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Biomedical subjects

R Berg

Publications and source records attributed to R Berg.

At least 109 records · Page 6Linked to original sources
PubMed1990

Femoral arteriovenous fistula as a complication of percutaneous transluminal coronary angioplasty. A report of five cases.

Arteriovenous fistula (AVF) associated with invasive and diagnostic angiographic procedures is rare. The incidence is increased with procedures such as percutaneous transluminal coronary angioplasty (PTCA) but is still quite low. We report five cases of AVF within a 17-month period, representing 0.15 per cent of all cardiac catheterizations and 0.87 per cent of PTCAs. All five patients presented with groin bruits. There were two associated pseudoaneurysms and one patient with deep vein thrombosis. All patients underwent uneventful division of the fistula. A thorough understanding of the anatomy of the femoral triangle is necessary in order to avoid this complication. That all fistulas were in the superficial or profunda femoris arteries emphasizes the importance of avoiding a low groin puncture. Early angiography and surgical intervention are recommended for optimal results.

Aged↗
PubMed1989

Medical and surgical management of early Q wave myocardial infarction. I. Effects of surgical reperfusion on survival, recurrent myocardial infarction, sudden death and functional class at 10 or more years of follow-up.

To define the outcome of patients given medical or surgical therapy for Q wave myocardial infarction, 387 patients were followed up for 10 to 13 years (mean 11.4). On study entry the groups had similar distributions for variables such as mean age, gender, previous myocardial infarction, abnormal creatine kinase activity, area of infarction, number of vessels diseased and clinical classification. The hospital mortality rate of the medical versus surgical group was 11.5% (23 of 200) versus 5.8% (11 of 187) (p = 0.07). Early reperfusion (that is, less than or equal to 6 h) resulted in a lower mortality rate than did medical therapy--2% (2 of 100) versus 11.5% (23 of 200) (p less than 0.05)--whereas the hospital mortality rate with late reperfusion was 10.3% (9 of 87). The long-term mortality rate of the medical and surgical groups was 41% (82 of 200) versus 27% (51 of 187) (p = 0.0007) with use of an adjusted Cox proportional hazards model. In the survivors, the differences between medical and surgical groups in recurrent myocardial infarction, mortality associated with reinfarction and sudden death were prospectively followed and evaluated by the life table method. Recurrent myocardial infarction was not prevented by surgical reperfusion or medical therapy (23% in both groups), however, the mortality rate in patients with recurrent infarction was higher in the medical therapy group--36.6% (15 of 41) versus 17.5% (7 of 40) (p = 0.04). The mortality difference did not depend on early or late surgical reperfusion. In the in-hospital survivors, the incidence of sudden death was 17.5% in the medical (31 of 177) versus 7.4% (13 of 176) in the surgical group (p = 0.01). This difference was much more pronounced in the early reperfusion group. Functional class was significantly lower than that for medical therapy in the early reperfusion but not the late reperfusion group. Thus, in comparable groups given medical and surgical therapy for acute myocardial infarction and followed up for greater than or equal to 10 years, surgical reperfusion appears to offer improved longevity in selected cases (when implemented early) but does not prevent recurrent myocardial infarction. The associated mortality with recurrent myocardial infarction is less as is the incidence of sudden death. Finally, lower functional class occurs most often in patients given early reperfusion.

Acute Disease↗
PubMed1989

Medical and surgical management of early Q wave myocardial infarction. II. Effects on mortality and global and regional left ventricular function at 10 or more years of follow-up.

To determine the long-term effect of surgical reperfusion on survival and left ventricular function of patients with anterior and inferior Q wave myocardial infarction, 387 patients were followed up for greater than or equal to 10 years after early Q wave infarction. In the anterior infarction group, 102 received conventional therapy and 101 underwent surgical reperfusion. The overall hospital mortality rate in the medically and surgically treated patients was different (16.7% [17 of 102] versus 6.9% [7 of 101], p less than 0.05). The cumulative 13 year actuarial mortality rate widened between the anterior medical and surgical groups (54% versus 31%, p = 0.0003) by the adjusted Cox proportional hazards model. The hospital mortality rate with early reperfusion (that is, less than or equal to 6 h of symptom onset) was 2% (1 of 51), whereas the mortality rate with late reperfusion was 12% (6 of 50). The 13 year actuarial cumulative mortality rate was significantly lower in both the early and late reperfusion groups (30% and 33%, respectively) than in the conventional therapy group (54%, p = 0.0006). The mortality rate in patients receiving surgery after surviving initial medical therapy was 50% (15 of 30). In the survivors of anterior Q wave myocardial infarction, improved global ejection fraction was seen in the patients undergoing early (54 +/- 13%) and late (50 +/- 10%) surgery relative to those receiving conventional therapy (43 +/- 11%, p less than 0.05). Only the early reperfusion group had better regional function of the anterior wall than that of the conventional therapy group. Thus, ventricular function correlated with improved long-term survival. In the patients with inferior Q wave myocardial infarction, the overall hospital mortality rate in the medical and surgical groups was not different (6.1% [6 of 98] versus 4.6% [6 of 86], p = NS). Likewise, the 13 year actuarial cumulative mortality rate was not different between the medical and surgical groups overall (32% versus 30%, p = 0.29) by the adjusted Cox proportional hazards model. The hospital mortality rate in the early reperfusion group was lower than that in the late reperfusion group (2.0% [1 of 49] versus 8.1% [3 of 37], p = NS). The 13 year actuarial cumulative mortality rate was lower in the early surgical group compared with that in the medical group (19% versus 32%, p = 0.04). The late surgical group had a similar 13 year actuarial cumulative mortality rate to that of the medical group (47% versus 32%, respectively, p = 0.47).(ABSTRACT TRUNCATED AT 400 WORDS)

Cardiac Catheterization↗
PubMed1989

[The applicable merit of untreated, HCl-treated and partly-hydrolysed straw meal in the feeding regimen of piglets after early weaning. 4. Histological findings in the digestive epithelium of the piglet].

In studies with piglets of the country race the applicability of variously treated straw materials was tested in comparison with conventional concentrate feeding (I) after an early weaning date (30th-35th day of life) over an 8-week period (1st-8th week of keeping). In the rations containing 10% straw (straw-concentrate mixtures), untreated (II), HCl treated (III: HCl treatment without steaming) and partly hydrolyzed straw meal (IV: HCl treatment with subsequent steaming) were used in the feeding. Samples were taken of 4 killed animals each in the 2nd and 8th weeks of keeping for the qualitative histologic assessment of palatum durum, oesophagus and stomach, duodenum and caecum, colon ascendens, colon descendens and rectum. Although significantly lower pH values in the stomach were registered after the feeding of feed mixtures III and IV due to increased acidity (pH value decrease by 1.3 to 1.5 units) in comparison to the values in I and II, the lamina epithelialis of the palatum durum remained intact in all groups and without any signs of cauterization. Equally, considerable changes in the comparison of the feeding groups could not be detected in the structures of the oesophagus and the stomach walls or in the qualitative histologic assessment of the duodenum and the caecum. However, there were clearly distinguishable group specifics with regard to the formation of lymphoreticular tissue in the stomach and for the colon ascendens.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed1989

Endotoxin induces bacterial translocation and increases xanthine oxidase activity.

Previously, we documented that endotoxin induces bacterial translocation from the gut and that inhibition or inactivation of xanthine oxidase activity reduces endotoxin-induced bacterial translocation. Consequently, experiments were performed to correlate endotoxin-induced bacterial translocation with changes in intestinal mucosal structure and xanthine dehydrogenase and oxidase activity. Segments of the jejunum, ileum, cecum, proximal colon, distal colon, and liver were harvested from ICR mice 24 hr after IP administration of E. coli 0111:B4 endotoxin (0.1 mg). Xanthine dehydrogenase and oxidase activities were measured in these samples and correlated with intestinal morphology. Bacteria translocated from the intestines to extraintestinal organs in 70% of the mice receiving endotoxin, while the organs of control mice were sterile (p less than 0.01). Endotoxin injured primarily the ileal and cecal mucosa and increased ileal and hepatic xanthine dehydrogenase and cecal oxidase activities (p less than 0.05). These results suggest that xanthine oxidase-induced mucosal damage plays a role in endotoxin-induced bacterial translocation.

Animals↗
PubMed1989

Nutritional status of patients with different levels of chronic renal insufficiency. Modification of Diet in Renal Disease (MDRD) Study Group.

This study evaluated the nutritional status of 95 patients with chronic renal insufficiency who participated in the feasibility phase of the NIH funded Modification of Diet in Renal Disease (MDRD) Study. All patients were seen monthly by a physician and dietitian. After a baseline period, the patients were randomly assigned either to a mildly protein-restricted control diet or to one of three low protein, low phosphorus diets. Patients with clear evidence for protein-calorie malnutrition were excluded from the study. Patients were followed for an average of 12.4 months (range, 0 to 22 months). The glomerular filtration rate (GFR) at the commencement of the experimental diets ranged from 8 to 56 ml/min/1.73 m2. Assessment of the nutritional parameters indicated that none of the four diet treatment groups developed protein-calorie malnutrition. At the end of treatment with the experimental diets, most nutritional parameters were normal and few had worsened. Nonetheless, the following observations indicated that some patients had developed subtle evidence for protein-calorie malnutrition. There were positive correlations between the GFR and the serum transferrin and creatinine:height ratio. In men, arm muscle area and, at the onset of the experimental diets, the % standard body weight also correlated with the GFR. In women, GFR correlated with dietary energy intake. When patients were grouped according to their GFR level, those with the lowest GFR also tended to have lower energy intakes, serum transferrin levels and creatinine:height ratios. Patients with a GFR of 24 ml/min/1.73 m2 or lower tended to lose body mass during the study. In all groups of patients, the estimated actual energy intake was significantly lower than the prescribed intake. On the other hand, in the patients assigned to one of the three low protein, low phosphorus diets, nitrogen intake was above the prescribed level. The low energy intake of those patients with the lower GFR levels may contribute to their propensity to become malnourished.

Body Weight↗
PubMed1989

Endotoxin-induced bacterial translocation: a study of mechanisms.

Previously, we documented that nonlethal doses of endotoxin cause the translocation (escape) of bacteria from the gut to systemic organs. The purpose of this study was to determine which portion(s) of the endotoxin molecule induces bacterial translocation and to examine the role of xanthine oxidase activity in the pathogenesis of endotoxin-induced bacterial translocation. Nonlethal doses of Salmonella endotoxin preparations (wild type, Ra, or Rb), containing the terminal portion of the core polysaccharide, induced bacterial translocation, whereas those preparations lacking the terminal-3 sugars (Rc, Rd, Re, or lipid A) did not induce bacterial translocation. Additionally, only those endotoxin preparations that induced bacterial translocation injured the gut mucosa, increased ileal xanthine dehydrogenase and oxidase activity, and disrupted the normal ecology of the gut flora, resulting in overgrowth with enteric bacilli. Inhibition of xanthine oxidase activity by allopurinol prevented endotoxin (Ra)-induced mucosal injury and reduced the incidence of bacterial translocation from 83% to 30% (p less than 0.01). These results suggest that endotoxin-induced bacterial translocation requires the presence of the terminal core lipopolysaccharide moiety and that xanthine oxidase-generated oxidants are important in the pathogenesis of endotoxin-induced mucosal injury and bacterial translocation.

Animals↗
PubMed1988

Hemorrhagic shock-induced bacterial translocation is reduced by xanthine oxidase inhibition or inactivation.

Experiments were performed to determine whether bacterial translocation (BT) after hemorrhagic shock is due to a reperfusion injury mediated by xanthine oxidase-derived oxidants. Rats were subjected to 30 minutes of shock (30 mm Hg) followed by reinfusion of shed blood. Twenty-four hours after hemorrhage and reinfusion, the mesenteric lymph node, liver, and spleen were harvested from each animal for bacterial culture, and the ileum and cecum were examined histologically. Sham-shocked (control) rats were instrumented, but blood was not withdrawn. The incidence of BT was higher in the shocked rats (61%) than in the sham-shocked animals (7%) (p less than 0.01). Allopurinol (50 mg/kg, administered orally), a competitive inhibitor of xanthine oxidase, reduced the incidence of shock-induced BT to 14% (p = 0.02). Similarly, rats fed a tungsten-supplemented molybdenum-free diet, which inactivates xanthine oxidase, reduced shock-induced BT to 10% (p = 0.02). The histologic damage cause by hemorrhagic shock was prevented by blocking xanthine oxidase activity. Thus hemorrhagic shock-induced bacterial translocation from the gut appears to be mediated by oxidants generated by activation of the xanthine oxidase system.

Allopurinol↗
PubMed1987

Endotoxin promotes the translocation of bacteria from the gut.

Experiments were performed in mice to determine whether endotoxin could cause bacteria normally colonizing the gut to spread systemically, a process termed bacterial translocation. Endotoxin given intraperitoneally promoted bacterial translocation in a dose-dependent fashion from the gut to the mesenteric lymph node (MLN). The incidence of bacterial translocation to the MLN was similar whether the endotoxin was administered intramuscularly or intraperitoneally, although the number of bacteria colonizing the MLN was greater with intraperitoneal endotoxin. The incidence and magnitude of endotoxin-induced bacterial translocation were similar between CD-1 and C3H/HeJ (endotoxin-resistant) mice, indicating that bacterial translocation is not prevented by genetic resistance to endotoxin. Thus, it appears that the gut may serve as a reservoir for bacteria causing systemic infections during endotoxemia.

Animals↗
PubMed1987

Effect of starvation, malnutrition, and trauma on the gastrointestinal tract flora and bacterial translocation.

We have previously shown, in an animal model, that viable indigenous bacteria will cross the intact gastrointestinal (GI) mucosa and spread systemically, a process termed bacterial translocation, if the normal bacterial ecology of the gut was sufficiently disrupted to allow bacterial overgrowth or if the animals were severely immunosuppressed. Starvation or protein malnutrition disrupts the normal indigenous GI tract microflora and impairs host antibacterial defenses. Consequently, we tested the effect of the combination of starvation or protein malnutrition plus burn trauma in promoting bacterial translocation from the GI tract. Bacterial translocation was measured by quantitatively culturing the mesenteric lymph nodes, spleens, livers, blood, and peritoneal cavities of normal or burned (30% of total body surface area) CD1 mice deprived of food for three days or fed a low-protein (0.03%) diet. The effect of starvation or protein malnutrition on the gut microflora was determined by quantitatively measuring the levels of bacteria present in the ceca. Both starvation and protein malnutrition increased the cecal levels of gram-negative enteric bacilli and decreased the levels of lactobacilli and strict anaerobes. Surprisingly, neither starvation nor protein malnutrition promoted bacterial translocation, even though these animals lost over 20% of their body weight and the ecology of the gut microflora was disrupted. In fact, the protein-malnourished animals exhibited lower incidences of bacterial translocation than normally nourished animals when both groups were monoassociated with Escherichia coli C-25 or monoassociated and burned. Thus, it appears that protein malnutrition does not promote bacterial translocation, even when combined with burn trauma.

Animals↗
PubMed1987

Characterization of synaptosomal dopamine uptake in post-mortem brain regions of schizophrenics.

The drug sensitivity of synaptosomal high-affinity dopamine (DA) uptake was investigated in post-mortem brain regions of schizophrenics, in comparison to controls matched for age, sex, and post-mortem delay, and in model experiments in rats. DA uptake was inhibited by nomifensine in the investigated regions of rat brain in a concentration-dependent manner; the regional rank order of inhibitory potency was: nucleus (n) caudatus greater than n. accumbens greater than frontal cortex. Furthermore, it was shown that the inhibitory potency of nomifensine is unchanged after in situ storage of rat brain tissue for 48 h and after the cryopreservation method used. In post-mortem brain of human controls, nomifensine inhibited DA uptake with the same regional differences as in rats; however, the inhibitory potencies were three-fourfold weaker. In schizophrenia, on the other hand, synaptosomal DA uptake inhibition by nomifensine was significantly weaker than in the corresponding control brains for all regions studied. This suggests a decreased affinity of the DA uptake carrier to nomifensine, similar to DA shown in recent studies with schizophrenic patients. The possible relevance of investigating functional parameters for understanding patho-biochemical mechanisms in schizophrenia is discussed.

Animals↗