[Gastric tube insertion without discomfort of the patient].
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Biomedical subjects
Publications and source records attributed to G Nylander.
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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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Colonic tumors were induced in Sprague-Dawley rats by weekly subcutaneous injections of 1,2 Dimethylhydrazine (DMH) for 4 months. The animals were thereafter laparotomized and a palpable tumor was transplanted into the same animal in a tumor-free area of the transverse colon. Autotransplanted tumors were considered those tumors growing in the wall of the transverse colon, covered by intact colonic mucosa. The frequency of autotransplanted tumors was 34%. The possibility that autotransplantation may also occur in humans by accident, during procedures to remove a colorectal adenocarcinoma, is discussed.
Intrinsic hepatic glycogenolysis was examined after hypovolemic stress. Hemorrhagic hypotension of 70 (P70) and 40 mm Hg (P40) for 60 min was inflicted for two postprandial groups and of 70 mm Hg (S70) in a 24-h starved group. The results were compared with three control groups; one postprandial (Pc), one 24-h starved (Sc), and one starved for 9 h (Sc:9) to mimic the glycogen depletion produced by 70 mm Hg hemorrhagic hypotension. Glucose output was studied in vitro using av recirculating isolated liver perfusion system with a perfusate free of glucose and endocrine stimulation. Liver glycogen determination was made before perfusion start. Although the glycogen stores were decreased after hemorrhage glucose yield was increased (P70) and unchanged (P40) as compared to controls (Pc and Sc: 9). Both starved groups delivered small amounts of glucose, but the released fraction of the S70 group was more than twice that from the Sc group. These data suggest a liver enzyme activation with increased velocity of the enzyme-substrate reactions responsible for glycogen degradation, induced during in vivo hemorrhage and persisting for at least 30 min in vitro perfusion.
Cold intolerance is a common problem after injuries to the hand. To elucidate the mechanism of this cold sensitivity, eight patients with successful replantations of amputations of the thumb or index finger were studied one and half years later. In six patients the Doppler signal from the anastomosed arteries was normal and in two patients signs of mild stenosis were found. All patients had normal or slightly reduced basal finger systolic pressure in the replanted finger. Six had signs of marked vasospasm. Alpha-receptor blockade had no effect on the cold-induced decrease in finger systolic pressure in the replanted finger. It is concluded that cold intolerance after hand injuries results from a defect in vasoregulation and is not caused by organic insufficiency of the circulation.
In traumatic injuries to the extremities, with a circulatory insufficiency, the resultant ischemia leads to decreasing levels of the energy-rich compounds adenosine triphosphate (ATP) and phosphocreatine (PCr) and increasing levels of lactate in muscle. A tourniquet model for temporary ischemia was used to determine if hyperbaric oxygen treatment could enhance the cellular metabolic restitution when the circulation was restored. The circulation of the rat hindlimb was interrupted for 1.5 and 3 hours. After 1.5 hours of ischemia, the levels of adenosine triphosphate, phosphocreatine, and lactate were restored to normal in muscle biopsies taken 5 hours after the ischemia. After 3 hours of ischemia, there were marked reductions of adenosine triphosphate and phosphocreatine and elevated lactate values in the postischemic muscle, indicating severe ischemic damage. Hyperbaric oxygen treatment at 2.5 atm for 45 minutes reduced these changes significantly. A certain number of hyperbaric oxygen treatments were necessary to maintain this effect. It is concluded that repeated hyperbaric oxygen treatments in the postischemic phase stimulate aerobic metabolism.
The purpose of the present study was to analyze changes of the myoelectric activity in experimental mechanical obstruction and paralytic ileus of the small intestine. Myoelectric activity was recorded in the upper small intestine of conscious, fasted rats by three bipolar electrodes implanted 10 cm apart. In the basal state regular myoelectric motility complexes (MMCs) were registered in all experimental animals. Obstruction of the small intestine (n = 13) was produced by a ligature between the middle and distal electrodes. Proximal to the obstruction regular MMCs continued. After 45 +/- 15 min at the middle (p less than 0.01), and 85 +/- 10 min at the duodenal electrode (p less than 0.01), MMCs disappeared. Another motility pattern was established, characterized by clusters of spikes, occurring regularly with 2-min intervals, separated by short silent periods, and a rapid aboral migration (p less than 0.01). Distal to the obstruction the propagation of MMCs was immediately disrupted. After a quiescent period of 13 +/- 3 min irregular spiking occurred and continued throughout the experiment (p less than 0.01). Intraperitoneal instillation of 0.1 M hydrochloric acid (n = 8) produced a prompt and long-lasting inhibition of the MMCs. The quiescence lasted for 70 +/- 23 min, until the MMCs reappeared (p less than 0.01). It is concluded that complete intestinal obstruction is followed by a series of significant and well-defined changes of myoelectric activity on both sides of the obstruction. Nociceptive stimulation of the peritoneum produces intestinal paralysis. The immediate inhibition of the motility indicates that the paralysis is not secondary to inflammatory reactions.