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- Hjelmqvist, H, et al.
(författare)
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Comparison between the effects of central and systemic hypertonic NaCl on hemodynamic responses to hemorrhage in sheep.
- 1995
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Ingår i: Shock. - 1073-2322 .- 1540-0514. ; 3:5, s. 355-61
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Tidskriftsartikel (refereegranskat)abstract
- Effects of treatment with systemic hypertonic (1.2M, 4 mL kg-1) NaCl (SHTNa) on tolerance to hemorrhage, accompanying systemic hemodynamics, and regional blood flow were investigated in conscious sheep. The results were compared with those obtained in animals subjected to hemorrhage during intracerebroventricular (ICV) administration of hypertonic (.5 M, .02 mL min -1) NaCl (CHTNa). Corresponding bleeding during ICV infusion of isotonic saline served as control. All treatments were started 30 min before commencement of a slow (.7 mL kg-1 min-1) hemorrhage, which was continued until the mean systemic arterial pressure (MSAP) suddenly dropped to about 50 mmHg. To reach the distinct fall in MSAP significantly more blood had to be withdrawn in the CHTNa (27.8 +/- 2.2 mL kg-1, p < .05) than in the SHTNa group (21.5 +/- 1.7 mL kg-1), which in turn showed a significantly higher tolerance to hemorrhage than the controls (15.1 +/- .7 mL kg-1, p < .01). The hemorrhage-induced reduction of cardiac output (CO) below basal level was less pronounced in the CHTNa group, where also the posthemorrhage CO recovery was most rapid. Spontaneous recovery of MSAP after bleeding was equally improved in both treatment groups with the central venous pressure being significantly higher in the SHTNa group. The hemorrhage-induced fall in renal blood flow (RBF) was more pronounced in the CHTNa group, which also had an impaired posthemorrhage recovery of RBF. In comparison to the SHTNa and control groups the renovascular resistance was significantly higher in the CHTNa group already during the prehemorrhage infusion period.(ABSTRACT TRUNCATED AT 250 WORDS)
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| 2. |
- Ljungdahl, M, et al.
(författare)
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Intestinal blood flow and intramucosal pH in experimental peritonitis.
- 1999
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Ingår i: Shock. - : Ovid Technologies (Wolters Kluwer Health). - 1073-2322 .- 1540-0514. ; 11:1, s. 44-50
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND AND AIMS: Experimental peritonitis causes gut intramucosal acidosis indicating intramucosal ischemia. However, tissue acidosis may reflect other conditions than ischemia. An increased mucosal-arterial Pco2 difference ( Pco2-gap) is suggested to be a more adequate measure of tissue ischemia than intramucosal pH (pHi). This study was performed to elucidate whether keeping cardiac index (CI) and splanchnic blood flow normal or supranormal by administration of colloids and an inotropic drug could prevent the acidosis as well as reduce the Pco2-gap. A secondary aim was to study to what degree the low pHi in peritonitis really reflects ischemia.SUBJECTS: 24 anesthetized pigs (18-27 kg) divided into four groups.MODELS: A Swan-Ganz catheter, transonic flow meters and catheters for blood sampling were applied. pHi was calculated using tonometry. Standardized fecal peritonitis was induced, except in controls. One peritonitis group was given dextran (Group P(DEX)) and another in addition dobutamine (Group PDOB) to keep CI normal or supranormal, respectively.RESULTS: After 4 h, a significant drop in pHi was found in all peritonitis groups, most pronounced in untreated peritonitis (to 7.09+/-.02). Corresponding values in Group P(DEX) and Group P(DOB) were 7.22+/-.03 and 7.22+/-.01, respectively, and in controls 7.30+/-.02. The Pco2-gap and the mucosal-arterial [H+] difference ([H+]-gap) increased significantly in untreated peritonitis but did not increase in groups given dextran and dextran + dobutamine.CONCLUSION: Maintaining CI in peritonitis attenuated the reduction in pHi and prevented the increased Pco2- and [H+]-gap. It seems justified from these data to conclude that the somewhat reduced pHi in treated peritonitis groups did not reflect tissue ischemia.
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| 3. |
- Ljungdahl, M, et al.
(författare)
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Small intestinal mucosal pH and lactate production during experimental ischemia-reperfusion and fecal peritonitis in pigs.
- 1997
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Ingår i: Shock. - : Ovid Technologies (Wolters Kluwer Health). - 1073-2322 .- 1540-0514. ; 7:2, s. 131-8
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to investigate mucosal pH and lactate production in a porcine model of ischemia/reperfusion and sepsis using both tonometry and a technique for segmental intestinal perfusion. Eighteen pigs (17-23 kg) were anesthetized and mechanically ventilated. They were divided into three groups and followed for 4 h. Group C (n = 6) served as controls. In the ischemia/reperfusion group (I/R; n = 6), the superior mesenteric artery was totally occluded for 60 min. In group P (n = 6), sepsis was induced by fecal peritonitis. Cardiac index (CI) was determined by thermodilution and blood flow in the superior mesenteric artery (QSMA), using a Transonic flow probe. Intramucosal pH (pHi) was calculated using tonometry. A special balloon tube for segmental perfusion was introduced in the midileum for lactate measurement. Lactate and oxygen saturation were measured in arterial blood and in the superior mesenteric vein. CI, QSMA, pHi, and lactate in blood and perfusate remained unchanged in controls. Occlusion of intestinal blood flow induced a fall in pHi from 7.28 +/- .02 to 6.76 +/- .04, a marked rise in lactate in the perfusate, and an increased arteriovenous lactate difference. During reperfusion, pHi tended to return to baseline values. Lactate in the perfusate and the arteriovenous lactate difference decreased. In sepsis there was a continuous reduction in CI and QSMA to 45 +/- 13% and 40 +/- 20% of baseline, respectively. pHi decreased moderately from 7.22 +/- .09 to 6.98 +/- .25. Lactate remained unchanged in blood and perfusate. Microscopic mucosal injury was observed in all animals subjected to ischemia/reperfusion and in three of six pigs in group P. A good association between pHi and lactate production was seen in ischemia/reperfusion. However, in sepsis, lactate in superior mesenteric venous blood or in intestinal perfusate did not increase, despite the fall in pHi. The mechanism causing ischemic mucosal injury has different characteristics in sepsis and in ischemia caused by arterial occlusion.
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| 4. |
- Nettelbladt, Carl Gustaf, et al.
(författare)
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Hyperosmotic glucose infusion during hemorrhage does not reduce bacterial translocation in 24 hour-starved rats
- 1995
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Ingår i: Shock. - : Lippincott Williams & Wilkins. - 1073-2322 .- 1540-0514. ; 4:2, s. 113-116
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Tidskriftsartikel (refereegranskat)abstract
- Food deprivation 24 h before stress increases bacterial translocation in hemorrhage. Presently it tested whether hyperosmolality, induced by exogenous glucose infusion to improve plasma refill, prevents or reduces bacterial translocation after experimental hemorrhage in 24 h food-deprived rats. Rats were given an i.v. infusion of either 2 mL of 30% glucose (G) or the same volume of .9% NaCl (C) while simultaneously being submitted to a standardized 60 min hemorrhage period, of moderate or more severe hemorrhage. Blood was not reinfused. Despite development of marked hyperglycemia (p < .001, G vs. C) resulting in significantly greater reductions in packed cell volume (p < .001, G vs. C), bacterial translocation was detected similarly in both groups regardless of whether moderate (10/12-G, 9/12-C) or severe (15/19-G, 15/18-C) hemorrhage was inflicted. It was concluded that hyperglycemic hyperosmolality did not prevent bacterial translocation in these models of hemorrhagic stress in 24 h-starved rats.
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