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Träfflista för sökning "WFRF:(Steen Stig) "

Sökning: WFRF:(Steen Stig)

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  • Li, Mei, et al. (författare)
  • Development and prevention of ischemic contracture (“stone heart”) in the pig heart
  • 2023
  • Ingår i: Frontiers in Cardiovascular Medicine. - : Frontiers Media SA. - 2297-055X. ; 10
  • Tidskriftsartikel (refereegranskat)abstract
    • Stone heart (ischemic contracture) is a rare and serious condition observed in the heart after periods of warm ischemia. The underlying mechanisms are largely unknown and treatment options are lacking. In view of the possibilities for cardiac donation after circulatory death (DCD), introducing risks for ischemic damage, we have investigated stone heart in pigs. Following cessation of ventilation, circulatory death (systolic pressure <8 mmHg) occurred within 13.1 ± 1.2 min; and a stone heart, manifested with asystole, increased left ventricular wall thickness and stiffness, established after a further 17 ± 6 min. Adenosine triphosphate and phosphocreatine levels decreased by about 50% in the stone heart. Electron microscopy showed deteriorated structure with contraction bands, Z-line streaming and swollen mitochondria. Synchrotron based small angle X-ray scattering of trabecular samples from stone hearts revealed attachment of myosin to actin, without volume changes in the sarcomeres. Ca2+ sensitivity, determined in permeabilized muscle, was increased in stone heart samples. An in vitro model for stone heart, using isolated trabecular muscle exposed to hypoxia/zero glucose, exhibited the main characteristics of stone heart in whole animals, with a fall in high-energy phosphates and development of muscle contracture. The stone heart condition in vitro was significantly attenuated by the myosin inhibitor MYK-461 (Mavacamten). In conclusion, the stone heart is a hypercontracted state associated with myosin binding to actin and increased Ca2+ sensitivity. The hypercontractile state, once developed, is poorly reversible. The myosin inhibitor MYK-461, which is clinically approved for other indications, could be a promising venue for prevention.
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  • Steen, Stig, et al. (författare)
  • Bröstkorgens organ.
  • 2002
  • Ingår i: Kirurgi för sjuksköterskor. - 9144074050 ; , s. 404-422
  • Bokkapitel (refereegranskat)
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  • Vagianos, Constantin, et al. (författare)
  • Control of traumatic liver hemorrhage in the cirrhotic rat by intraportal infusion of norepinephrine
  • 1987
  • Ingår i: Research in Experimental Medicine. - 0300-9130. ; 187:5, s. 339-346
  • Tidskriftsartikel (refereegranskat)abstract
    • The effect of intraportal infusion of norepinephrine (NE) on primary hemostasis in the cirrhotic rat was investigated at standardized liver trauma. Cirrhosis was induced by simultaneous administration of increasing amounts of carbontetrachloride (CCl4) and phenobarbitone. Infusion of norepinephrine took place after cannulation of the gastroduodenal vein. Intraportal infusion of NE resulted in a significant increase in arterial blood pressure and portal pressure in all animals. No difference was observed between cirrhotic and control rats. Cirrhotic animals bled longer and more profusely as compared with the controls. Infusion of NE resulted in significant decrease in bleeding time and blood loss. NE did not affect hematocrit, hemoglobin, platelet, or white cell count. Platelet aggregation was not influenced by the compound. In conclusion, intraportal infusion of NE proved effective in decreasing hemorrhage at liver trauma in cirrhotic rats.
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  • Vagianos, Constantin, et al. (författare)
  • Increased uptake of 5-FU in experimental liver tumours by simultaneous infusion of norepinephrine
  • 1987
  • Ingår i: European journal of cancer & clinical oncology. - : Elsevier BV. - 0277-5379. ; 23:9, s. 1323-1327
  • Tidskriftsartikel (refereegranskat)abstract
    • The effect of the simultaneous administration of norepinephrine and 5-fluorouracil (5-FU) on the uptake of radiolabelled 5-FU by liver tumours was studied in rats. Three different concentrations of 5-FU were used (15, 1.5 and 0.15 microgram/g body weight). The drugs were infused over a 30 min period via the hepatic artery, following cannulation of the gastroduodenal artery. The radioactivity in liver tumour, normal liver, lungs and intestines was estimated by liquid scintillation counting. At all concentrations tested, an increased uptake of radioactive 5-FU was found in the tumour when norepinephrine was infused. Tumour/liver ratios also increased significantly in all these cases. No significant differences were noted between norepinephrine infused and control animals in the radioactivity in normal liver, lungs and intestines. The effects noted were possibly due to changes in blood flow within the liver, but the possibility of a direct effect of norepinephrine on DNA metabolism is discussed.
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  • Zoucas, Evita, et al. (författare)
  • Arrest of haemorrhage at experimental liver trauma by intra-portal infusion of nor-epinephrine
  • 1989
  • Ingår i: Surgical Research Communications. - 0882-9233. ; 7:1, s. 19-25
  • Tidskriftsartikel (refereegranskat)abstract
    • The efficacy of intraportal (i.p.) nor-epinephrine infusion in controlling bleeding upon liver trauma in the presence of normal as well as defective platelet function was evaluated in the rat. Infusion of nor-epinephrine (10-4 M, NE) took place after cannulation of the gastro-duodenal vein, during 5 min prior to liver trauma. Simultaneously blood pressure (BP) was registered. Platelet aggregation was rendered defective by per os administration of acetyl-salicylic acid (2.5 mg/100 g bW ASA) 30 min prior to liver trauma. Liver trauma constituted of a standardized liver resection involving 2-3 per cent of the total liver weight, bleeding time and blood loss from the wound being registered. Haemoglobin (Hb), Haematocrit (Hct), platelet count (PC), APT-time and platelet aggregation were studied upon resection. I.p. infusion of NE resulted in significant increase of BP from 122.5 3.2 mm Hg in controls to 166.2 ± 3.2 mm Hg. NE infusion significantly decreased bleeding time at liver trauma from 270 ± 15 sec in controls to 154 ± 10 sec. Simultaneously blood-loss was decreased from 0.9 ± 0.1 g to 0.4 ± 0.1 gr. Administration of ASA increased bleeding time to 513 ± 17 sec and blood loss to 2.1 ± 0.1 gr. Infusion of NE in ASA pretreated rats reduced bleeding time to 253 ± 24 sec and blood loss to 1.1 ± 0.2 gr compared with animals receiving only ASA. Hb, Hct, PC and APT-time were not affected. Platelet aggregation was diminished after administration of ASA, but was not affected by NE.
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