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Biomedical subjects

U Haglund

Publications and source records attributed to U Haglund.

At least 73 records · Page 4Linked to original sources
PubMed1990

Stress ulcers.

Gastric stress ulceration occurs rapidly in patients after severe trauma. However, bleeding from stress ulceration is a rare but very serious complication after trauma and major surgery. Important risk factors for stress ulcer bleeding are shock, especially septic shock, and the development of other components of the multiple system organ failure syndrome. The pathophysiology and treatment of stress ulceration is reviewed in this paper. Prophylaxis is the best form of treatment, and the most effective prophylaxis is optimal resuscitation and intensive care. In addition, pharmacologic prophylaxis, including antacids, sucralfate, or acid secretory inhibitors, has been advocated. Once profuse bleeding has started, measures other than aggressive treatment of shock and sepsis are usually unsuccessful.

Anti-Ulcer Agents↗
PubMed1990

Feline E. coli bacteremia--effects of misoprostol/scavengers or methylprednisolone on hemodynamic reactions and gastrointestinal mucosal injury.

Live E. coli were infused i.v. in cats to induce gastrointestinal mucosal injury and the gastric mucosa was exposed to bile and a luminal pH of 1. A gastric lesion index was calculated and intestinal injury was graded. The effects of i.v. methylprednisolone before and after induction of bacteremia were compared with those of intragastric misoprostol combined with i.v. superoxide dismutase (SOD) and catalase and with a control group. Methylprednisolone, but not misoprostol/SOD/catalase, significantly reduced the gastric lesion index (p less than 0.05). The duodenum/small intestine was significantly injured in 4/6, 2/6 and 4/6 cats in the misoprostol/SOD/catalase, methylprednisolone and control groups, respectively (NS). End gastric luminal pH was 3.9, 2.7 and 4.5 in the respective groups (p less than 0.05), with systemic arterial pH 7.15, 7.15 and 7.32 (NS). Mean arterial pressure and cardiac output were improved with methylprednisolone. Misoprostol/SOD/catalase reduced late hypotension. Pulmonary arterial pressure rose to c. 200% of basal in all groups. Methylprednisolone, but not misoprostol/SOD/catalase, thus protected the gastric mucosa from sepsis-induced gastric injury concomitant with reduced disappearance of protons from the gastric lumen, but did not significantly affect small-bowel damage. Hemodynamic responses were significantly improved in methylprednisolone-pretreated cats.

Acid-Base Equilibrium↗
PubMed1990

Tension leads to increased neutrophil accumulation and decreased laparotomy wound strength.

Wound margin strength was measured immediately after and at 72 hours after median laparotomy in rats. The laparotomy wound was sutured with or without tension, and wound margin strength was measured as breaking strength with the sutures in situ. In wounds sutured without tension, no decrease in breaking strength was observed at 72 hours; in rats sutured with tension, breaking strength decreased by 77%, and in almost half of the animals the sutures cut through. There was markedly increased accumulation of neutrophil leukocytes around the sutures in the tension group, as indicated by increased tissue myeloperoxidase activity. The decrease in breaking strength was abolished by treatment with an inhibitor of the collagen-degrading proteinases of the neutrophils (the soybean trypsin inhibitor). Although the decrease in breaking strength should be due to collagenolysis, there were no changes in collagen content or solubility around the sutures, indicating that the changes in collagen were too delicate to be revealed by the methods used. We conclude that the decrease in breaking strength was caused by the neutrophils.

Abdominal Muscles↗
PubMed1990

The sequence of development of intestinal tissue injury after strangulation ischemia and reperfusion.

Tissue injury at reperfusion has been reported after partial ischemia. However, previous attempts to demonstrate a component of injury caused by reperfusion after total ischemia have failed. This study was performed to evaluate the hypothesis that in such situations the extent of the tissue injury caused by ischemia itself prevented detection of a reperfusion component. Rats were subjected to near-total intestinal ischemia by means of a hydrostatic pressure clamp that produced preferential venous occlusion (strangulation) for periods from 1 to 90 minutes. Tissue injury was evaluated microscopically by a blinded examiner. Ischemic periods of 20 minutes or less did not induce detectable tissue injury. Longer durations of ischemia caused villous injury: the longer the period of ischemia, the more extensive the tissue injury. However, there was no exacerbation of injury seen after reperfusion, regardless of the duration of ischemia. In a separate series of rats, total arterial occlusion was employed without concomitant venous congestion. Such isolation arterial occlusion of 40 to 60 minutes' duration was followed by a statistically significant exacerbation of tissue injury at reperfusion. Thus total intestinal ischemia may be followed by reperfusion injury if there is no concomitant congestion and if ischemic injury is not too extensive.

Animals↗
PubMed1990

Role of the renin-angiotensin system in liver blood flow reduction produced by positive end-expiratory pressure ventilation.

Positive end-expiratory pressure (PEEP), often used in critically ill patients, reduces cardiac output, and its adverse effects on splanchnic circulation imply a risk of regional secondary organ failure. To investigate if the renin-angiotensin system (RAS) mediates PEEP-induced circulatory changes, hemodynamic effects of PEEP were measured in four groups of pigs: controls (C), nephrectomized (N), or given enalaprilate, an angiotensin-converting enzyme inhibitor (E), or saralasin, a competitive inhibitor of angiotensin II (S). Groups N, E and S represented interference with RAS effects at different sites. With PEEP at 10 cmH2O, mean arterial pressure, cardiac index, portal venous and hepatic arterial blood flow decreased in all groups, while portal and central venous pressures rose, without significant intergroup difference. Systemic and preportal bloodflow resistance increased in groups S and N, and hepatic arterial resistance in group C. Accentuation of the flow and pressure changes occurred with 20 cm PEEP in all groups, with increase of systemic and hepatic resistance in S and N, or preportal resistance in group N and protal resistance in group C. The study suggested that RAS is not a major mediator of PEEP-induced circulatory changes. Differing responses within groups N, S and E may have been due to interference with the action of RAS and of other vasoactive substances.

Animals↗
PubMed1990

Lack of beneficial effects of milrinone in severe septic shock.

The effects of milrinone were investigated in a porcine septic shock model. Septic shock was induced by i.v. infusion of live Escherichia coli. Anesthetized pigs were treated with milrinone before the E. coli infusion or were left untreated as septic controls. E. coli caused a significant reduction of cardiac index, renal blood flow, and portal blood flow. Pulmonary vascular resistance was significantly increased, as were the systemic and preportal vascular resistances. One of the seven septic control pigs died. In milrinone-treated septic animals cardiac index was maintained for a longer period of time but blood pressure was significantly reduced compared with the control pigs. Pulmonary vasoconstriction was little affected by pre-treatment with milrinone. Four out of seven milrinone-treated pigs died during the observation period. It is concluded that in the settings of the used porcine septic shock model milrinone treatment has no beneficial effect.

Animals↗
PubMed1990

Early detection of gastrointestinal mucosal ischemia in porcine E. coli sepsis.

The aim of this study was to investigate the oxygenation of the gastrointestinal tract mucosa using indirect pH measurements in a porcine septic model (intravenous infusion of live E. coli). By means of intraluminally placed balloon catheters (Tonomitior) permeable to CO2, intramucosal pH (pHi) was calculated using the Henderson-Hasselbalch equation. Cardiopulmonary hemodynamics and portal blood flow were measured using Swan-Ganz catheters. Samples were taken from the gastrointestinal tract for histological examination. Nine pigs were given i.v. E. coli infusion while six pigs served as sham controls and were given an equivalent amount of Ringer's solution only. All septic animals developed hemodynamic signs of septic shock. Gastric, small intestinal and sigmoid colonic pHi decreased gradually during the four hour observation period. In the small intestine and the sigmoid colon the decrease was significant already after one hour (p less than 0.01 and p less than 0.02, respectively). Microscopic examination of tissue specimens obtained 4 hours following induction of sepsis revealed normal or close to normal findings in all the sham and in more than half of the septic animals. These findings indicate that abnormally low gastrointestinal intramucosal pH may be found early in septicemia, preceding microscopically detectable damage by several hours. It is concluded that the tonometer technique does provide early detection of gastrointestinal ischemia in septic shock.

Animals↗
PubMed1989

Thromboxane A2-receptor blockade and prostacyclin in porcine Escherichia coli shock.

Septic shock was induced by intravenous infusion of live Escherichia coli in pigs to investigate the influences on central hemodynamic, coagulation, and fibrinolytic reactions by a thromboxane A2 (TxA2)-receptor blocker (BM 13.177; n = 6) and a prostacyclin analogue (iloprost or ZK 36,374; n = 7). The early pulmonary vasoconstriction following E coli infusion was attenuated, but not abolished, by BM 13.177. Only minor effects were seen after pretreatment with iloprost. Neither drug had any major effect on the coagulation and fibrinolytic activation. These results confirm that TxA2 is an important, but not the only, mediator of early pulmonary vascular response in porcine septicemia and that neither TxA2 nor prostacyclin is of major importance for the hemostatic reactions in this shock model.

Animals↗
PubMed1989

Esophageal and jejunal motor function after total gastrectomy and Roux-Y esophagojejunostomy.

Emptying and peristaltic activity of the esophagus and proximal jejunum were studied using scintigraphy and fluoroscopy documented on videotape in 11 patients after total gastrectomy and Roux-Y loop reconstruction. Impaired esophageal motor function, as judged by both methods, was seen in five patients who were all 50 years of age or older. This was in contrast to the findings in a group of healthy control subjects, all over 50 years of age, in whom esophageal function appeared normal on scintigraphy in five of seven. Disturbed jejunal function, as judged by radiography, was found in eight patients, whereas the emptying rate according to scintigraphy was judged normal in all but two patients. Five of the patients complained of various adverse alimentary tract symptoms, but the scintigraphic and radiographic findings did not correlate with these symptoms.

Adult↗
PubMed1989

Influence of prostanoids on gastrointestinal mucosal injury in experimental septic shock.

Capillary stasis and mucosal injury in the stomach and small intestine were studied in septic shocked pigs. Septicemia was induced by live E. coli i.v. in 28 animals. Additionally, five animals were infused with Ringer's solution and served as sham controls. The 28 E. coli-infused animals were pretreated with either a cyclooxygenase inhibitor--indomethacin, n = 6, a thromboxane (TxA2)-synthetase inhibitor--UK 38,485 alone, n = 6, or combined with a serotonin-antagonist--ketanserin, n = 9. Seven E. coli-infused animals were left untreated and served as septic controls. The sham controls were hemodynamically stable and had normal histological findings. All bacteria-infused animals exhibited signs of septic shock with pronounced hemodynamic reactions. Attenuation of the bacteria-induced increase in pulmonary arterial blood pressure was found in all pretreated animals but most pronounced in the indomethacin-pretreated group which also showed protection against gastric mucosal injury and capillary stasis. TxA2-inhibited animals had aggravated capillary stasis and mucosal injuries. It is concluded that gastric mucosal damage could be modified by drugs influencing the prostanoid system. The "cytoprotective" effect of prostaglandins seem to be of minor importance for the prevention of the gastro-intestinal mucosal injury seen in some series.

Animals↗
PubMed1989

Influence of aprotinin, a protease inhibitor, on porcine E. coli shock. Studies on coagulation, fibrinolytic and hemodynamic response.

The effect of a protease inhibitor, aprotinin, on hemostasis (a2M, a2AP, AT III, prothrombin-convertin activity, fibrinogen, fibrinogen monomers and fibrinolytic activity on fibrin plates) was investigated in pigs with septic shock. Anesthetized pigs were given live Escherichia coli i.v. (n = 7), or aprotinin (1,000,000 KIE i.v.) 15 min before live E. coli (n = 6), or Ringer's solution only (sham controls, n = 8). Septic shock developed in all E. coli-infused pigs. Pulmonary vascular resistance increased, platelet and leukocyte counts fell and signs of systemic activation of the coagulation and fibrinolytic systems appeared in the E. coli groups, but aprotinin attenuated the effects on these systems and also on the pulmonary circulation. Five of the six aprotinin-pretreated pigs survived, but none of the seven with septic shock and no pretreatment. Thus the shock induced by infusion of live E. coli and the resultant changes in the coagulation and fibrinolytic systems and in cardiopulmonary hemodynamics were diminished by aprotinin pretreatment.

Animals↗
PubMed1989

Intramucosal pH measurement with tonometers for detecting gastrointestinal ischemia in porcine hemorrhagic shock.

Intraluminal pCO/ was measured in the stomach, small intestine, and sigmoid colon of pigs using balloon catheters (Tonomitor). With the simultaneously determined arterial blood HCO3 concentration, the intramucosal pH (pHi) could be calculated using the Henderson-Hasselbalch equation. Cardiac output and portal venous flow were measured using Swan-Ganz catheters. A series of 35 normotensive pigs were studied to achieve normal values of cardiac output, gastrointestinal pHi, and blood flow in pigs. In another series of pigs (n = 12), hemorrhage was induced in two steps and followed by retransfusion. Five additional animals served as controls. Gastric, small intestinal, and colonic pHi decreased with increasing degree of hemorrhage but remained unchanged in the controls. Following severe hemorrhage, pHi fell below the normal range in all pigs but one. It recovered only partly following retransfusion. Histological examination of specimens obtained following retransfusion revealed normal mucosa in six of eight investigated animals and superficial mucosal injury in the remainder, indicating that abnormal pHi may be found for a period in the microscopically normal gastro-intestinal mucosa. Monitoring pHi in the stomach, small intestine, or colon using tonometers could be a useful technique to reveal insufficient mucosal blood flow in the alimentary canal.

Animals↗
PubMed1989

Cardiopulmonary dysfunction in a feline septic shock model: possible role of leukotrienes.

The aim of the present study was to explore the possible involvement of leukotrienes (LTs) in the development of cardiopulmonary dysfunction in experimental septic shock. Sepsis was induced in anesthetized cats by infusion of liver Escherichia coli bacteria. One series (N = 6) was pretreated with diethylcarbamazine (DEC), a 5-lipooxygenase inhibitor; another series (N = 7) was pretreated with FPL 55712, a LTC4-D4 antagonist; and a third series (N = 8) served as septic controls. After 2 hr of bacteremia, there were no differences in cardiac function in the three series. By subjecting the heart to volume load, two points on a Starling curve were obtained, indicating the limits of the functional cardiac reserve. This loading procedure disclosed a significantly better preserved left ventricular function in the DEC-pretreated group as compared with the other two groups. Pretreatment with DEC and FPL 55712 had no effects on early pulmonary vascular reactions. However, the tracheal pressure response was less pronounced after pretreatment compared with septic controls. Calculated airway resistance was less increased and pulmonary compliance less decreased in the two pretreated groups. Furthermore, arterial hypoxia was prevented by pretreatment. It is concluded that this study suggests that LTs are involved in the development of myocardial insufficiency in experimental bacteremic septic shock. Moreover, the results strongly indicate that LTs may be of importance in compromising pulmonary gas exchange, partly by effects on the smaller airways.

Airway Resistance↗
PubMed1988

Effects of a calcium antagonist (nifedipine) on cats in live E. coli bacteriemic shock.

The effects of a calcium antagonist, nifedipine, on cardiovascular reactions and on gastrointestinal mucosal integrity was studied in a standardized feline bacteriemic model. Nifedipine pretreatment delayed the development of cardiovascular derangement and reduced the severity of the intestinal but not the gastric mucosal injury. The effect on the intestinal mucosa could be due to the delayed development of hypotensive shock but also to a protective effect on the superficial mucosal cells.

Animals↗