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Biomedical subjects

J Swedenborg

Publications and source records attributed to J Swedenborg.

At least 91 records · Page 5Linked to original sources
PubMed1988

Interposition graft fistulas for hemodialysis.

When a radiocephalic arteriovenous (AV) fistula is not feasible for vascular access in hemodialysis, the second choice is interposition AV fistula using synthetic graft. Experience concerning patency and complications of interposition graft fistula and need for additional surgery in 49 grafts (41 patients) is reviewed. All 40 polytetrafluoroethylene (PTFE) and nine bovine grafts were placed in the forearm--22 straight between the radial artery and an antecubital vein and 27 as loops connecting the brachial artery to an antecubital vein. At the end of follow-up (mean 13, range 1-46 months), nine grafts were still in use and nine had failed, 15 patients had received a renal transplant and 15 were dead. One patient was lost to follow-up. Reoperation was necessitated by complications in 30 instances and permitted resumption of dialysis in 25. Reoperation was more common with straight than with loop graft (p less than 0.01). Interposition PTFE loop graft fistula is recommended as second choice for angioaccess, after radiocephalic fistula.

Adult↗
PubMed1988

Long and short term patency of radiocephalic arteriovenous fistulas.

Eighty-three radiocephalic fistulas in 71 uremic patients were retrospectively investigated. The fistulas were grouped according to construction, viz. side of radial artery to side of cephalic vein and end of cephalic vein to side of radial artery. The aim was to find and evaluate factors influencing fistula patency rate, with special emphasis on type of anastomosis. The early failure rate was significantly higher in the end-to-side group. The late failure rate was not influenced by mode of fistula construction. The fistula failure rate showed no correlation to patient age. Diabetes did not influence failure rate, but significantly shortened the mean patency time.

Adult↗
PubMed1987

Antithrombin III binding to surface immobilized heparin and its relation to F Xa inhibition.

The mode of F Xa inhibition was investigated on a thromboresistant surface with end-point attached partially depolymerized heparin of an approximate molecular weight of 8000. Affinity chromatography revealed that one fourth of the heparin used in surface coating had high affinity for antithrombin III (AT). The heparin surface adsorbed AT from both human plasma and solutions of purified AT. By increasing the ionic strength in the AT solution the existence of high and low affinity sites could be shown. The uptake of AT was measured and the density of available high and low affinity sites was found to be in the range of 5 and 11 picomoles/cm2, respectively. Thus the estimated density of biologically active high and low affinity heparin respectively would be 40 and 90 ng/cm2. The heparin coating did not take up or exert F Xa inhibition by itself. With AT adsorbed on both high and low affinity heparin the surface had the capacity to inhibit several consecutive aliquots of F Xa exposed to the surface. When mainly high affinity sites were saturated with AT the inhibition capacity was considerably lower. It was demonstrated that the density of AT on both high and low affinity heparin determines the F Xa inhibition capacity whereas the amount of AT on high affinity sites limits the rate of the reaction. This implies that during the inhibition of F Xa there is a continuous surface-diffusion of AT from sites of a lower class to the high affinity sites where the F Xa/AT complex is formed and leaves the surface. The ability of the immobilized heparin to catalyze inhibition of F Xa is likely to be an important component for the thromboresistant properties of a heparin coating with non-compromised AT binding sequences.

Animals↗
PubMed1987

Uptake and inactivation of thrombin on the subendothelium: comparisons with endothelium.

One aspect of the non-thrombogenicity of endothelium is the property to bind and inhibit thrombin. Loss of the endothelial layer gives rise to a thrombogenic surface. The present study concerns uptake and inactivation of thrombin on endothelium as well as subendothelium. Both the immediate subendothelial layer and the media were investigated. Binding and inhibition of thrombin was assayed using both a synthetic chromogenic substrate and fibrinogen. In the latter case thrombin enzymatic activity was assessed by measuring liberation of fibrinopeptide A. There was a linear relationship between thrombin in the solution and thrombin enzymatic activity recovered on the surface on both endothelium and media. 30-50 per cent of the surface bound thrombin measured with the chromogenic substrate was also active towards fibrinogen. Preincubation of endothelium with plasma gave rise to an increased loss of thrombin from the solution at the same time as less thrombin was recovered on the surface. This indicates increased inactivation. Increased inactivation could also be obtained by pretreatment with antithrombin (AT) but not with AT-depleted plasma. The same general pattern was seen on the subendothelium but not on the media. It is concluded that inhibition of thrombin occurs on the endothelium and can be augmented by prior binding of AT to the surface. This effect although less pronounced can also be obtained on the subendothelium. The deeply injured vessel is much less capable of inhibiting thrombin.

Animals↗
PubMed1987

Synthetic arterial grafts cause prolonged increase in the in vivo formation of thromboxane and prostacyclin in humans.

To evaluate the in vivo production of thromboxane A2 and prostacyclin their major urinary metabolites were measured in patients following graft replacement of the abdominal aorta. Specific methods based on gas chromatography-mass spectrometry were used to measure the urinary excretion of 2,3-dinor-TxB2 and 2,3-dinor-6-keto-PGF1 alpha. The excretion of these metabolites increased tenfold and almost fortyfold during post-operative Day 1 and remained elevated 6-10 days p.o. In a group undergoing cholecystectomy smaller changes of shorter duration were seen. It is concluded from this study that synthetic grafts cause prolonged increase in the in vivo formation of thromboxane A2 and prostacyclin. The reason for the increased TxA2 formation is probably platelet interaction with the foreign surface, whereas the increase of PGI2 could be part of a vascular defense against induced thrombotic activity. Those increases may have pathophysiologic implications.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Long-term stability in vivo of a thromboresistant heparinized surface.

A surface with covalently bonded heparin was tested in an in vivo model. Heparinized and non-heparinized tubings were inserted in the pig aorta. They were left in place for up to 16 wk. After removal they were analysed for their capacity to take up and inhibit thrombin. A comparison was also made with tubings that had not been inserted in animals. The heparin surface showed some specific alterations after implantation but its capacity to inhibit thrombin was not impaired. The heparinized tubings caused less intimal hyperplasia and thrombi than non-heparinized tubings.

Animals↗
PubMed1986

Thrombin inactivation on surfaces with covalently bonded heparin.

About 8000 Daltons porcine mucosa heparin fragments were covalently bonded by end-point attachment to polyethylene. The interaction between the immobilized heparin, added thrombin, and antithrombin III [AT] was investigated. The heparin surface was adsorbed with either albumin, AT dissolved in albumin or Tyrode, or platelet free plasma. Irrespective of the pre-treatment procedure, exposure of the surface to thrombin resulted in the same substantial decrease of thrombin in solution and the same degree of surface-confined thrombin activity. It was concluded that the heparin surface has a large capacity to bind thrombin and that the thrombin inhibitory capacity of high affinity heparin fragments is limited. On exposure of the thrombin-loaded surfaces to defibrinogenated plasma or AT, the surface-confined thrombin was inhibited within 30 seconds. Successive dilutions of plasma or AT decreased the inhibition rate but not the inhibition capacity. It is concluded that inhibition of thrombin adsorbed on the heparin surface occurs as follows: Added AT adheres to high affinity heparin fragments on the surface whereupon adsorbed thrombin migrates in the hydrophilic heparin coating towards the reaction site of AT and becomes inhibited. The inactivated thrombin-AT complex leaves then the surface, thus enabling the process to be repeated.

Antithrombin III↗
PubMed1986

Ruptured abdominal aortic aneurysms: a study of incidence and mortality.

The incidence of ruptured abdominal aortic aneurysms (AAA) during 1980 in the Stockholm county and the clinical fate of the patients were evaluated. Eighty-eight patients with ruptured AAA were found, an incidence of 0.06 per thousand. The overall mortality was 94 per cent. Sixty-four patients reached hospital, twenty-three received a correct diagnosis; thirteen were operated upon and five survived. Autopsy or operation revealed that most ruptures were retroperitoneal (88 per cent) and that only two aneurysms (2 per cent) extended above the renal arteries. It is concluded that the high mortality rate following rupture is more dependent upon failure to operate than on operative mortality.

Age Factors↗
PubMed1986

Results of surgical treatment for iliofemoral venous thrombosis.

The long-term results after venous thrombectomy combined with a temporary arteriovenous fistula were evaluated in 19 patients. Clinical status, isotope phlebography, venous occlusion plethysmography and foot volumetry were performed after a mean follow-up time of 38 months (range 13-75). The primary operation was successful in 17 of the 19 patients; the 2 remaining had chronic occlusions of their iliac veins. At the time of closure of the arteriovenous fistula, i.e. 3 months after thrombectomy, 14 patients had a patent iliac vein. At follow-up eight patients were considered to have a patent iliac vein, eight had a partial restitution and three had an occluded iliac vein. The group as a whole had no impaired venous emptying of the leg, but the small group of patients with occlusion at follow-up according to isotope phlebography seemed to have an impaired venous emptying. Foot volumetry showed only minor signs of valvular insufficiency, mainly in limbs with distal extension of the initial thrombus or only partial restitution of venous patency. A good long-term result can be expected after venous thrombectomy with a temporary arteriovenous fistula particularly in younger patients where the thrombosis is limited to the iliofemoral segment. This emphasizes the importance of early operation before distal extension of the thrombus occurs.

Adolescent↗
PubMed1986

Thrombin uptake and inhibition on endothelium and surfaces with a stable heparin coating: a comparative in vitro study.

The endothelial lining and two differently heparin-coated surfaces were compared in vitro regarding thrombin uptake and inhibition. One heparin surface was based on stabilized ionic binding of heparin, the other on covalent binding of partially degraded heparin. Both heparin surfaces have previously been shown to have pronounced thromboresistant properties. The two heparinized polyethylene surfaces and the endothelial surface of segments of the porcine aorta were studied. After exposure to the surfaces, thrombin disappeared from the solution and appeared bound to the surfaces. The disappearance rate of thrombin from the solution was the same on exposure to the endothelium and the covalently bonded heparin surface, but less following exposure to the ionically bonded heparin surface. The thrombin activity appearing on the endothelium was lower than on the heparin surfaces, indicating that the endothelium exerted a slow thrombin inhibiting capacity. On exposure of the thrombin-loaded endothelium to plasma, thrombin was rapidly inhibited. Thrombin bound to the covalently bonded heparin surface was inhibited at a slower rate than on the ionically bonded surface, but still faster than the rate at which free thrombin was inhibited in nonheparinized plasma. It is concluded that the endothelium and stabilized heparin coatings bind thrombin and accelerate its inhibition by plasma.

Animals↗
PubMed1985

Thrombin activity appearing on the vessel wall after trauma.

Thrombin activity was assayed on the aortic surface of rabbits after soft tissue trauma or endothelial injury caused by a balloon catheter. The animals were sacrificed by exsanguination 20 minutes or 3 hours after either type of trauma. Thrombin amidolytic activity on the luminal surface of the aorta was measured by exposing it to a synthetic chromogenic substrate. Thrombin activity appeared on the aortic endothelium 3 hours but not 20 minutes after soft tissue trauma. Heparin prevented the appearance of thrombin activity completely only if given just before the trauma. After endothelial injury, thrombin activity appeared on the vascular surface after 3 hours but not after 20 minutes. Thrombin activity appearing on the endothelium after soft tissue trauma may explain posttraumatic thrombotic events. The thrombin activity could, however, also be directed towards activation of protein C in which case an anticoagulant effect is obtained. Thrombin appearing after endothelial injury may enhance reactivity on the damaged vessel wall.

Animals↗
PubMed1985

Uptake and inactivation of thrombin on rabbit aortic endothelium studied with two different substrates.

The endothelium is an important compartment for uptake and inhibition of thrombin. The amount of enzymatically active bound thrombin can be detected with both small synthetic substrates and with aid of fibrinogen as substrate. The present study was designed to investigate the relation between endothelially bound thrombin with amidolytic activity towards a synthetic substrate (S-2238) and thrombin capable of converting fibrinogen by measuring generation of fibrinopeptide A (FPA). The luminal surfaces of rabbit aortae (2 cm2) were exposed in vitro to thrombin (0.625-5.0 NIH units/ml). Thrombin disappeared from the solution and a certain fraction was recovered on the surface. There was a linear relationship between the amount of thrombin on the surface and the concentration of thrombin in the incubation mixture. Approximately one third of the thrombin measured with S-2238 was also able to cleave fibrinogen. After incubation with defibrinogenated plasma almost total inhibition of fibrinogen splitting activity occurred within 30 sec. The inhibition of the amidolytic activity was less complete. When endothelially bound thrombin was exposed to plasma much less FPA was generated than in a fibrinogen solution. A minor fraction of endothelially bound thrombin was inhibited also upon incubation with Tyrode without recovery of any enzymatic activity in the solution. The results indicate that a fraction of thrombin bound to the endothelium has retained enzymatic activity and that a fraction of the enzymatically active thrombin is capable of converting fibrinogen. Inhibition of thrombin enzymatic activity occurs rapidly upon exposure to plasma. The endothelium itself has a minor inhibitory effect also in the absence of plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Growth rate of abdominal aortic aneurysms as measured by computed tomography.

The risk of rupture of an abdominal aortic aneurysm increases with size. It has thus been recommended that small aneurysms be continuously followed with some type of imaging technique to detect when aneurysm size constitutes an indication for surgery. The present study focuses on the growth rate of abdominal aortic aneurysms in 35 patients who were subjected to repeated computerized tomographic examinations of their abdominal aortic aneurysms. Several aneurysms were measured more than twice resulting in 57 different examinations. The mean growth rate of the transverse diameter was 0.52 cm/year. The individual growth rates were, however, variable. Aneurysms with an initial transverse diameter exceeding 6 cm showed a slightly but not significantly faster increase in size compared with smaller aneurysms. No correlation between initial size and growth rate could be established. Six patients died during the study period, two from myocardial infarction, three after elective aneurysm operations and one, refused for elective operation, died after rupture. It is concluded that the growth rate measured with computed tomography agrees well with previously reported estimates obtained with ultrasonography. It is recommended that small aneurysms particularly in patients with relative contraindications to surgery be followed with repeated examinations of size.

Aged↗
PubMed1985

Infected pseudo-aneurysm of the femoral artery caused by a monitoring catheter.

A patient suffering from severe burns developed a mycotic aneurysm in the femoral artery as a result of insertion of a monitoring catheter. Treatment with antibiotics and repeated arterial surgery failed and a below knee amputation was finally performed. The use of monitoring intraarterial catheters in burn patients is to be avoided, because of impaired immunity, wound infection and septicaemia in this type of patient which could facilitate the development of septic aneurysm. If, however, a monitoring catheter is mandatory, it should be inserted and cared for by highly experienced staff who appreciate the risks involved. A peripheral site of insertion should reduce morbidity.

Adult↗
PubMed1985

Uptake and inactivation of thrombin on aortic endothelium and neo-intima.

The aim of this study was to investigate the uptake and inactivation of thrombin on aortic endothelium and neo-intima developing on vascular grafts in pigs and dogs. Thrombin, measured with a synthetic chromogenic substrate, was found on the grafts, particularly on grafts with an incompletely developed neo-intima. After incubation of grafts and aortic segments with thrombin in vitro, significantly more thrombin was taken up on the grafts as compared to aortic endothelium. In the presence of plasma, surface-bound thrombin was inactivated much faster on aortic endothelium than on neo-intima. If surfaces loaded with thrombin in vitro were incubated with a balanced salt solution the enzyme was inhibited much more slowly. Thrombin activity on the neo-intima may contribute to graft thrombosis.

Animals↗
PubMed1985

Blood coagulation and fibrinolytic factors as well as their inhibitors in trauma.

Tests generally accepted in the diagnosis of DIC were evaluated in 13 patients with multiple trauma. The blood samples were drawn on admission before treatment with blood, blood products or heparin. The tests included platelet count, prothrombin complex (Normotest/Thrombotest), Factor V, Factor VIII:C, fibrinogen, fibrinogen degradation products (FDP), thrombin and Reptilase times as well as the ethanol gelation test (fibrin monomer). Based on the results of the tests, the patients were categorized into DIC, suspected DIC and no DIC groups. It was found that those patients who were referred to the DIC group were also those who later developed the most severe organ dysfunction and who stayed the longest time in the Intensive Care Unit. Thus, the clinical and laboratory findings agreed. The Normotest/Thrombotest ratio, thrombin times and Reptilase times, and presence of fibrin monomers were of limited value for the diagnosis of DIC. To make a correct diagnosis, the results of several of the conventional tests had to be combined. Additional tests were then evaluated. An increase of the fibrinopeptide A (FPA) level and the Factor VIIIR:Ag (vWF:Ag)/Factor VIII:C ratio in all the DIC patients as well as a decrease of the antithrombin (AT) level in some DIC patients indicated thrombin activity and a risk of thromboembolic events. A decrease of plasminogen and alpha 2-antiplasmin indicated activation of the fibrinolytic system. It is concluded that these new tests are useful in the diagnosis and treatment of DIC and similar proteolytic states.

Adolescent↗