42 +/- 1 minutes. Two grafts were studied after 3 days and six grafts, after 60 days. Ring segments were cut from all vessels, and isometric contractions were recorded in organ baths. The vessel segments were constricted with noradrenaline, a thromboxane A2 mimic (U-46619), or prostaglandin F2 alpha. Concentration-response curves with acetylcholine, which was used as the endothelium-stimulating substance causing release of EDRFs, were obtained. The patency of the grafts was 100%. Acetylcholine induced relaxation in all vessel segments with intact intima, whereas no relaxation was seen when the endothelium was manually removed. No significant differences were found between the grafts and the normal control vessels. Histology of the 60-day grafts showed elastomuscular arteries without intimal thickening and a media consisting of eight to ten muscle layers interrupted by five to six elastic lamellae. Scanning electron microscopy showed no major differences between normal endothelium and the endothelium of 3-day or 60-day grafts. This study indicates that free elastomuscular arterial grafts, in which the morphology of the intima is preserved, will retain their full ability to release EDRFs.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1991

Pulmonary sequelae of prolonged total venoarterial bypass: evaluation with a new experimental model.

Total normothermic venoarterial bypass was established in 6 healthy pigs over a period of 18 hours. A heparin-coated closed extracorporeal system was used and no heparin was administered systemically. During the bypass period the main pulmonary artery was occluded and the heart was maintained in a beating state. All the animals maintained stable hemodynamics and normal blood gases during the entire period of bypass. In the postbypass period, the central hemodynamics continued to be stable while the arterial oxygen tension (inspired oxygen fraction = 0.21) decreased significantly (p less than or equal to 0.05). The total body oxygen uptake, on the other hand, remained unaltered. All the animals died within 4 hours after weaning off the venoarterial bypass circuit on account of pulmonary edema in 2 and cardiac arrest in 4. Death was preceded by progressive pulmonary hypertension and lactacidosis in all the animals. Histological examination of the lungs showed pulmonary parenchymal damage ranging from interstitial edema to intraalveolar hemorrhage and parenchymal necrosis involving more than 80% of the pulmonary parenchyma. A normothermic total venoarterial bypass of 18 hours duration or more produces pulmonary edema of varying severity, pulmonary hypertension, pulmonary parenchymal necrosis, and lactacidosis in healthy juvenile pigs, resulting uniformly in their death. Despite these sequelae the systemic arterial hypoxemia may only be mild to moderate.

Acidosis↗
PubMed1991

Might free arterial grafts fail due to spasm?

The rat femoral artery was used as a free graft and was studied after 2, 7, 14, 30, and 60 days. The patency of the grafts was 100% (2 days, n = 6), 78% (7 days, n = 9), 63% (14 days, n = 8), 33% (30 days, n = 12), and 18% (60 days, n = 11). Histology showed an intimal thickening after 14 days and the media, which in the controls consisted of eight to ten layers of myocytes, was reduced to six to eight cell layers. During the first 2 weeks the graft segments had an impaired contraction when exposed to Krebs solution with 124 mmol/L K+, whereas after 1 month and later the graft segments approached the controls or had even higher contractile force. The thromboxane mimic U-46619 elicited full contractile force at all times whereas the potency was significantly lower during the first 14 days. Noradrenaline was unable to induce contraction in the graft segments during the first 14 days, but at 30 and 60 days it had regained full contractile force and was significantly more potent (approximately 60 times) in the graft segments compared with the controls. This study suggests that intimal thickening and hypercontractility might be a problem in free muscular arterial grafts.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1991

High potassium contents in organ preservation solutions cause strong pulmonary vasocontraction.

Euro-Collins (ECS) and UCLA-formula organ preservation solutions induced strong vasocontraction in porcine pulmonary arteries when studied in organ baths at temperatures of 37 degrees C and 30 degrees C. At 20 degrees C ECS induced a 30% contraction, but at 6 degrees C no contraction (n = 5) or a weak contraction (n = 1) was elicited. Neither prostaglandin E1 nor nifedipine caused any significant reduction of the vasocontraction elicited by ECS and UCLA. Krebs solution, enriched with potassium in amounts corresponding to those in ECS (115 mmol/L) or UCLA (30 mmol/L), induced vasocontraction comparing well with those induced by ECS or UCLA, indicating that it is the high potassium content that causes the vasocontraction. In a second experiment lung segments were stored at 4 degrees C for 9 hours in ECS, UCLA, or Krebs solution. Pulmonary arterial segments were then studied in organ baths at 37 degrees C. The choice of preservation solution did not significantly affect the contractile properties of potassium, noradrenaline, or the thromboxane mimic U-46619. To conclude, high potassium contents in organ preservation solutions induce strong pulmonary vasocontraction in lung temperatures greater than 20 degrees C but not in temperatures less than 10 degrees C. These vasocontractions are not significantly reduced by prostaglandin E1 or nifedipine. We suggest that the initial preservation solution used to cool down the lungs should contain 4 mmol/L or no potassium. When the lung temperature is less than 10 degrees C, a second perfusion might be done, and then a high potassium content (if thought to be essential) will not cause vasocontraction.

Alprostadil↗
PubMed1991

Contractile properties of lymphatics from the human lower leg.

Lower leg lymphatics, taken from seven volunteers, were investigated in vitro. Isometric contractions were induced by noradrenaline, 5-hydroxytryptamine (5-HT), prostaglandin F2 alpha (PGF2 alpha), and the thromboxane A2 (TXA2)-mimetic U-44069. Noradrenaline induced phasic contractions in 6 of 7 segments. The amplitude of the contractions were up to 100% of a previous K+ (124mM)-induced contraction and the frequency at 10(-6)M of noradrenaline was 5-13 min-1. These contractions were unaffected by propranolol (10(-6)M), but they were abolished by phentolamine (10(-6)M). Noradrenaline had an Emax (tonic contraction) of 7% of the K+ (124mM) contraction (n = 7) and the pEC50-value was 6.9 (n = 3). The corresponding values for 5-HT were 21% (n = 5) and 6.4 (n = 3). PGF2 alpha elicited contractions in all segments investigated (Emax = 87%, pEC50 = 5.8, n = 5). U-44069 had high contractile capacity and potency in all investigated segments (Emax = 137%, pEC50 = 8.9, n = 7). Phasic contractions were elicited also by 5-HT, PGF2 alpha and U-44069. Compared to earlier studies of human peripheral lymphatics, these results show that there are regional differences in susceptibility to these vasoactive agents.

Adult↗