Nutrition education in medical schools (NEMS) project: Joining ESPEN and university point of view.

BACKGROUND & AIMS: Nutrition education is not well represented in the medical curriculum. The aim of this original paper was to describe the Nutrition Education in Medical Schools (NEMS) Project of the European Society for Clinical Nutrition and Metabolism (ESPEN). METHODS: On 19 January 2020, a meeting was held on this topic that was attended by 51 delegates (27 council members) from 34 countries, and 13 European University representatives. RESULTS: This article includes the contents of the meeting that concluded with the signing of the Manifesto for the Implementation of Nutrition Education in the Undergraduate Medical Curriculum. CONCLUSION: The meeting represented a significant step forward, moved towards implementation of nutrition education in medical education in general and in clinical practice in particular, in compliance with the aims of the ESPEN Nutrition Education Study Group (NESG).

European Society of Coloproctology consensus on the surgical management of intestinal failure in adults.

Intestinal failure (IF) is a debilitating condition of inadequate nutrition due to an anatomical and/or physiological deficit of the intestine. Surgical management of patients with acute and chronic IF requires expertise to deal with technical challenges and make correct decisions. Dedicated IF units have expertise in patient selection, operative risk assessment and multidisciplinary support such as nutritional input and interventional radiology, which dramatically improve the morbidity and mortality of this complex condition and can beneficially affect the continuing dependence on parenteral nutritional support. Currently there is little guidance to bridge the gap between general surgeons and specialist IF surgeons. Fifteen European experts took part in a consensus process to develop guidance to support surgeons in the management of patients with IF. Based on a systematic literature review, statements were prepared for a modified Delphi process. The evidence for each statement was graded using Oxford Centre for Evidence-Based Medicine Levels of Evidence. The current paper contains the statements reflecting the position and practice of leading European experts in IF encompassing the general definition of IF surgery and organization of an IF unit, strategies to prevent IF, management of acute IF, management of wound, fistula and stoma, rehabilitation, intestinal and abdominal reconstruction, criteria for referral to a specialist unit and intestinal transplantation.

ESPEN Guidelines on Parenteral Nutrition: pancreas.

Assessment of the severity of acute pancreatitis (AP), together with the patient's nutritional status is crucial in the decision making process that determines the need for artificial nutrition. Both should be done on admission and at frequent intervals thereafter. The indication for nutritional support in AP is actual or anticipated inadequate oral intake for 5-7 days. This period may be shorter in those with pre-existing malnutrition. Substrate metabolism in severe AP is similar to that in severe sepsis or trauma. Parenteral amino acids, glucose and lipid infusion do not affect pancreatic secretion and function. If lipids are administered, serum triglycerides must be monitored regularly. The use of intravenous lipids as part of parenteral nutrition (PN) is safe and feasible when hypertriglyceridemia is avoided. PN is indicated only in those patients who are unable to tolerate targeted requirements by the enteral route. As rates of EN tolerance increase then volumes of PN should be decreased. When PN is administered, particular attention should be given to avoid overfeeding. When PN is indicated, a parenteral glutamine supplementation should be considered. In chronic pancreatitis PN may, on rare occasions, be indicated in patients with gastric outlet obstruction secondary to duodenal stenosis or those with complex fistulation, and in occasional malnourished patients prior to surgery.

Doctors and nurses on wards with greater access to clinical dietitians have better focus on clinical nutrition.

BACKGROUND: According to the Council of Europe, clinical dietitians should assume a more central role in nutritional support. The aim of this study was to assess the opinions among doctors, nurses and clinical dietitians regarding the use of clinical dietitians' expertise in the hospital units and, further, to assess whether the presence of clinical dietitians in hospital departments influenced doctors and nurses focus on clinical nutrition. METHODS: A questionnaire about the use of clinical nutrition was mailed to 6000 doctors and 6000 nurses working in hospital units where undernutrition is documented to be common, as well as to 678 clinical dietitians working in Scandinavian hospitals. RESULTS: The response rate of clinical dietitians, nurses and doctors were 53%, 46% and 29%, respectively. Nurses and doctors who saw clinical dietitians often found it less difficult to identify undernourished patients and found that insight into the importance of adequate nutrition was better than those who saw clinical dietitians seldom. Clinical nutrition had a higher priority in units with frequent visits by clinical dietitians. CONCLUSIONS: The present study shows that doctors and nurses on wards with greater access to clinical dietitians had better focus on clinical nutrition.

Alteration of hepatic fatty acid metabolism after burn injury in pigs.

BACKGROUND: The primary goal of this study was to investigate hepatic fatty acid (FA) metabolism after severe thermal injury. METHODS: Sixteen pigs were divided into control (n = 8) and burn (n = 8, with 40% full thickness total body surface area burned) groups. Catheters were inserted in the right common carotid artery, portal vein, and hepatic vein for blood sampling. Flow probes were placed around the hepatic artery and portal vein for blood flow measurements. Animals were given pain medication and sedated until the tracer study on day 4 after burn. The pigs were infused for 4 hours with U-13C16-palmitate in order to quantify hepatic FA kinetics and oxidation. RESULTS: Liver triglyceride (TG) content was elevated from 162 +/- 16 (control) to 297 +/- 28 micromol TG/g dry liver wt. (p < .05). Hepatic FA uptake and oxidation were similar between the 2 groups, as were malonyl-coenzyme A (CoA) levels and activities of acetyl-CoA carboxylase and adenosine monophosphate (AMP)-activated protein kinase. In contrast, incorporation of plasma-free fatty acids into hepatic TG was elevated (p < .05) and very low density lipoprotein TG (VLDL-TG) secretion was decreased from 0.17 +/- 0.02 (control) to 0.03 +/- 0.01 micromol/kg per minute in burned pigs (p < .05). CONCLUSIONS: The accumulation of hepatic TG in burned animals is due to inhibition of VLDL-TG secretion and to increased synthesis of hepatic TG. Fatty acids are not channeled to TG because of impaired oxidation.

Surfactant phosphatidylcholine in thermally injured pigs.

OBJECTIVE: To investigate the effect of a thermal injury on pulmonary surfactant phosphatidylcholine kinetics. DESIGN: Random, controlled study. SETTING: University research laboratory. SUBJECTS: Yorkshire swine (n = 8) with and without a 40% total body surface area burn. INTERVENTIONS: A new isotope tracer methodology was used to quantify surfactant phosphatidylcholine kinetics. Four days after burn, [1,2-13C2]acetate and [U-(13)C16]palmitate were infused continuously for 8 hrs to quantify surfactant phosphatidylcholine synthesis, secretion, recycling, and irreversible loss. MEASUREMENTS AND MAIN RESULTS: The total surfactant phosphatidylcholine pool size was reduced from the control value of 2.65 +/- 0.05 to 1.61 +/- 0.08 micromol/g wet lung in burned animals (p <.05), as was the proportional contribution of palmitate to lung surfactant phosphatidylcholine composition. This reduction was associated with a significant decrease in lung dynamic compliance from the control value of 66 +/- 6 to 55 +/- 6 mL/cm H2O for burned pigs (p <.05). The most prominent response of lung phosphatidylcholine kinetics was a decrease in the total lung phosphatidylcholine synthesis from a control value of 12.7 +/- 1.2 to 5.5 +/- 0.3 nmol phosphatidylcholine-bound palmitate x hr(-1) x g of wet lung(-1) in burned animals (p<.05). CONCLUSIONS: Pulmonary phosphatidylcholine content and palmitate composition decrease after burn injury because of a decrease in the rate of phosphatidylcholine synthesis. These responses likely contribute to impaired lung compliance.

Caval backflow: a potential problem during blood sampling from the hepatic vein.

A proper measurement of splanchnic metabolism involves sampling blood from the hepatic vein without backflow contamination of blood from the caval vein. We have investigated the potential problem of caval backflow in human volunteers with an indwelling hepatic vein catheter by sampling blood with different amounts of suction on the syringe (ie, sampling speeds). We also investigated the potential problem in pigs in which a balloon catheter was inserted in the hepatic vein. Pure hepatic vein samples were obtained with the balloon inflated and compared with samples obtained from the same catheter in the conventional manner. In overnight fasted humans, drawing blood samples from the hepatic vein with minimal suction ("slow" drawing) resulted in glucose values 9.6% higher than drawing the samples with greater suction ("fast" drawing). The calculated arterial-venous balance across the splanchnic bed was 4.8 times greater with "slow" blood drawing as compared with "fast" drawing. Values obtained from the pigs showed no concentration differences between pure hepatic vein samples and "slow" drawing from the hepatic vein. The current study indicates that it is possible to obtain a "true" hepatic vein sample, but backflow from the caval vein is a potential pitfall that can have a physiologically significant impact on calculated balance data.

Glucose effects on lung surfactant kinetics in conscious pigs.

The primary goal of this study was to investigate the effects of glucose infusion on surfactant phosphatidylcholine (PC) metabolic kinetics in the lungs. A new stable isotope tracer model was used in which [1,2-(13)C(2)]acetate and uniformly labeled [U-(13)C(16)]palmitate were infused in 12 normal overnight-fasted pigs to quantify lung surfactant kinetics with or without glucose infusion (24 mg. kg(-1). min(-1)). With glucose infusion, the rate of surfactant PC incorporation from de novo synthesized palmitate increased from the control value of 2.1 +/- 0.2 to 15.5 +/- 1.9 nmol PC-bound palmitate. h(-1). g wet lung(-1) (P < 0.05), whereas the incorporation rate from plasma preformed palmitate decreased from the control value of 20.9 +/- 1.9 to 11.6 +/- 1.1 nmol palmitate. h(-1). g wet lung(-1) (P < 0.05). The palmitate composition in lamellar body surfactant PC increased from the control value of 61.7 +/- 2.1% to 75.9 +/- 0.6% (P < 0.05). The surfactant PC secretion rate decreased from the control value of 239.0 +/- 26.1 to 81.9 +/- 5.3 nmol PC-bound palmitate. h(-1). g wet lung(-1) (P < 0.05). We conclude that, whereas surfactant secretion was inhibited by glucose infusion, neither total surfactant PC synthesis nor the surfactant PC pool size was significantly affected due to an increased reliance on de novo synthesized fatty acids.

Myocardial metabolism and efficiency after warm continuous blood cardioplegia.

BACKGROUND: Warm continuous blood cardioplegia (WCBCP) has been recommended during prolonged cardiac arrest to minimize functional deterioration. Myocardial metabolism and efficiency after this cardioplegic modality are not well described. METHODS: Substrate oxidation, blood flow, and myocardial function were measured before, during, and after 3 hours of WCBCP in 7 pigs. RESULTS: Free fatty acid and glucose oxidation decreased by 60% +/- 3.8% and 94% +/- 1.2%, respectively, during cardioplegia (both p < 0.05) and increased to 62% +/- 28% and 122% +/- 62% of baseline during the early recovery phase (p < 0.05 for glucose). One hour after WCBCP oxidation rates were similar to baseline. The transient postcardioplegic increase in substrate oxidation was associated with a 43% +/- 23% elevation of oxygen consumption (MVO2) compared with baseline and a 62% +/- 18% increase in myocardial blood flow. Cardiac output and mean arterial pressure did not change significantly after WCBCP, although myocardial function (stroke work, left ventricular end-systolic pressure, end-diastolic pressure, contractility, and efficiency) was depressed (p < 0.05). End-diastolic pressure and contractility improved from early to late phase of recovery, whereas the other indicators of ventricular function remained depressed. CONCLUSIONS: Myocardial substrate oxidation was preserved after 3 hours of WCBCP, although ventricular function was moderately impaired. Thus, WCBCP with a seemingly normal substrate and oxygen supply was associated with a reduced cardiac efficiency.

Gut epithelial apoptosis after severe burn: effects of gut hypoperfusion.

BACKGROUND: Severe cutaneous burn causes transient mesenteric vasoconstriction and altered gut mucosal integrity. We recently showed that burn also increases gut epithelial cell death by apoptosis. The goal of this study was to determine whether changes in gut perfusion after burn contribute to burn-associated gut apoptosis. STUDY DESIGN: We first correlated superior mesenteric artery blood flow with measurement of gut perfusion at the tissue level by laser doppler in four nonburned rats before, during, and after arterial clamping to validate our measurements of gut perfusion. We then characterized gut perfusion sequentially over time after burn; gut perfusion was measured 3 cm from the ligament of Treitz before burn and hourly for 6 hours. A group of control rats underwent the exact same protocol without the burn to exclude effects of anesthesia and laparotomy on tissue perfusion (n = 4). We studied a third group of rats with hypoperfusion of the same duration and magnitude induced mechanically without burn (n = 7). Sections of the proximal gut from all three groups (control without burn, burn, and hypoperfusion without burn) were examined for epithelial apoptosis. RESULTS: Linear regression analysis demonstrated a strong correlation between superior mesenteric artery blood flow and intestinal tissue perfusion measured by laser doppler under both low and high flow conditions (r = 0.85). Laser doppler measurements of gut perfusion after burn showed deceased gut perfusion that was maximal at 2 hours postburn (p < 0.05), and that persisted for 4 hours (p < 0.05). By 6 hours, gut perfusion returned to baseline. Apoptosis increased significantly in the burn group (2.11 +/- 0.17%) compared with control (0.52 +/- 0.2%) and the mechanically decreased perfusion group (0.51 +/- .03) (p < 0.001). CONCLUSIONS: We conclude that burn-induced gut hypoperfusion is insufficient to cause burn-related increased gut epithelial apoptosis. We speculate that the signal for increased gut epithelial apoptosis is primarily related to proinflammatory mediators induced by the burn wound.

Methysergide reduces nonnutritive blood flow in normal and scalded skin.

Methysergide is a serotonin antagonist and has been demonstrated to reduce wound blood flow and edema formation. We have determined the effect of methysergide on protein kinetics in normal and scalded skin of anesthetized rabbits. L-[ring-(13)C(6)]- or L-[ring-(2)H(5)]phenylalanine was used to reflect skin protein kinetics by use of an ear model, and L-[1-(13)C]leucine was used to reflect whole body protein kinetics. The results were that infusion of methysergide (2-3 mg. kg(-1). h(-1)) reduced the blood flow rate in normal skin by 50% without changing skin or whole body protein kinetics. After scald injury on the ear, administration of methysergide for 48 h reduced the weight of scalded ears (43 +/- 4 vs. 30 +/- 5 g, P < 0.01) and ear blood flow rate (42.6 +/- 4.9 vs. 5.8 +/- 1.0 ml. 100 g(-1). min(-1), P < 0.0001) and did not change wound protein kinetics. Methysergide reduced arteriovenous shunting and maintained inward phenylalanine transport from the blood to the skin pool. Using the microsphere technique, we found that the infusion of methysergide decreased blood perfusion by 33-36% in both normal and scalded ear skin. We conclude that methysergide administration reduces nonnutritive, as opposed to nutritive, blood flow in normal and scalded skin.

Comparison of wound culture and bronchial lavage in the severely burned child: implications for antimicrobial therapy.

BACKGROUND: The relationship of the burn wound flora to microbial pathogens in the tracheobronchial tree has important implications for antimicrobial therapy in the severely burned patient. Management of septic complications is bolstered by surveillance quantitative wound cultures (QWC) and bronchial lavage fluid (BLF) cultures. OBJECTIVES: To compare the organisms present in BLF with those found in QWC and to determine if QWC can predict BLF results. DESIGN: Results of BLF cultures from all patients who underwent bronchial lavage from January 1, 1996, to December 31, 1996, at our institution were compared with QWC data from the same date. Criteria for a positive match included an identical antibiotic susceptibility pattern and biotype. Match rates were calculated qualitatively and quantitatively. RESULTS: In 30 (48%) of the 62 BLF cultures, there was a match between the organism identified in the BLF and the QWC. When strict quantitative criteria were applied, the match rate was only 9 (14%) of 62. Burn size and inhalation injury had no significant effect on match rate. CONCLUSIONS: Whereas the microbial pathogens were similar in the QWC and BLF, linear regression showed no value of QWC in predicting BLF culture results. The difference between qualitative and quantitative match rates suggests cross-colonization between the burn wound and tracheobronchial tree, but little to no cross-infection. The QWC and BLF cultures must be performed independently in determining antimicrobial specificity in the burned patient.

Is the general practitioner hospital a potential "patient trap"? A panel study of emergency cases transferred to higher level hospitals.

OBJECTIVES: 1. To find out whether a stay in local general practitioner hospitals (GP hospitals) prior to an emergency admission to higher level hospitals aggravated or prolonged the course of the disease, or contributed to permanent health loss for some patients. 2. To detect cases where a transitory stay in a GP hospital might have been favourable. DESIGN: A retrospective expert panel study based on records from GP hospitals and general hospitals. The included patients had participated in a previous prospective study of consecutive admissions to GP hospitals during 8 weeks. SETTING: Fifteen out of 16 GP hospitals in Finnmark county, Norway. SUBJECTS: Seventy-three patients transferred to higher level hospitals from a total of 395 admitted to GP hospitals. MAIN OUTCOME MEASURES: Three outcome categories were considered for each patient: "possible permanent health loss", "possible significantly prolonged or aggravated disease course", and "possible favourable effect on the disease course". RESULTS: There was agreement about the possibility of negative effects in two patients (2.7%), while a possible favourable influence was ascribed to six cases (8.2%). CONCLUSION: Negative health effects due to transitory stays in GP hospitals are uncommon and moderate, and balanced by benefits, particularly with regard to early access to life saving treatment for critically ill patients.

High cardioplegic perfusion pressure entails reduced myocardial recovery.

OBJECTIVE: The cardioplegic solution is often given at high flow and pressure following aortic clamping clamping to ensure rapid diastolic arrest. With standard setup in clinical practice, it is easy to exceed 200 mmHg in the aortic root. To investigate whether cardioplegic solution delivery pressure has an influence on myocardial protection, intermittent infusions of crystalloid cardioplegia were given at two different pressures using an in vivo pig model. METHODS: Fourteen pigs (48-57 kg) were put on cardiopulmonary bypass, aorta-clamped (2 h) and 500 ml St. Thomas' cardioplegia (4 degrees C) was delivered antegradely at either 75 mmHg (group 1, n = 7) or 175 mmHg (group 2, n = 7) pressure via 9-F aortic root cardioplegic needle. Every 20 min, 100 ml cardioplegic were delivered at either one of the two pressures. After 2 h, the aorta was unclamped and the hearts reperfused. Attempts were made to wean pigs from bypass following 20 min reperfusion or, if they were failing, after 40 min. If failing once again, the pigs were reperfused for the last 20 min on the heart-lung machine. RESULTS: Hearts in group 1 (n = 7) needed significantly longer time to stop after aortic clamping (38 +/- 9 s) than did group 2 hearts (n = 7) (21 +/- 5 s) (P = 0.043). In group 1, all pigs were weaned from bypass, whereas in group 2 only 2 out of 7 pigs were able to sustain circulation without cardiopulmonary bypass (P = 0.01), and then with lower hemodynamic performances. At the end of cardiac arrest, group 1 had significantly higher adenosine triphosphate (19.4 +/- 1.1 mumol/g dry weight and 15.05 +/- 1.8 mumol/g dry weight, respectively) (P = 0.05) and significantly lesser fall in energy charge than group 2 (0.02 +/- 0.01 and 0.05 +/- 0.02, respectively) (P = 0.05). Also at the end of reperfusion, group 1 had significantly higher adenosine triphosphate (16.54 +/- 1.4 mumol/g dry weight and 12.53 +/- 0.95 mumol/g dry weight, respectively) (P = 0.016) than group 2. CONCLUSIONS: Despite a swifter diastolic cardiac arrest, the high cardioplegic solution delivery pressure caused significantly poorer postischemic recovery than a moderate pressure with the same amount of cardioplegic solution.

Exogenous reactive oxygen species deplete the isolated rat heart of antioxidants.

The effects of reactive oxygen species (ROS) on myocardial antioxidants and on the activity of oxidative mitochondrial enzymes were investigated in the following groups of isolated, perfused rat hearts. I: After stabilization the hearts freeze clamped in liquid nitrogen (n = 7). II: Hearts frozen after stabilization and perfusion for 10 min with xanthine oxidase (XO) (25 U/l) and hypoxanthine (HX) (1 mM) as a ROS-producing system (n = 7). III: Like group II, but recovered for 30 min after perfusion with XO + HX (n = 9). IV: The hearts were perfused and freeze-clamped as in group III, but without XO + HX (n = 7). XO + HX reduced left ventricular developed pressure and coronary flow to approximately 50% of the baseline value. Myocardial content of hydrogen peroxide (H2O2) and malondialdehyde (MDA) increased at the end of XO + HX perfusion, indicating that generation of ROS and lipid peroxidation occurred. Levels of H2O2 and MDA normalized during recovery. Superoxide dismutase, reduced glutathione and alpha-tocopherol were all reduced after ROS-induced injury. ROS did not significantly influence the tissue content of coenzyme Q10 (neither total, oxidized, nor reduced), cytochrome c oxidase, and succinate cytochrome c reductase. The present findings indicate that the reduced contractile function was not correlated to reduced activity of the mitochondrial electron transport chain. ROS depleted the myocardium of antioxidants, leaving the heart more sensitive to the action of oxidative injury.

Myocardial substrate oxidation during warm continuous blood cardioplegia.

BACKGROUND: Although long-chain fatty acids are a major energy substrate utilized by the myocardium, changes in the substrate balance toward a predominating fatty acid utilization could jeopardize the myocardium during cardiac operative procedures. METHODS: In the present study myocardial substrate utilization was examined during warm continuous blood cardioplegia (4 hours, 37 degrees C), using pigs undergoing cardiopulmonary bypass. Hearts were perfused antegradely in a closed extracorporeal circuit in which cardioplegic donor blood (hematocrit, 22%) containing 14C-glucose and 3H-oleate was delivered to the heart. Arterial and coronary sinus blood samples were taken at intervals for determination of plasma concentrations of energy substrates, as well as glucose and oleate oxidation rates (14CO2 and 3HOH production). RESULTS: The concentration of fatty acids in the cardioplegic perfusate did not change significantly during the cardiac arrest period. The mean concentration of glucose showed a 30% decline (not significant), whereas the lactate concentration increased from a starting value of 3.12 +/- 0.27 to 6.31 +/- 0.72 mmol/L at the end (mean +/- standard error of the mean; n = 8; p < 0.05). Only fatty acid levels showed a significant (positive) arterial-coronary sinus difference. Myocardial oxidation of oleate varied between 302 +/- 71 and 650 +/- 66 nmol.min-1.heart-1, whereas the range of variation for glucose oxidation was 144 +/- 64 to 355 +/- 107 nmol.min-1.heart-1. However, the changes in fatty acid levels and glucose oxidation rates during the cardiac arrest period were not statistically significant. We calculated that overall glucose oxidation accounted for less than 5% of the total aerobic energy production. CONCLUSIONS: The present results demonstrate overreliance on fatty acids as a source of energy during warm continuous blood cardioplegia, consistent with a condition of myocardial insulin resistance.

Normotherm continuous blood cardioplegia for 4 hours in an in vivo pig model.

Warm, continuous blood cardioplegia should theoretically maintain cardiac arrest for hours without ischaemic or hypothermic injury. In the absence of in vivo studies of myocardial metabolism and ultrastructural and/or functional preservation during and after more than 2 hours of cardiac arrest and after weaning from bypass, we devised a porcine model with a closed extracorporeal circuit for the heart alone. Normothermic blood cardioplegia was administered antegrade and recirculated for 2 or 4 hours, each in seven pigs. After aortic declamping all were successfully weaned from bypass and reperfused for 1 hour. Thereafter we found no significant intergroup difference in haemodynamic characteristics (average fall in mean arterial pressure 31.7 +/- 3.2% and 26.9 +/- 2.6%) or blood analyses. After 5 and 60 minutes of cardiac arrest there was minimal lactate production (5.7 +/- 10.7 and 0.5 +/- 10.5 nmol/l, respectively), whereas in the remainder of the arrest period there was lactate uptake, indicating aerobic heart metabolism. Our setup avoids systemic hyperkalaemia, gives good cardiac protection with no deterioration between 2 and 4 hours and is well suited for studies on the quiescent, blood-perfused oxygenated heart.

Coronary autoregulation protects against harmful effects of commonly used cardioplegia delivery pressure.

OBJECTIVE: Hearts or parts of hearts are often ischemic prior to infusion of the cardioplegic solution and have a more or less dilated coronary bed. We made an investigation whether coronary dilation just prior to induction of cardiac arrest by aortic clamping and infusion of crystalloid cardioplegic solution would influence cardioprotection. METHODS: Isolated buffer-perfused rat hearts (100 cm H2O pressure (= 73.5 mmHg), 37 degrees C) were used. After a stabilization period the perfusion of 8 rats (group 1) was stopped and the hearts arrested with 5 ml CS (100 cm H2O, 12 degrees C). Equal amounts of cardioplegic solution were then delivered every 20 minutes for the entire 3 1/2 hour hypothermic ischemic period. Following ischemia the hearts were reperfused for 60 minutes. In group 2 (n = 8) 1 ml 10(-2) mmol Papaverine was given into the aortic root just prior to the first cardioplegic solution infusion in order to induce coronary vasodilation. The procedure was identical in the two groups during ischemia and reperfusion. RESULTS: During the ischemic period coronary resistance increased in group 2. During reperfusion group 2 had lower coronary flow (P = 0.001), left ventricle developed pressure (P = 0.002) and a higher creatine kinase release (P = 0.003) than group 1 hearts. Group 2 also had a lower adenosine-triphosphate (6.51 +/- 0.40 mumol.g-1 and 14.03 +/- 0.59 mumol.g-1, respectively, P = 0.011), creatine phosphate (24.70 +/- 1.02 mumol.g-1 and 36.50 +/- 1.31 mumol.g-1, respectively, P = 0.020) and a larger fall in dry/wet-weight ratio (1.7 +/- 0.4 and 0.8 +/- 0.5, respectively, P = 0.043). CONCLUSIONS: Vasodilation (i.e. ischemia) just prior to infusion of crystalloid cardioplegic solution may impair myocardial protection even when the cardioplegic solution is delivered at a relatively low and presumably safe pressure.

Delivery pressure of the cardioplegic solution influences myocardial protection.

To investigate whether cardioplegic solution (CS) delivery pressure influences myocardial protection, intermittent infusions of CS at different pressures were used in an isolated Langendorff rat heart preparation. In group 1 the hearts were kept arrested for 210 min at 12 degrees C with intermittent infusions of 5 ml CS every 20 min at 30 cm H2O (22 mmHg) pressure, in group 2 the same volume of CS was infused at 100 cm H2O (73.5 mmHg) pressure, in group 3 at 145 cm H2O (106.5 mmHg) pressure and in group 4 at 238 cm H2O (175 mmHg) pressure. There was a significantly higher coronary resistance in groups 1 and 4 (7.3 +/- 0.2 RU and 6.9 +/- 0.2 RU) than in groups 2 and 3 (4.2 +/- 0.2 RU and 4.2 +/- 0.2 RU) (P < 0.05) during the ischemic period. There were no significant differences between group 2 and 3 in the reperfusion period. Groups 2 and 3 showed higher coronary flow and left ventricle developed pressure than group 1 and 4. Hearts from group 1 and 4 had lower adenosine triphosphate (7.88 +/- 0.44 mumol.g-1, 5.56 +/- 0.56 mumol.g-1) (P < 0.05) and creatine phosphate (24.66 +/- 0.47 mumol.g-1, 15.34 +/- 0.94 mumol.g-1) (P < 0.05) content at the end of the reperfusion period than group 2 (10.56 +/- 0.41 mumol.g-1, 30.06 +/- 0.38 mumol.g-1) and group 3 (14.13 +/- 0.69 mumol.g-1, 35.25 +/- 0.78 mumol.g-1).(ABSTRACT TRUNCATED AT 250 WORDS)

[Varices of the great saphenous vein]. / Varicer i vena saphena magna.

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.