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D Arvidsson

Publications and source records attributed to D Arvidsson.

51 records · Page 3Linked to original sources

Splanchnic and total body oxygen consumption in experimental fecal peritonitis in pigs: effects of dextran and iloprost.

Tissue oxygenation in the gastrointestinal tract and in the liver was studied in a porcine model where septic shock was induced by fecal peritonitis. The effects of different fluid regimes were compared. In one group (n = 8) a moderate amount of crystalloid fluids was given, in another (n = 7) crystalloids and colloids, and in a third group (n = 6) iloprost, a prostacyclin analogue, was administered intra-arterially (10 ng x kg-1 b.w. x min-1) in combination with the crystalline and colloid fluid regime. Septic shock induced by fecal peritonitis reduced cardiac index and oxygen supply to splanchnic organs. Iloprost improved the hepatic arterial blood flow, and tended to attenuate the reduction in liver oxygen delivery. Oxygen consumption (VO2) in the gastrointestinal tract and the liver was significantly increased in the group given crystalloids. These animals developed a hypovolemic/hypodynamic septic shock. Liver VO2 in these animals became flow dependent reflected by increasing hepatic venous lactate values and inversion of lactate turnover by the liver. In the two other groups gastrointestinal and liver VO2 remained constant during the observation period. Oxygen extraction over the liver increased when oxygen delivery decreased. The increased liver VO2 is suggested to be secondary to impaired microcirculation and accumulation of macrophages and leukocytes in the septic liver.

Animals↗

Effects of positive end-expiratory pressure on splanchnic circulation and function in experimental peritonitis.

Splanchnic and central hemodynamic effects of positive end-expiratory pressure (PEEP) were studied in anesthetized pigs using mechanical ventilatory assistance, with or without sepsis (fecal peritonitis). One hour after sepsis, PEEP (10 cm H2O) was applied (n = 6). Another group (n = 6) had sepsis without PEEP. In one group (n = 6) without sepsis, PEEP was applied after 1 hour, while a fourth group (n = 5), without sepsis or PEEP, served as a control. The group with PEEP and sepsis had reduced cardiac index, portal venous blood flow, and liver surface blood flow. The group with PEEP alone had reduced splanchnic circulation by increasing gastrointestinal vascular resistance, while the group with sepsis alone had increased portal vascular resistance. In a separate series with sepsis, intermittent PEEP, and vigorous fluid resuscitation, it was demonstrated that avoiding hypovolemia did not seem to protect from the PEEP effects on the splanchnic circulation. The combination of sepsis and PEEP was not additive on portal blood flow reduction but reduced bile production.

Animals↗

Laparoscopic cholecystectomy during pregnancy.

Pregnancy is by some considered a contraindication for laparoscopic cholecystectomy. However, no evidence exists to support this opinion. We describe herein a laparoscopic cholecystectomy in a pregnant woman in the 22nd week of gestation with an uneventful postoperative recovery and normal completion of pregnancy. Laparoscopic cholecystectomy can be performed during pregnancy with a slight modification of the operative technique and is less traumatic than open surgery.

Adult↗

Splanchnic oxygen consumption in septic and hemorrhagic shock.

Oxygen consumption (VO2) is dependent on oxygen delivery (DO2) in septic shock. Local hypoxia with later secondary organ failure may develop, however, despite an often hyperdynamic circulation. The splanchnic organs seem to be of vital importance in this context. In experiments performed in pigs we compared total body VO2 and DO2 with oxygen consumption and delivery in the gastrointestinal organs and the liver in two different shock states: (1) septic shock induced by peritonitis (n = 6) and (2) hemorrhagic shock (n = 6). Another group of six animals not in shock served as controls. Total, gastrointestinal, and liver DO2 decreased in a similar pattern in both septic and hemorrhagic shock. Gastrointestinal and liver VO2 increased in sepsis, whereas it was unchanged in hemorrhage. In the later phase of sepsis, liver VO2, but not gastrointestinal VO2, again decreased, because liver oxygen extraction was almost total and liver DO2 decreased further. The development of flow-dependent liver hypoxia was reflected in a decrease in liver lactate turnover (increased liver lactate release) during late sepsis. Early hypoxia in the splanchnic region is suggested as a plausible mechanism behind the development of secondary organ failure, especially in sepsis.

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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.

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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.

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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.

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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↗

The early platelet uptake and distribution of platelets in small-diameter polytetrafluoroethylene (PTFE) vascular grafts in vivo.

Platelet deposition onto the surface of biomaterial is an important component of the interaction between blood and a prosthetic arterial graft. To understand the thrombotic process in small-diameter by-pass grafts, we used pigs to study the early in vivo uptake of 111In-oxine-labelled platelets in polytetrafluoroethylene (PTFE; GoreTex) grafts. In each experimental animal, 12 PTFE grafts (internal diameter, 3 mm; length, 5 cm) were placed in the femoral artery as interposition grafts. 111In-Labelled autologous platelets were injected. Sequential-scintillation camera images of the graft area were taken over a period of 3.5 h. Platelet deposition in vivo was calculated as an activity ratio for the entire grafts as well as for different segments of the graft. The grafts were harvested, cut into 0.6-cm pieces and weighed, and the 111In activity was measured. The distribution along the graft surface was calculated. Blood flow was measured continuously. The activity ratios rapidly increased, and a maximum was reached 60 min after the re-establishment of blood flow; thereafter the activity ratios slowly decreased. The distribution of platelets along the graft surface was found to be non-uniform where more platelets were deposited towards the distal anastomoses.

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Platelet adhesion in polytetrafluoroethylene (PTFE) vascular grafts in vivo and the influence of increased intramuscular pressure--an experimental model.

Thrombogenicity of graft material is involved in early graft failure in small diameter grafts. The frequently seen postoperative swelling of the leg after distal revascularization may cause an increased intramuscular pressure and early graft failure. Pairs of 4 mm polytetrafluoroethylene (PTFE) grafts were implanted. Autologous platelets were labeled with 111In-oxine. Platelet adhesiveness onto the grafts were analyzed from gamma camera images. Intramuscular pressures were measured with wick technique. Blood flow was measured. One graft served as control the other as test graft. Ninety minutes after declamping the i.m. pressure was increased in the test-leg to 30 mmHg, and later to 60 mmHg. In the control-graft platelet uptake increased to a maximum 60 min after declamping. Blood flow and i.m. pressure remained uneffected. The test-grafts were initially similar but when i.m. pressure was increased to 30 mmHg activity in the grafts increased significantly. Blood flow decreased with 12% of initial flow. When i.m. pressure was raised to 60 mmHg platelet uptake continued to increase. An increased intramuscular pressure of 30 mmHg or more significantly increase the amount of platelets adhering onto PTFE grafts, emphasizing the need for measuring intramuscular pressures after lower limb vascular revascularizations.

Animals↗

A comparison of two methods of labelling autologous platelets with 111In-oxine in five different species.

Several different methods for labelling autologous platelets with 111In-oxine have been described. However, no comparative study has been reported. In the present investigation two different labelling methods were compared in terms of labelling efficiency and platelet function in five species: human, dog, pig, rabbit and rat. One of the labelling methods, utilising among other things a serum albumin gradient separation of platelets and incubation of 111In-oxine in a water bath at 37 degrees C, was superior in all species with significantly higher labelling efficiency and unchanged platelet function.

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