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Biomedical subjects

K Rådegran

Publications and source records attributed to K Rådegran.

At least 37 records · Page 2Linked to original sources

Autotransfusion of mediastinal blood in cardiac surgery.

A series of 135 adults undergoing cardiac surgery was randomized to an autotransfusion group (n = 67) or a control group (n = 68). In the autotransfusion group mediastinal blood was collected and reinfused during the first 6 postoperative hours. Blood from the reservoir was taken for bacteriologic culture at the end of that time. The postoperative blood was comparable in the two groups. The average requirement of bank blood was 2.7 units in the autotransfusion group and 3.3 units in the controls (p less than 0.05). The average volume of autotransfusion blood was 336 ml. There were no clinical infections in the autotransfusion group, although 19% of the cultures were positive, and no apparent alteration of the coagulation mechanisms arose from infusion of autologous blood. No clinically significant intergroup differences were found in hematologic, renal or hepatic parameters, neurologic function or use of antibiotics.

Aged↗

Comparison of two protocols for heparin neutralization by protamine after cardiopulmonary bypass.

Twenty patients undergoing cardiac operations were randomly assigned to two protocols for heparin neutralization by protamine after cardiopulmonary bypass. In all patients protamine chloride was given at a ratio of 1 unit of protamine to 1 unit of injected heparin. In Group I (10 patients) all protamine was infused within 10 minutes after termination of cardiopulmonary bypass. Group II (10 patients) received 75% of the calculated protamine dose within 10 minutes after termination of bypass and the remainder after transfusion of all blood in the heart-lung machine. Plasma heparin levels were significantly lower in Group II 5 minutes after transfusion of all blood in the heart-lung machine and were 0.13 units/ml (standard deviation 0.04) in Group I and 0.06 units/ml (standard deviation 0.05) in Group II (p less than 0.001) 60 minutes after bypass. Activated partial thromboplastin time mirrored the changes in plasma heparin, whereas activated clotting time (Hemochron) was too insensitive to detect these low plasma heparin levels. We conclude that the two-dose protocol resulted in more complete heparin neutralization than the one-dose protocol.

Cardiopulmonary Bypass↗

Cerebral blood flow and metabolism during cardiopulmonary bypass with special reference to effects of hypotension induced by prostacyclin.

Cerebral blood flow and metabolism of oxygen, glucose, and lactate were studied in 43 patients undergoing aortocoronary bypass. Twenty-five patients received prostacyclin infusion, 50 ng per kilogram of body weight per minute, during cardiopulmonary bypass (CPB), and 18 patients served as a control group. Regional cerebral blood flow (CBF) was studied by intraarterially injected xenon 133 and a single scintillation detector. Oxygen tension, carbon dioxide tension, oxygen saturation, glucose, and lactate were measured in arterial and cerebral venous blood. Mean arterial blood pressure decreased during hypothermia and prostacyclin infusion to less than 30 mm Hg. The regional CBF was, on average, 22 (standard deviation [SD] 4) ml/100 gm/min before CPB. It increased in the control group during hypothermia to 34 (SD 12) ml/100 gm/min, but decreased in the prostacyclin group to 15 (SD 5) ml/100 gm/min. It increased during rewarming in the prostacyclin group. After CPB, regional CBF was about 40 ml/100 gm/min in both groups. The cerebral arteriovenous oxygen pressure difference decreased more in the control group than in the prostacyclin group during hypothermia. The cerebral metabolic rate of oxygen decreased in both groups from approximately 2 ml/100 gm/min to about 1 ml/100 gm/min during hypothermia, increased again during rewarming, and after CPB was at the levels measured before bypass in both groups. There was no difference between the groups in regard to glucose and lactate metabolism.

Adult↗

Effects of prostacyclin infusion on renal function during cardiopulmonary bypass.

Infusion of prostacyclin inhibits platelet activation during cardiopulmonary bypass (CPB) but also results in systemic arterial hypotension. Therefore, the effects of CPB and prostacyclin on renal function were studied in 36 male patients undergoing aortocoronary bypass. Nineteen patients (Group 1) received prostacyclin, 50 ng per kilogram of body weight per minute, during CPB, and 17 patients (Group 2) served as controls. There was pronounced hypotension in Group 1 only. Urine production during CPB averaged 88 +/- 140 ml and 2,306 +/- 1,112 ml in Groups 1 and 2, respectively. No patient had renal failure. Glomerular filtration rate (GFR), as measured by clearance of chromium 51-labeled ethylenediaminetetraacetic acid, was increased in Group 1 from 86 +/- 14 to 99 +/- 22 ml/1.73 m2/min (p less than 0.05) the day after operation, but remained unchanged in Group 2 (81 +/- 15 to 82 +/- 21 ml/1.73 m2/min). The increased GFR in Group 1 can be regarded as an expected adaptation to the change in body fluids after CPB. Therefore, the unchanged GFR in Group 2 must be regarded as caused by insufficient adaptation or impaired renal function. Proximal tubular function was evaluated by determination of beta 2-microglobulin in urine. In both groups, urinary beta 2-microglobulin and the ratio of urinary beta 2-microglobulin to urinary creatinine were increased the day after operation. The hypotension in Group 1 did not exacerbate the damage to tubular function.

Aged↗

Effects of cardiopulmonary bypass and prostacyclin on plasma catecholamines, angiotensin II and arginine-vasopressin.

Infusion of prostacyclin during cardiopulmonary bypass (CPB) reduces platelet activation, diminishes postoperative blood loss and decreases arterial blood pressure. In spite of continuous prostacyclin infusion, there is a delayed gradual rise in arterial pressure and resistance from low initial levels. We measured epinephrine (E), norepinephrine (NE), serotonin (5-HT), angiotensin II (ATII) and arginine-vasopressin (AVP) in plasma and carried out hemodynamic studies in 19 patients operated for coronary vascular disease. Eight patients served as a control group and were subjected to routine CPB. Eleven patients received prostacyclin 50 ng/kg/min during CPB. E and NE increased four- to sixfold during CPB from about 0.5 ng/ml (P less than 0.001). There was no difference between the groups. During CPB AVP increased sixfold from about 20 pg/ml in both groups (P less than 0.001), decreased early after CPB and increased again to high levels 3 h after CPB. The combined action of E, NE and AVP is of likely importance for the rise in systemic vascular resistance and/or need of vasodilation during CPB in the control group. ATII did not increase in the control group, but increased fourfold to about 20 pg/ml (P less than 0.01) during CPB in the prostacyclin group. The addition of AT II to E, NE and AVP seems responsible for the gradual return of arterial pressure and resistance during prostacyclin infusion. Postoperative hypertension and/or need of vasodilation 3 h after CPB was associated with high AVP levels in both groups. Hypotension caused by prostacyclin infusion did not increase E, NE or AVP above levels produced by CPB and moderate hypotension alone.

Anesthesia↗

Somatosensory evoked potentials and cerebral metabolism during cardiopulmonary bypass with special reference to hypotension induced by prostacyclin infusion.

Somatosensory evoked potentials and cerebral metabolism were studied during cardiopulmonary bypass in 41 patients undergoing coronary bypass. Twenty-two patients received prostacyclin 50 ng/kg/min during cardiopulmonary bypass for platelet protection and 19 patients served as controls. Mean arterial blood pressure in the prostacyclin group was below 30 mm Hg during the first 30 minutes of bypass, but it remained above 50 mm Hg in the control group. Central conduction time, a measure of the electrical conduction time in the central nervous system, was prolonged in both groups during bypass up to 30 minutes of rewarming. The prolongation was greater in the control group early during bypass. At 20 minutes of cardiopulmonary bypass, central conduction time was increased by 81% (standard deviation 38) of the prebypass value in the control group and by 44% (standard deviation 17) in the prostacyclin group (p less than 0.001). Arteriovenous oxygen difference across the brain was greater in the prostacyclin group early during bypass. It was 36 ml/L (standard deviation 9) in the control group and 60 ml/L (standard deviation 18) in the prostacyclin group (p less than 0.001) at 10 minutes of bypass. There was no difference between the groups in regard to glucose and lactate. We conclude that cardiopulmonary bypass with hypothermia prolongs central conduction time. The hypotension induced by prostacyclin (50 ng/kg/min) did not further impair conduction in the central nervous system.

Blood Platelets↗

Effects of prostacyclin infusion on platelets and hemodynamics in coronary bypass surgery.

Twenty patients undergoing aorto-coronary bypass were randomly assigned to a prostacyclin treatment group or control group. Eight patients received 2 mg/kg heparin and 10 ng/kg/min prostacyclin before cardiopulmonary bypass (CPB) and 50 ng/kg/min during CPB. Twelve patients, serving as controls, received 3 mg/kg heparin. Heparinization resulted in a slight but significant increase of plasma beta-thromboglobulin in the control group but not in the prostacyclin group, and of plasma platelet factor 4 (PF-4) in both groups. After 90 minutes of CPB, beta-thromboglobulin was 408 (SD 128) ng/ml in the control group and 111 (SD 50) ng/ml (p less than 0.001) in the prostacyclin group. Platelet count, corrected for hemodilution, was 92% (SD 10) of the pre-CPB value after 10 minutes of CPB and 89% (SD 7) one hour after CPB in the control group, as compared to 113% (SD 10) and 145% (SD 18), respectively, in the prostacyclin group. Prostacyclin infusion before CPB reduced systemic vascular resistance to half of that of the control group, lowered mean arterial blood pressure, and increased cardiac index by 60% to 80%. An infusion of prostacyclin before CPB does not add to the already excellent platelet protective effect of 50 ng/kg/min prostacyclin during CPB, but may be used for vasodilation.

Blood Platelets↗

Hypotension induced by prostacyclin treatment during cardiopulmonary bypass does not increase the risk of cerebral complications.

High-dose prostacyclin treatment during cardiopulmonary bypass reduces platelet activation and possibly postoperative blood loss. A side-effect is arterial hypotension. We studied the incidence of cerebral complications in 79 patients requiring coronary bypass. Only patients without known cerebrovascular disease were studied. Thirty-nine patients received prostacyclin 50 ng/kg/min during cardiopulmonary bypass and 40 patients served as controls. Mean arterial blood pressure in the group given prostacyclin was below 30 mm Hg during the first 30 minutes of bypass but remained above 60 mm Hg in the control group. Postoperative neurological examination revealed transient cerebral dysfunction in six control patients and two prostacyclin-treated patients. Investigation of cerebrospinal fluid showed signs of blood-brain barrier damage in 12 control and seven prostacyclin-treated patients. Cytologic changes in cerebrospinal fluid consistent with brain tissue damage occurred in two control patients but in no patient given prostacyclin. Myelin basic protein and adenylate kinase in cerebrospinal fluid were assayed as being markers of brain damage. Myelin basic protein was within the normal range in all patients. Adenylate kinase was moderately increased (greater than 0.035 U/L) in five of 15 control patients and six of 13 prostacyclin-treated patients. We conclude that treatment with prostacyclin 50 ng/kg/min during cardiopulmonary bypass does not increase the risk of postoperative cerebral damage.

Adenylate Kinase↗

Effects of prostacyclin infusion on platelet activation and postoperative blood loss in coronary bypass.

The effects of infusion of prostacyclin were studied in 41 patients undergoing aortocoronary bypass. Twenty-three patients received heparin (2 mg per kilogram of body weight) and prostacyclin (50 ng per kilogram per minute) during cardiopulmonary bypass (CPB). Eighteen patients received heparin (3 mg per kilogram). One hour after CPB, the platelet count was 98 +/- 16% of the value obtained before CPB in the prostacyclin group and 73 +/- 18% in the control group (p less than 0.001). The plasma level of platelet factor 4 rose only initially during CPB in the prostacyclin group, but increased continuously in the control group; at 90 minutes of CPB it was 92 +/- 35 ng per milliliter and 376 +/- 119 ng per milliliter, respectively (p less than 0.001). Beta-thromboglobulin showed a similar pattern. Postoperative chest drainage was 386 +/- 87 ml in the prostacyclin group and 596 +/- 342 ml in the control group (p less than 0.05). Blood transfused during and five days after operation was 1,359 +/- 751 ml in the prostacyclin group and 2,047 +/- 915 ml in the control group (p less than 0.05).

Aged↗

Prostacyclin infusion during extracorporeal circulation foe coronary bypass.

The effects of prostacyclin on whole blood platelet count, blood coagulation factors, and postoperative bleeding were investigated in 20 patients undergoing aorta-coronary bypass. Eleven patients received heparin 2 mg/kg and prostacyclin 50 ng/kg/min during cardiopulmonary bypass (CPB). Nine patients received only heparin 3 mg/kg. CPB was by roller pump and bubble oxygenator primed with Ringer's acetate. Hypothermia to 28 degrees C was induced. In the control group, platelet count, corrected for hemodilution, was 70% +/- 15% (mean +/- SD) of pre-CPB value after 30 minutes of bypass and remained at this level 1 hour after CPB. In the prostacyclin group, the platelet count after 30 minutes was 85% +/- 17%, after 120 minutes 111% +/- 20%, and 1 hour after CPB 92% +/- 17%. There was a significant difference between the groups (p less than 0.05) from 60 minutes of CPB up to 1 hour after CPB. Prostacyclin allowed reduction of the heparin dosage while retaining anticoagulation as measured by activated coagulation time (ACT), fibrinopeptide A, and fibrinogen determinations. The ACT was more than 900 seconds in the prostacyclin group after 30 minutes of CPB, as compared to 523 +/- 118 seconds (p less than 0.05) in the control group. This difference diminished later during CPB. In the prostacyclin group, arterial blood pressure was 30 mm Hg or less during the first hour of CPB and the systemic vascular resistance was half of that in the control group. All patients survived. There were no clinical signs of neurologic damage. Postoperative bleeding was 352 +/- 61 ml in the prostacyclin group and 550 +/- 338 ml (NS) in the control group.

Aged↗

Use of the activated coagulation time in cardiac surgery. Effects on heparin-protamine dosages and bleeding.

A standard heparin-protamine protocol was used for a series of 44 patients. In a second series of 82 patients. Activated Clotting Time (ACT) by the Hemochron method was used to control heparinization and its reversal with protamine. The two groups was similar in regard to surgical procedures, pump-times and perfusion technique. Patients in group II controlled by Hemochron received in average 13% less heparin and 48% less protamine than patients in group 1 (p less than 0.001 Student's t-test). The intra-operative blood loss was on an average 50% less in group II than in group I (p less than 0.001). There was, however, no significant difference in regard to postoperative bleeding. The introduction of the ACT test thus resulted in reduced dosages of heparin and protamine and in a reduction of intra-operative bleeding, while surgical technique seems to be the main factor in the control of postoperative bleeding.

Adult↗

Influence of cardiopulmonary bypass on some host defence functions in man.

Four different functions of the immune defence were studied in six men undergoing open-heart surgery with cardiopulmonary bypass (CPB). Pre-operatively, a few hours after and three days after surgery the following tests were performed: (I) in vivo phagocytic and metabolic functions of the reticuloendothelial system (RES), (II) haemolytic activity of blood monocytes, (III) nitroblue tetrazolium (NBT) reduction by granulocytes, and (IV) bactericidal capacity of granulocytes. Compared to the pre-operative values, the RES functions were unchanged postoperatively, whereas there was a significant increase in the haemolytic activity of monocytes and in the NBT reduction of granulocytes. The capacity of the granulocytes to kill bacteria was normal a few hours after surgery, but significantly increased on day 3. No infectious complications occurred and all patients recovered uneventfully. These results suggest that, at the present time, open-heart surgery under CPB is accompanied by an increased activity of granulocytes and monocytes in the early postoperative period.

Adult↗

Bleeding complications following invasive cardiac studies in anticoagulated patients with artificial heart valves.

The number and nature of bleeding complications subsequent to cardiac catheterization and angiography were determined in 50 anticoagulated and 50 control patients. There were six bleeding complications in the anticoagulated group and five in the control group. Although the complications were somewhat more severe in anticoagulated patients, the difference was not enough to justify a change in our general policy of continuing anticoagulant treatment in patients with artificial heart valves who are admitted for postoperative invasive cardiac investigations.

Adult↗

Prevention of platelet adhesion and aggregation by a glutardialdehyde-stabilized heparin surface.

A stable heparinized surface was prepared by sequential treatment of polyethylene with water solutions of hexadecylamine hydrochloride, heparin and glutardialdehyde. In order to explain the "non-thrombogenic" properties of this surface, it was evaluated with regard to prevention of platelet adhesion and aggregation. Human heparinized blood (2 and 10 IU/ml) with 51Cr-labelled autologous platelets was rotated for 60 minutes in untreated and heparin-treated circular tubings. The surface area/blood volume ratio was varied and an air-blood interface was present. In untreated tubings, platelet adhesion and aggregation increased in proportion to the size of the surface area/blood volume ratio, irrespective of the heparin concentrations of the blood. In the heparin-treated tubings, there was no measurable platelet adhesion to the surface and no platelet aggregation in the blood. The difference between the heparinized and the untreated surfaces with regard to platelet adhesion was discernible even after 10 minutes storage of stagnant blood. It is concluded that platelet adhesion and aggregation induced by exposure of blood to a foreign surface in an in vitro experimental model can be prevented by a stable heparin coating of the surface.

Aldehydes↗