PubMed HealthSearch

Biomedical subjects

D Sørlie

Publications and source records attributed to D Sørlie.

At least 19 recordsLinked to original sources

A new protective solution for hypothermic storage of free vein grafts in cardiovascular surgery.

In order to reduce the operative injury of the endothelium in free reversed vein grafts, cultured human endothelial cells were used to test the optimal concentration of the constituents of a flushing solution for improved protection of the endothelium. The following solution proved to be the most suitable when tested at 20 degrees C; mannitol 160 mmol l-1, glucose 15 mmol l-1, NaCl 30 mmol l-1, KHCO3 5 mmol l-1, K2SO4 10 mmol l-1, KH2PO4 4 mmol l-1, MgSO4 20 mmol l-1, CaCl2 1.5 mmol l-1, potassium citrate 1.0 mmol l-1, Pluronic F-68 20 mg l-1, HEPES 4 mmol l-1, HEPES-Na 6 mmol l-1, pH 7.25, osmolality 325 mosmol kg-1 H2O. When endothelial cell injury was measured by a 51Cr-release assay, the new solution protected human endothelial cells in culture during hypothermic incubation better than isotonic NaCl, St Thomas' cardioplegic solution or Krebs-Henseleit's buffer. Transmission and scanning electron microscopy showed that the endothelium of human saphenous vein grafts was well preserved following 6 h of incubation at 20 degrees C with the new solution. As determined by morphometry using scanning electron microscopy, the endothelium of free porcine vein grafts was better preserved after incubation for 2 h at 20 degrees C with the new solution than with either isotonic NaCl (p = 0.02) or diluted, heparinized blood (p = 0.02) as the incubation medium, all cases observed following 2 h of subsequent arterial flow. The present study indicates that the endothelium of free vein grafts can be well protected against hypothermia when the flushing and irrigation fluid has a composition favouring endothelial protection. It appears likely that such treatment of vein grafts will reduce the frequency of vein graft narrowing and occlusion, post-operatively.

Animals

[Carotid endarterectomy. Surgical complications and long-term prognosis].

227 patients underwent 259 carotid endarterectomies because of transitory ischemic attacks (TIA). All had a 50% or more carotid lumen reduction as revealed by angiography, and symptoms from the arteriosclerotic lesion. Surgical mortality/morbidity at 30 days was 2.6%. 5.3 years after the operation (1 month-13 years) the probability of stroke was 4.9%, which corresponds to a postendarerectomy stroke rate of 1% per year. The procedure may be of value if the rate of surgical complication is very low, but the net effect still depends upon the occurrence of other vascular complications during the follow-up period. The incidence of vascular diseases in this series of seriously affected arteriosclerotics was higher than in a matched normal population, and mortality was much higher. At present a somewhat restrictive indication for surgery seems justified.

Adult

[Improved treatment of abdominal aortic aneurysms. Progress over 17 years].

During the period 1970-86, 155 men and 24 women were operated on for abdominal aortic aneurysms at the University Hospital in Tromsø. Elective operations were performed in 76 patients with an operative mortality of 5 (7%), impending rupture in 49, of whom 14 died (29%) and ruptured aneurysms in 54 patients, of whom 33 (61%) died. There has been a substantial increase in the number of patients per year admitted with abdominal aneurysms, from an average of 4.5 during the years 1970-76 inclusive, to over 20 during the years 1984-86. Operative and early postoperative mortality have been reduced and there has been no death following elective operations during the last three years of the reported period. Mortality was 8% for impending rupture and 45% for ruptured aneurysms. Electively abdominal aortic aneurysms can be operated safely even in patients over the age of 80. Ruptured aneurysms, however, still carry a high operative mortality in patients over the age of 70.

Age Factors

[Arteria gastroepiploica dextra in coronary surgery. Complete revascularization in angina pectoris].

We have used the right gastroepiploic artery as a viable jump graft to the distal right coronary artery in two patients. The first patient was a 37 year-old man with recurrent angina after coronary bypass surgery with three vein grafts eight years previously. The second patient was a man aged 45 with angina in New York Heart Association Class III to IV. In both cases coronary angiography revealed severe triple vessel disease with multiple proximal and distal occlusions or stenosis. Both internal mammary arteries were also used in the two patients to revascularize the LAD and circumflex systems. Thus, a complete revascularization was achieved by use of only viable arteries as conduits. Both patients recovered well and were free from angina. At present only the first patient has had a postoperative angiogram, which showed good patency of the gastroepiploic artery jump graft. If the long-term patency of this type of graft is similar to that of the internal mammary arteries, it is another suitable arterial conduit for revascularization of the ischemic myocardium.

Adult

[Enterobacter cloacae infections at the Regional Hospital in Tromsø].

Enterobacter cloacae was isolated from 69 patients hospitalized at the University Hospital of Tromsø, Norway, during a period of 18 months. The total lethality was 11.6% (8/69) and death occurred most often in patients with a serious underlying condition. Death due to septicaemia occurred in 4/10 patients. Multiple beta-lactam resistant strains were present in 15 patients and were associated with septicaemiae (7/10, p less than 0.0005). Cephalosporin treatment had been given to every third patient (24/69), and nearly half of them (10/24) were infected by multiple beta-lactam resistant E cloacae. E cloacae occurred mainly as a nosocomial infection, since more than 70% of all patients infected had been treated by an invasive procedure prior to isolation of the bacterium. A high number of E cloacae strains were from operation wounds, especially among patients at the Department of Surgery (22/30). At this Department, the total number of E cloacae, and especially the number of multiresistant strains, was markedly reduced during restricted use of cefalosporins.

Adolescent

Amelioration of reperfusion injury following hypothermic, ischemic cardioplegia in isolated, infarcted rat hearts.

The left coronary artery was ligated and myocardial infarction developed in 28 rats. Three weeks later, the hearts were excised and mounted in an apparatus for perfusion of non-working isolated hearts (Langendorff). Hypothermic (15 degrees C), ischemic cardioplegia was induced for either 2 or 3 1/2 h followed by reperfusion for 45 min. Half of the hearts were reperfused with an initially gradual rise in temperature and pressure of the perfusion fluid, whereas the other half was reperfused directly with the perfusate at 37 degrees C and 100 cm H2O pressure. The hearts were examined by transmission electron microscopy and randomized for stereological analysis based on point counting on electron micrographs. Cardioplegia of 2 h duration was tolerated better than cardioplegia for 3 1/2 h (interstitial edema; P = 0.03, fraction of altered mitochondria; P = 0.001). Particularly in the hearts undergoing the longest cardioplegia, myocardial injury was less severe following a gentle reperfusion as compared with those exposed to the clinically common abrupt technique (fraction of mitochondria in the myocyte; P = 0.03, fraction of altered mitochondria; P = 0.008). In the interstitium, the luminal area of capillaries was significantly increased and the endothelial swelling less pronounced in the groups undergoing the gentle reperfusion technique, (luminal/endothelial fraction; P = 0.01). The study shows that previously infarcted hearts are susceptible to ischemic damage even after 2 h of regular hypothermic, ischemic cardioplegia and that a gentle reperfusion technique significantly ameliorates reperfusion injury.

Animals

Effects of initial reperfusion temperature and pressure after prolonged cardioplegic ischemic arrest. A metabolic and functional study in rat hearts.

The effects of temperature and pressure during early cardiac reperfusion after 3.5 hours of hypothermic, cardioplegic ischemia were investigated in isolated Langendorff-perfused rat hearts. The hearts were randomized in two groups and subjected to different techniques of reperfusion. The group I hearts were exposed to rapidly rising perfusion pressure and temperature, and in group II slowly rising pressure and temperature were employed. After 60 min of reperfusion, left ventricular developed pressure, coronary flow and tissue content of high-energy phosphates were evaluated. Left ventricular pressure and coronary flow were significantly better preserved in group II. Recovery of adenosine triphosphate and creatine phosphate was significantly lower in group I (5.27 +/- 0.38 and 8.72 +/- 0.62 mumol x g dry weight-1) than in group II (9.31 +/- 0.41 and 14.97 +/- 0.62). The study thus demonstrated that functional recovery, restoration of coronary flow and normalization of high-energy phosphate stores after long periods of hypothermic cardioplegic ischemia can be considerably influenced by the employed reperfusion technique.

Adenosine Triphosphate

Ultrastructural changes in rat hearts following cold cardioplegic ischemia of differing duration and differing modes of reperfusion.

Morphologic consequences of prolonged global hypothermic (15 degrees C), cardioplegic ischemia and two reperfusion techniques were studied in Langendorff-perfused rat hearts. A 'gentle' reperfusion technique, with gradual rise in perfusate temperature and pressure to physiologic levels over 30 min, was used for 12 hearts following 2-hour or 3 1/2-hour (6 in each group) ischemia. Abrupt reperfusion, with perfusate at 37 degrees C and 70 mmHg, was performed on 13 hearts (6 ischemic for 2 hours and 7 for 3 1/2 hours). Six nonischemic, perfused hearts served as controls. Randomly selected specimens from the left ventricle after 45-60 min reperfusion were prepared for transmission electron microscopy. Volume fractions of myocardial structural components were calculated from stereologic point-counting on the electron micrographs. Two-way analysis of variance revealed that interstitial edema developed with increasing ischemic time and was not influenced by reperfusion technique. The degree of endothelial damage was independent of ischemic time, but was lessened by 'gentle' reperfusion. Both mitochondrial injury and myocyte edema were less when perfusate temperature and pressure were slowly raised after 3 1/2-hour ischemia.

Animals

Coronary trapping of a complement activation product (C3a des-Arg) during myocardial reperfusion in open-heart surgery.

Accumulation of complement factors has been found to occur in the myocardium after infarction. We studied the possibility that the complement activation product C3a des-Arg is trapped within the coronary circulation during reperfusion of the ischemic myocardium. In 11 patients undergoing routine coronary artery bypass grafting, arterial blood was sampled before, during and after cardiopulmonary bypass. Blood was drawn from the coronary sinus concomitantly with arterial blood sampling 5 and 30 min after release of the aortic cross-clamp (n = 10). From a preoperative value of 92 +/- 13 ng/ml, C3a des-Arg rose during CPB to a maximum of 1816 +/- 393 at the end of CPB. Following reperfusion for 5 min, C3a des-Arg was 1284 +/- 232 ng/ml in arterial and 1106 +/- 100 in coronary sinus blood, a significant difference (p less than 0.05). The amount of C3a des-Arg trapped in the heart at 5-min reperfusion showed positive correlation with its arterial concentration (p less than 0.05). No significant difference was found after 30 min of reperfusion. Complement activation products trapped in the heart in the early reperfusion period may play a pathogenetic role in myocardial ischemia-reperfusion injury.

Cardiopulmonary Bypass

Lack of ability to synthesize tissue factor by endothelial cells in intact human saphenous veins.

It is well established that cultured endothelial cells are induced to generate tissue factor activity when incubated with either endotoxin or thrombin. In this study a perfusion system was used on 3-4 cm long human saphenous veins. The veins were perfused with thrombin (2.5 U/ml), endotoxin (30 ng/ml) or just medium for 3 h at 37 degrees C. After the perfusion, the veins were treated with collagenase, and EC were collected and subjected to tissue factor activity measurements. Some perfused veins were examined for tissue factor activity on the vessel wall by allowing factor VII and factor X to interact with the lumen of the intact vessels, followed by quantitation of generated factor Xa in a chromogenic assay. No formation of tissue factor activity could be found after perfusion in either collagenase-dissolved endothelial cells or in the coupled chromogenic assay for tissue factor activity performed in the lumen of the vessel. Our data strongly suggest that endothelial cells in intact endothelium may behave quite differently from isolated endothelial cells stimulated in cell cultures.

Adult

[Varices of the great saphenous vein].

During a 7-year period, 237 patients were treated surgically at Tromsø Hospital for varices of the great saphenous vein. At follow-up (mean 7.5 years) the overall results were excellent in 30%, good in 47%, and poor in 21% of the patients. The recurrence rate of varicose veins was 47%. However, 50% of these patients had no symptoms or only minor symptoms, from the recurrence. 37 patients noticed the occurrence of troublesome varicose veins within one year after operation. At clinical reexamination it was found that in 32 of these patients the surgery had been inadequate. This probably explains the rapid recurrence.

Adolescent

[Nosocomial infections with resistant Enterobacter cloacae. Effects on the disease and the treatment].

We describe five patients with serious nosocomial infection caused by resistant Enterobacter cloacae. Four of the patients underwent cardiovascular operations and were infected with an identical, multiple beta-lactam resistant E cloacae strain. The fifth patient was admitted with several wounds and skin-ulcers containing both resistant and sensitive E cloacae of other types. The resistant strain caused septicemia in four patients; three developed multiorgan failure and one died. The most probable causes of these infections were an abundant and constant reservoir of E cloacae in a sink at the operating unit, periodical breakdown of barriere routines, and heavy use of cephalosporins.

Adult

Multiply beta-lactam resistant Enterobacter cloacae infections linked to the environmental flora in a unit for cardiothoracic and vascular surgery.

During the period March 1987-May 1988, postoperative infection or colonization with Enterobacter cloacae occurred in 9/379 (2.4%) patients who underwent cardiovascular surgery. Five of the patients were infected with multiply beta-lactam resistant E. cloacae, of whom 4 had been infected with an identical, resistant strain during intervals of months. This strain was also found in the environmental flora of the cardiovascular operating suite and in a sink reservoir in the surgery department. All 4 patients with the identical resistant strain had serious complications during the postoperative period with symptoms of septicaemia in 3, multiorgan failure and shock in 2, and mediastinitis in 3. The single resistant strain of a different serotype was also associated with severe postoperative complications. The 4 sensitive strains were all different serotypes. None caused septicaemia, one was associated with mediastinitis, another with an uncomplicated sternum infection, and 2 were from sputum. In the 3 latter patients with sensitive strains and few postoperative complications, cephalosporins had not been used during the pre- or postoperative period.

Adult

Endothelial cells of the cardiac microvasculature during and after cold cardioplegic ischaemia. Comparison of endothelial and myocyte damage.

Ultrastructural changes in endothelial cells of the myocardial microvasculature were studied in 18 patients who underwent aortocoronary bypass surgery under cold ischaemic cardioplegia. Biopsy specimens for electron microscopy were taken from the right atrium before and at the end of aortic cross-clamping and after 20 and 60 min of reperfusion. At the end of the cold ischaemic cardioplegia, the endothelial cells showed reduced numbers of pinocytotic vesicles, moderate intracellular oedema and slight nuclear changes. During reperfusion the endothelial changes became more pronounced and interstitial oedema developed. These changes persisted, or even increased in the first 60 min of reperfusion, in contrast to the myocytic changes, which tended to regress. The endothelial cells of the myocardial microvasculature thus appeared to be more vulnerable than the myocytes to cold ischaemic cardioplegia and reperfusion. Focally reduced blood reperfusion due to endothelial swelling and interstitial oedema did not seem to be the main cause of the focal postischaemic myocytic damage.

Adult

Improved energy preservation following gentle reperfusion after hypothermic, ischemic cardioplegia in infarcted rat hearts.

The influence of temperature and pressure during early reperfusion after 2 h of hypothermic, cardioplegic ischemia was investigated. Adenosine triphosphate (ATP) and creatine-phosphate (CP) were measured after 45-min reperfusion. The experiments were carried out in normal and previously infarcted rat hearts (the left coronary artery having been ligated 3 weeks earlier). Four groups, each containing six hearts, were studied. Group 1 consisted of normal hearts reperfused with an abrupt rise in temperature and pressure, group 2 of normal hearts exposed to slowly rising temperature and pressure, and group 3 and 4 of previously infarcted hearts. Reperfusion procedures in groups 3 and 4 were the same as in group 1 and 2, respectively. The study showed that previously infarcted hearts have a lowered tolerance to ischemia and that the reperfusion technique may influence the preservation of myocardial energetics, although this influence was not statistically significant in normal hearts following only 2 h of ischemia. The gently reperfused infarcted hearts had energy stores equal to the normal hearts after 2 h of ischemia and 45 min of reperfusion, whereas the infarcted hearts reperfused in a rougher mode had significantly lowered values (P less than 0.05 for ATP and P less than 0.01 for CP).

Adenosine Triphosphate

Mortality in rats on long-term parenteral nutrition.

The long-term effect of total parenteral nutrition (TPN) was studied in rats. A failure to thrive developed and all animals died within 40 days of TPN. Autopsy invariably demonstrated the increased weight and volume of the liver and spleen. Multiple fat emboli were found in the lungs of all animals, and multiple epithelioid cell granulomas in the liver of all and in the spleen of most animals. Chronical low grade infection could not be demonstrated. Microorganisms were not found in blood or tissue specimens and endotoxin could not be demonstrated in plasma samples.

Animals

Use of dextran to prevent pericardial adhesions caused by maize starch powder.

Maize starch powder, used as lubricant in surgical gloves, was administered into the pericardial cavity of rats and was found to induce granulomatosis with formation of pericardial adhesions. The effect of dextran 70 on the formation of these adhesions was investigated. It was found that intrapericardial dextran reduces the occurrence of pericardial adhesions.

Animals

Direct effect of high-dose insulin on the depressed heart after beta-blockade or ischemia.

The direct cardiac effects of high-dose insulin (HDI) were assessed in 13 canine hearts supported by cardiopulmonary bypass. Isovolumic peak developed pressure (PDP, mmHg), coronary blood flow (CBF, ml/beat/100 g LV) and myocardial oxygen consumption (MVO2, ml O2/beat/100 g LV) were determined during incremental left ventricular balloon inflation before and after functional depression by beta-blockade (0.2 mg/kg propranolol) or 2 hours cardioplegic ischemia at 28 degrees C. The 2 regimens gave an overall functional reduction of 46 +/- 3% and 42 +/- 2%, respectively. The hearts were then challenged with an aortic root bolus of 1000 IU insulin. A glucose clamp was maintained at physiological levels. Insulin reversed the negative inotropic effect of propranolol to 80% of control function and normalized heart rate. Despite the significant amelioration of systolic function by HDI, MVO2 indexed for cardiac effort did not change. Neither systolic function nor heart rate was changed in the ischemically depressed hearts. In conclusion, HDI reverses the negative inotropic effect of beta-adrenergic receptor blockade without augmenting oxygen utilization. Apart from effects ascribable to systemic vasodilation and metabolic shifts, no direct cardiac inotropic stimulation can be expected on the post-ischemically depressed, nondiabetic myocardium unless there is a persistent negative effect of beta-blockers.

Animals