[A survey in Malmö. The frequency of venous thromboembolism has not changed during the last 30 years].
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Biomedical subjects
Publications and source records attributed to G Nylander.
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Conclusions reached at an expert meeting arranged by the Medical Products Agency (Läkemedelsverket) in Sweden on the treatment of gynaecological bleeding disorders are presented. An active approach to endometrial diagnosis is recommended when bleeding is protracted and does not respond to medication, and when bleeding occurs more than one year after menopause. A period of expectation is permissible in women younger than 45 years. Exfoliative endometrial diagnosis is highly sensitive and specific and, in recent years, the traditional curettage has been reappraised as the first method of choice. Bleeding during anovulatory cycles is usually managed by treatment with progestagens. Menorrhagia may be diminished by oral contraception, tranexamic acid or NSAID. Endometrial resection offers a promising alternative to hysterectomy. Genital infection is another common cause of irregular bleeding in sexually active women and must be treated before invasive procedures are undertaken. Abnormal bleeding in patients with endometriosis often improves as a result of the treatment given to alleviate other symptoms such as pain. Bleeding irregularities caused by gynaecological malignancy, particularly contact bleeding in cancer of the cervix, are seen during the reproductive years and are accessible for diagnosis. The authors also discuss irregular bleeding caused by coagulopathia or treatment with hormones, as well as the effect of antifibrinolytic drugs.
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Urine from 32 road tanker drivers handling petrol, diesel, paraffin and white spirit was tested in the Salmonella/microsome mutagenicity system using tester strains TA98 anbd TA100. Urine samples were collected before and after tanking and were concentrated 250-fold on XAD-2 columns before testing. Controls were 33 office employees from the same plant. No effect on urinary mutagenicity of occupational exposure to petroleum products was found. Significant differences in mutagenic effect were demonstrated between smokers and non-smokers. Methodological experiments demonstrated a dose/response effect of smoking on urinary mutagenicity. A modified test using a preincubation period and an increased concentration of bacteria was more sensitive than the standard Ames test to mutagens from tobacco smoking.
Feeding routines in the maternity ward were investigated in 204 mother-infant pairs before and in 203 after a change towards earlier, more frequent breastfeeding and elimination of routine substitute feeds. In the intervention group, the volume of breast-milk increased, while the use of formula and sugar solution decreased correspondingly. The infants in the intervention group lost more weight during the first 2-3 days (6.4% versus 4.6%), but regained their birth weight faster than the supplemented control group. The incidence of hyperbilirubinemia was not significantly different in the two groups. No cases of hypoglycemia were diagnosed. At 6 months, 87% of the infants in the intervention group were still fed at the breast, compared with 66% in the control group. The weight curves were comparable up to 9 months, when intervention group infants were found to weigh slightly less. These follow-up results must be interpreted with some caution due to the low but comparable response rate of the two groups. Thus the intervention study demonstrated that healthy, full-term infants usually have no need for supplements to their mothers' milk provided they have had a satisfactory start in life with early and frequent feeds at the breast. The follow-up study indicated that a more "physiological" start of breastfeeding may have had a positive long term effect on the overall duration of the lactational period.
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In the present study we have evaluated the activity of myeloperoxidase (MPO) in ischemic reperfused skeletal muscle of rats, as an index of polymorphonuclear leukocyte (PMNL) accumulation and its time course. A tourniquet model for temporary ischemia was used, in which one hindleg was made ischemic for 1.5, 3 or 5 hours. Muscle biopsies were taken after 12 hours reperfusion from both the injured and the uninjured legs. Controls received anesthesia only. No increase in the MPO levels was observed after 1.5 hours of ischemia followed by 12 hours of reperfusion. With the same reperfusion time and 3 or 5 hours of ischemia, there was a five-fold increase in MPO activity. Prolonging the ischemia from 3 to 5 hours did not cause any further significant MPO increase. With 3 hours of ischemia, biopsies were also taken after 0, 1, 5, 24 and 74 hours reperfusion. The results showed a time dependent increase in MPO activity. A significant increase was first seen after 5 hours reperfusion with the peak at 24 hours. After 74 hours of reperfusion the MPO activity had almost returned to control levels. The uninjured leg had MPO levels similar to those in the control. However, there was a small reduction at 5 and 12 hours of reperfusion. During the ischemic period before reperfusion, the ischemic leg showed a significant decrease in MPO activity. Severe ischemia in skeletal muscle results in a time dependent accumulation of PMNLs during reperfusion, as measured by the changes in MPO activity in the tissue.
The relationship between blood flow (xenon washout method), edema formation (percent total water content), and the number of polymorphonuclear leukocytes (PMNLs), as measured by the level of the enzyme myeloperoxidase, has been investigated in post-ischemic skeletal muscle of rats. A tourniquet model of temporary, complete ischemia of one hindlimb for 3 or 4 hours was used. Biopsies were taken after 0.5, 5 and 12 hours of reperfusion (6 experimental groups) and from a control group that had received only anesthesia. After 4 hours, but not 3 hours of ischemia there was a restricted blood flow during the early reperfusion phase, the "no-reflow" phenomenon, indicating severe ischemia. There was no significant accumulation of PMNLs in the skeletal muscle nor was there a correlation between the number of PMNLs in the post-ischemic muscle and the restricted bloodflow. With 4 hours of ischemia and 0.5 hours of reperfusion there was a statistically significant, positive correlation between the number of PMNLs and the amount of edema; no such correlation was evident in either of the other groups. These results suggest that PMNLs are not the major cause of reduced bloodflow or of edema in the early reperfusion phase after total ischemia.
A study of 885 women who had given birth in Oslo, Norway in 1985 disclosed that 80% were still breastfeeding three months after delivery. Forty percent of the mothers smoked cigarettes daily. Only 7% had stopped smoking because of pregnancy or lactation. High social class and educational level was positively correlated to prolonged breastfeeding. Smoking was negatively correlated to breastfeeding when the infant was three and four months old. While 93% of non-smokers with an education of 17 or more years still breastfed four months after delivery, this was true of only 6% of heavy smokers with an education of nine years or less. Also within each social group and educational level the prevalence of breastfeeding was lower among the smokers, with a dose/response effect of the number of cigarettes smoked. More smokers than non-smokers stopped breastfeeding because they had "too little milk". Forty percent of infants breastfed by smokers suffered from colic or excessive crying, as compared with 26% of the children of non-smokers.
A free flap transfer in a case of Adriamycin necrosis on the dorsum of the hand is reported. The advantages of this method of reconstruction are discussed.
A new mechanical anastomotic device--the UNILINK system--for small vessels, designed for work under the operating microscope was used in four patients for microvascular, hand surgical operations. All procedures were successful with regard to tissue survival and wound healing. Basal skin temperature and systolic blood pressure distal to the mechanical anastomoses were normal 12 to 26 months after the operation. Doppler investigation also confirmed that all mechanical anastomoses were patent. At the time of this report, 32 to 45 months after the operations, no adverse effects of the method have been found. The device offers increased safety and speed in microvascular operations.
Earlier studies from our laboratory have shown that hyperbaric oxygen (HBO) treatment reduces edema, enhances aerobic metabolism and improves the recovery of the phosphorylase activity in postischemic rat skeletal muscle. However, as it has become increasingly apparent that oxygen in excess may have harmful effects, it was of interest to study if HBO caused an increased formation of oxygen free radicals. Toxic peroxides, as a result of oxygen free radicals, were quantitated in the postischemic skeletal muscle of rat and with HBO treatment by measuring the thiobarbituric acid reaction which includes the lipid peroxides and the alkydes including malondialdehyde (MDA), a key intermediate in the formation of peroxides. A tourniquet model of temporary ischemia of the rat hindlimb was used for 3 hours. Muscle biopsies were taken at various intervals before and after tourniquet release with and without hyperbaric oxygen at 2.5 atmospheres absolute (ATA) for 45 min after tourniquet release. Three hours of anesthesia caused a significant rise of thiobarbituric acid reactive material (TBAR) concentration in muscle compared to normal controls without anesthesia. An increase of similar magnitude was seen after 3 hours of ischemia, with or without reperfusion. These values were normalized after 45 min. HBO in the postischemic phase did not cause a further increase in the TBAR concentration in muscle immediately postischemically. However, the levels remained increased at 45 min after the onset of reperfusion, immediately after HBO treatment and had returned to normal values 2 hours postischemically.(ABSTRACT TRUNCATED AT 250 WORDS)
Haemorrhagic hyperglycemia has been demonstrated to have beneficial effects on fluid homeostasis, and insulin resistance has been reported in vitro after haemorrhage. In the present study the interrelation of peripheral levels of insulin, glucagon, and adrenalin and the rate of glucose disappearance (Rd) in haemorrhagic hyperglycemia were determined in vivo. Rd was determined by single injection of 3-3H-glucose in three groups of postprandial rats: controls, rats submitted to rapid blood loss, and rats receiving a constant 30% glucose infusion. The level of hyperglycemia after bleeding was 22.9 +/- 1.9 mmol x 1(-1) (mean +/- 1 S.E.), and during infusion it was 20.4 +/- 1.4 mmol x 1(-1). The Rd value of controls was 8.2 +/- 0.5 mmol x 100 g-1 x min-1, during glucose infusion it was 34.1 +/- 0.6, and after haemorrhage it was 9.7 +/- 0.4. Both treatments increased insulin levels by greater than 200%. These results show an important role of insulin resistance in causing hyperglycemia after experimental haemorrhage in the rat.
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Glycogen and lactate metabolism was studied in livers from three groups of postprandial rats sustaining 70 mm Hg hemorrhagic hypotension for variable periods, 60 min (60H group), 120 min (120H group), and nonbled controls. The donor livers were investigated after completed hemorrhage using an in vitro perfusion system with L-lactate as substrate, together with U-C14-lactate. The residual glycogen stores were determined after perfusions. The incorporation of labelled lactate to glucose was increased in the 120H group by 66.7% and 116.8% compared to the 60H group and controls (p less than 0.01), but glycogenolysis was still the main source of glucose released in the 120H group. Glycogen formation from labelled lactate was 46.6% higher in the 120H group compared to controls (p less than 0.05) and lactate oxidation was decreased by 67.5% (p less than 0.05). The data suggest that hepatocytes are capable of rapid change from glycolysis to gluconeogenesis during hemorrhagic hypovolemia. However, energy-sparing glycogen breakdown is given priority over gluconeogenesis as long as glycogen remains available.
In chronic gastric fistula (GF) rats, hyperosmolal 0.20 M HCl infused into a duodenal loop anastomosed to the jejunum (Roux-en-Y) produced a greater inhibition of the maximal acid response to pentagastrin than HCl or 1200 mosmol kg-1 solution of polyethylene glycol (PEG) alone, suggesting that HCl and hyperosmolal solution inhibit secretion by different mechanisms. In the present study on chronic GF rats with Thirty-Vella loops of the proximal or distal duodenum (bile and pancreatic ducts transplanted to the jejunum), perfusion of the proximal or distal loop with 0.20 M HCl significantly inhibited the maximal acid response to pentagastrin, but perfusion with hyperosmolal PEG solution did not alter the response. The results suggest different anatomical sites for the inhibitory mechanisms, sensitive to acid and hyperosmolal solution.
In the post-ischemic muscle, hyperbaric oxygen (HBO) treatments have been shown to reduce post-ischemic edema and enhance aerobic metabolism. In the present paper histological, histochemical and ultrastructural methods were used to study the influences of HBO treatment on the morphology of post-ischemic skeletal muscle. The changes were also quantified using morphometry. The circulation of the rat hindlimb was interrupted for 3 hours and muscle biopsies were taken 5 and 12 hours post-ischemia. Light microscopy showed signs of ischemic changes in the muscle. Morphometrically, the area with activity of the muscle enzyme phosphorylase was greatly reduced post-ischemia. HBO treatment at 2.5 atmospheres of absolute pressure (ATA) for 45 min significantly increased muscle cross sectional area with a positive phosphorylase reaction 5 hours post-ischemia. Three HBO treatments were necessary to maintain this effect, 12 hours post-ischemia. Ultrastructurally, the ischemic changes seen using light microscopy were confirmed. Morphometrically, there was a significant increase of mitochondrial size in the ischemic muscle compared with the control uninjured muscle but HBO did not markedly reduce these ultrastructural changes. It was concluded that the reduction of phosphorylase activity, a sensitive marker for muscle cell damage, is to a great extent prevented by HBO treatment in the post-ischemic phase.
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