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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

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↗
PubMed1988

Liver metabolic effects of intestinal shock and naloxone treatment in the rat.

The liver metabolic response of rats following a standardized intestinal shock, induced by applying a pressure of 120 cm water on the mesenteric vessels for 60 min, was studied. Immediately prior to the release of the pressure on the vessels saline or naloxone was given either as a single injection or as a continuous infusion. After the reperfusion of the intestine no early disturbances in liver metabolism were found as evidenced from the ATP, glucose and lactate levels in liver biopsies taken 15 min following reflow. Within 60 min of reflow reduction of ATP and increases of glucose and lactate levels occurred. There were no major hemodynamic or liver metabolic differences between saline- and naloxone-treated shocked rats. When saline or naloxone was given as a continuous infusion, the changes in liver metabolism were, however, less severe than those observed in the single injection situation pointing toward a non-specific effect of volume replacement rather than a blockade of opioid receptors. Hepatic hypoxia and/or cellular effects of "shock factors" could be mechanisms of pathophysiologic importance for the disturbed liver metabolism in this shock model.

Acid-Base Equilibrium↗
PubMed1988

Laser-Doppler flowmetry for estimating liver blood flow.

Whether laser-Doppler flowmetry can be used to monitor liver blood flow was evaluated in a porcine model in which portal venous blood flow was followed indirectly by electromagnetic flowmetry applied to the superior mesenteric artery, and total hepatic venous outflow was measured directly by using an extracorporeal circuit. Hepatic venous outflow at rest was 23.5 +/- 5.7 ml.kg body wt-1.min-1. Occlusion of the hepatic arterial supply reduced hepatic laser-Doppler blood flow to 22%, but hepatic venous outflow only to 80%. Portal venous blood flow remained unchanged or increased slightly. Occlusion of the portal vein, on the other hand, decreased hepatic laser-Doppler blood flow values to 37% and hepatic venous outflow to 13%. Increased hepatic venous outflow pressure, caused by a positive end-expiratory pressure or elevation of the draining cannula, reduced flow and caused approximately equal changes in the three variables, as did reduced flow by step-wise bleeding. From these experiments in the pig it is concluded that laser-Doppler flowmetry on the liver surface clearly reflects relative changes of the total liver blood flow, as exemplified in this study, during venous stasis and bleeding. The technique is, however, more sensitive to blood flow changes in the hepatic artery as compared with the portal vein.

Animals↗
PubMed1988

Neutrophil-induced decrease in wound margin strength after intestinal anastomosis--influence on collagen and mechanisms of granulocyte action.

A marked decrease in strength occurs early after surgery in tissues adjacent to an incisional wound. In this study measurement of collagen and a histological examination were carried out in a rat intestinal anastomosis. The decrease in tissue strength of the bowel wall did not correlate to the amount of collagen or to changes in collagen solubility. At histology the collagen layer was seen unaffected. Our previous studies showed that the decrease in strength was eliminated if the number of circulating neutrophils was reduced by antineutrophil serum. In addition, the decrease was counteracted by a proteinase inhibitor, the soybean trypsin inhibitor (STI), and the oxygen-free-radical scavengers superoxide dismutase (SOD) and catalase. To further examine the mechanisms of the decrease, neutrophil accumulation in the anastomosis was examined by myeloperoxidase (MPO) assay, and at histology, after treatment of the animals with the proteinase inhibitor, the scavengers or saline solution. MPO activity increased by 110% 24 h after the operation in saline-treated animals, but the increase was not influenced by STI or SOD and catalase. At the histological examination neutrophil accumulation was not seen affected by the drugs. Thus, the proteinase inhibitor and the scavengers counteract the decrease in strength in some other way than by reducing the number of neutrophils in the wound edges, for instance by local inhibition of neutrophil proteolytic enzymes and oxygen-free radicals.

Anastomosis, Surgical↗
PubMed1988

The pentagastrin-induced gastric acid response in humans.

The pentagastrin-induced acid response, alone and versus different doses of cimetidine, was studied in humans. The inhibitory effect of the histamine H2-receptor antagonist cimetidine could only in part be counteracted by increasing doses of pentagastrin. The maximal gastric acid response was significantly decreased by cimetidine, and the ED50 values for pentagastrin showed a minor but still statistically significant increase, indicating both a competitive and a non-competitive inhibition by cimetidine of pentagastrin-induced gastric acid secretion. The pA2 characterization of the receptor mediating the pentagastrin-induced gastric acid response gave a value of 6.2, compared with the pA2 value of the human H2 receptor of 6.1. This suggests that the pentagastrin-induced gastric acid response in humans is mediated via the histamine H2-receptor.

Adult↗
PubMed1988

Arachidonic acid cascade metabolites in porcine E. coli shock. Coagulation, fibrinolytic and hemodynamic response.

Cardiopulmonary hemodynamics and changes in various hemostatic factors (alpha 2M, alpha 2AP, AT III, prothrombin-proconvertin activity, fibrinogen concentration, ethanol gelation test and fibrinolytic activity on fibrin plates) were investigated in pigs during shock induced with live Escherichia coli. Anesthetized pigs were treated with indomethacin or with the combined cyclooxygenase/lipoxygenase inhibitor BW755C before the E. coli infusion or were left untreated as septic controls. Septic shock developed in all of these animals. Pretreatment attenuated the early deterioration of pulmonary circulation but did not modify the coagulation/fibrinolytic activation or the disturbed cardiopulmonary hemodynamics seen in the delayed phase of shock. The arachidonic acid cascade metabolites thus seems to mediate the early, but not the delayed cardiopulmonary reaction and to have minor importance for activation of coagulation and fibrinolysis in E. coli-shocked pigs.

Animals↗
PubMed1988

Cardiopulmonary function as related to thromboxane A2 synthesis in experimental septic shock.

The aim of the present study was to explore the possible involvement of thromboxane A2(TxA2) in the development of cardiopulmonary dysfunction in experimental septic shock. Sepsis was induced in anesthetized cats by intravenous (i.v.) infusion of live Escherichia coli. One series (No. = 12) was pretreated with a specific TxA2 synthetase inhibitor, dazmegrel; another (No. = 8) served as a septic control series. In both series a systemic arterial hypotension developed after 2 hr; no differences in cardiac function were detected. After 2 hr bacteremia cardiac preload was increased by a rapid infusion of dextran. This showed that cardiac function was significantly more preserved in dazmegrel-pretreated cats compared with septic controls. Pretreatment with dazmegrel totally prevented the pulmonary vascular response to bacterial infusion. The pulmonary compliance decreased to 40% in controls but to only 75% in the dazmegrel series, and airway resistance increased to 300% and 140%, respectively. The ventilation-perfusion ratio was less impaired in the pretreated series. Pretreatment with dazmegrel abolished the increase in thromboxane B2 (TxB2), the stable metabolite of TxA2, seen in the untreated series. The rise in 6-keto-prostaglandin F1a (6-keto-PGF1a), the stable metabolite of prostaglandin I2PGI2, was evident in both series. We concluded that TxA2 is important for the impaired cardiac performance in septic shock. Furthermore, TxA2 is involved, but not as the only factor, in the development of pulmonary dysfunction.

Airway Resistance↗