Search PubMed⌕ Search

Biomedical subjects

J Swedenborg

Publications and source records attributed to J Swedenborg.

At least 109 records · Page 6Linked to original sources
PubMed1985

Acute nontraumatic extremity ischaemia in Sweden. A one-year survey.

An attempt was made to evaluate the results of treatment for acute nontraumatic extremity ischaemia in Sweden during one year. A questionnaire was sent to all surgical units, and 61% replied. Of the total 586 evaluated cases, 497 were classified as embolism and 89 as acute thrombosis. Patient age strongly influenced results in both groups as regards limb salvage and mortality rates. The site of embolic occlusion also influenced mortality, with greatly heightened rate in aortic occlusion. Delay of operation for more than 12 hours after onset of symptoms was associated with increase in amputation rate and mortality. Adequate heparin therapy significantly improved results after embolectomy, but had no such effect after surgical treatment of thrombosis. The amputation rate was higher after acute thrombosis than after embolism. The authors conclude that patient age should be considered in comparisons between different case series of acute ischaemia, that embolus site and time of surgery are important determinants of mortality and amputation rate, and that heparin significantly improves results of embolectomy.

Adult↗
PubMed1983

Effect of glycosaminoglycans and antithrombin III on uptake and inhibition of thrombin by the vascular wall.

Thrombin binds to and is inactivated by the endothelium. The inactivation is potentiated by plasma. The present investigation was designed to clarify the role of vessel wall glycosaminoglycans (GAG) and plasma antithrombin III (AT III) in the inactivation and binding of thrombin by endothelium. Thrombin was shown to bind to vascular endothelium and artificial surfaces containing GAG:s. The binding could be inhibited on both types of surfaces by pretreating them with protamine. Thrombin bound to endothelium was rapidly inactivated in the presence of plasma but only slowly if the plasma was replaced by AT III, AT III-depleted plasma or a balanced salt solution. It is concluded that thrombin binds to vessel wall GAG:s and is inactivated by the endothelium. Potentiation of the inhibition of the endothelially bound thrombin by plasma is dependent upon presence of AT III but an additional plasma factor is also required.

Animals↗
PubMed1983

Inactivation of thrombin by the aortic endothelium.

The aim of the investigation was to clarify the uptake of thrombin on vascular endothelium and the inhibition of thrombin on the endothelium in the presence or absence of plasma. Segments of porcine aorta were used. Thrombin was labelled with 125I and its enzymatic activity was assayed amidolytically using a specific chromogenic substrate. After exposure to the endothelium both enzymatic activity and radioactivity disappeared from the thrombin solution and were recovered as surface bound activities. The enzyme activity confined to the endothelium rapidly disappeared in the presence of plasma but no activity was recovered in the plasma. The surface confined radioactivity, however, decreased slowly and was quantitatively recovered in the plasma. In the absence of plasma, i.e. in the presence of a balanced Ringer's solution, only slow disappearance of thrombin enzymatic activity occurred although the rate of disappearance was higher than that of release of radioactivity. It is concluded that thrombin, taken up on the endothelium, is almost instantaneously inhibited by an interaction mechanism with plasma and then released in an inactive state. The endothelium itself, however, seems to slowly inhibit bound thrombin and then release it.

Animals↗
PubMed1983

The vascular endothelium as an inhibitor of thrombin.

Uptake and inhibition of thrombin on the endothelium of porcine aorta was studied in vitro. The thrombin was labelled with 125J and its enzyme activity was measured with an amidolytic assay. After exposure to the aorta both the enzyme activity and radioactivity disappeared from the solution and were recovered as surface bound activities. The rate of inhibition of the surface bound thrombin was determined in presence or absence of plasma. In presence of plasma the endothelially confined enzymatic activity was rapidly inhibited, no enzymatic activity was recovered in plasma. The surface bound radioactivity, however, decreased slowly and was recovered in plasma. In absence of plasma only slow inhibition took place. It is concluded that thrombin taken up on the endothelium is rapidly inhibited there by an interaction with plasma and then released in an inactivated state. An alternative conclusion, based on the anticoagulant and antithrombotic actions of the endothelial fibrin lining is briefly discussed.

Animals↗
PubMed1983

The vascular endothelium as an inhibitor of thrombin.

Uptake and inhibition of thrombin on the endothelium of porcine aorta was studied in vitro. The thrombin was labelled with 125J and its enzyme activity was measured with an amidolytic assay. After exposure to the aorta both the enzyme activity and radioactivity disappeared from the solution and were recovered as surface bound activities. The rate of inhibition of the surface bound thrombin was determined in presence or absence of plasma. In presence of plasma the endothelially confined enzymatic activity was rapidly inhibited, no enzymatic activity was recovered in plasma. The surface bound radioactivity, however, decreased slowly and was recovered in plasma. In absence of plasma only slow inhibition took place. It is concluded that thrombin taken up on the endothelium is rapidly inhibited there by an interaction with plasma and then released in an inactivated state. An alternative conclusion, based on the anticoagulant and antithrombotic actions of the endothelial fibrin lining is briefly discussed.

Adsorption↗
PubMed1982

Uptake and inhibition of thrombin by the vascular wall.

Thrombin activity and inhibition were assayed on the aortic surface of dogs and pigs. After sacrifice, the aortae were excised and thrombin activity was measured with an amidolytic assay. A small thrombin activity was found on the endothelium. Heparinization of the animals lowered endothelial thrombin activity. After exposure of the aortic endothelium to a thrombin/albumin solution in vitro, thrombin activity disappeared from the solution and was recovered on the surface. De-endothelialized vessels took up more thrombin than those with intact endothelium. Endothelium confined thrombin was rapidly inactivated when exposed to plasma. A slow inactivation was seen upon exposure to a modified Ringer's solution. Thrombin confined to de-endothelialized aortae, i.e. to medial structures, was always inactivated at a slow rate irrespective as to whether it was exposed to plasma or Ringer's solution. It is concluded that endothelium and subendothelium bind thrombin and subsequently inactivate it. The inactivation proceeds faster on endothelium when exposed to plasma. The possible role of glycosaminoglycans is discussed.

Animals↗
PubMed1982

Septic false aneurysms. Report of three cases.

Three cases of septic false aneurysms are reported. They appeared as palpable pulsating masses shortly after severe septic episodes and were diagnosed by angiography. Two aneurysms were located in the common iliac artery and one in the superficial femoral artery. Operation was performed under antibiotic coverage and included ligation of the artery and excision of the aneurysm. Immediate reconstruction was performed in one case, in the two remaining, such reconstruction was abstained from since intraoperative ankle pressures were judged adequate. In one case reconstruction was performed later to relieve claudication. All patients survived with functioning extremities.

Adult↗
PubMed1982

Thrombectomy and arteriovenous fistula for iliofemoral venous thrombosis in fertile women.

Thirteen women of fertile age with left-sided iliofemoral venous thrombosis were treated with thrombectomy and a temporary arteriovenous fistula in the groin. In nine patients, the appearance of thrombosis could be related to pregnancy; in three of these, obstetric complications occurred. Diagnosis was obtained by antegrade and retrograde phlebography. After three months, the arteriovenous fistula was closed. Anticoagulant treatment was given from the time of diagnosis and for a total of six months. Patency of the iliac vein was determined by phlebography or venous occlusion plethysmography, or both. Based upon these findings, a short term patency rate of 85 per cent was achieved. Analysis of the material indicates a multifactorial pathogenic mechanism in the development of iliofemoral venous thrombosis. Important factors are pregnancy, obstetric complications, mechanical factors causing flow resistance in the iliac vein, hormonal factors and defective fibrinolysis.

Adult↗
PubMed1982

Acute thrombosis and embolism of the extremities: factors influencing the result of treatment.

Eighty-five cases treated for acute nontraumatic ischemia of the extremities have been reviewed. Eighty per cent were diagnosed as emboli and the remaining 20% were considered to have acute thrombosis. The most common embolism source was the heart and the most common heart disease causing embolism was atrial fibrillation. Seventy patients were treated surgically (80 surgical procedures) and 14 conservatively. All surgical patients received pre-, per- and postoperative anticoagulants. Limb-salvage rate was 76% in patients with emboli and 60% in the thrombosis group. The amputation rate was significantly higher in the thrombosis group. The overall mortality was 12% and was slightly but not significantly higher in the embolism group. It is concluded that acute arterial emboli should be treated rapidly by embolectomy. Acute thromboses carry a higher amputation rate if treated by thrombectomy alone and thus reconstruction should be considered. The relatively low mortality rate in the present material could be due to the routine use of anticoagulants.

Adolescent↗