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Am J Physiol. 1992 Dec;263(6 Pt 2):H1892-900.
Microvascular ischemia-reperfusion injury in striated muscle: significance of "no reflow".

Menger MD, Steiner D, Messmer K.

Institute for Surgical Research, University of Munich, Federal Republic of Germany.

"No reflow" has been implicated as prominent phenomenon in microvascular injury associated with ischemia-reperfusion (I/R). The objectives of this study were 1) to elucidate the significance of no reflow in microvascular I/R injury of striated muscle and 2) to determine whether reactive oxygen metabolites play a role in the development of postischemic no reflow. By use of the hamster dorsal skinfold preparation and intravital microscopy, microvascular perfusion of capillaries and postcapillary venules of striated muscle was quantitatively assessed before and 30 min, 2 h, and 24 h after 4 h of tourniquet-induced ischemia. I/R was characterized by a significant reduction (P < 0.01) in functional capillary density to 35% of baseline values during initial reperfusion, with incomplete recovery after 24 h (n = 9). In addition, capillary perfusion was found to be extremely heterogeneous, and wall shear rate in postcapillary venules was significantly decreased (P < 0.01). Treatment with either superoxide dismutase (SOD; n = 9) or allopurinol (n = 9) resulted in maintenance of capillary density of 60% of baseline (P < 0.05). Furthermore, I/R-induced capillary perfusion inhomogeneities and decrease of wall shear rate in venules were attenuated significantly (P < 0.01) by SOD and allopurinol. Thus part of capillary perfusion disturbances during I/R in striated muscle may be caused by increased postcapillary vascular resistance, probably mediated by reactive oxygen metabolites. However, the fact that in SOD- and allopurinol-treated animals 40% of the capillaries were still found to be nonperfused indicates that mechanisms other than oxygen radicals play an important role in the development of postischemic no reflow.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1481913&dopt=Abstract




Transplantation. 1999 Jan 27;67(2):200-6.
Ablating the ischemia-reperfusion injury in non-heart-beating donor kidneys.

Hernandez A, Light JA, Barhyte DY, Mabudian M, Gage F.

Washington Hospital Center, Transplantation Services, Washington, DC 20010, USA.

BACKGROUND: The objective of this study was to determine if allopurinol (AL) and/or trifluoperazine (TFP) added to the Belzer machine preservation solution (MPS) improves the function of non-heart-beating donor (NHBD) canine kidneys. METHODS: Anesthetized canines underwent bilateral dissection of the renal vessels, obtaining baseline flow. After removing one kidney (heart-beating donor [HBD]), the dog was exsanguinated. After remaining in situ for 120 min (30-min warm ischemia time, 90-min cold ischemia time), the second kidney was removed (NHBD), flushed, biopsied, and weighed. The kidneys were machine-perfused separately for 20 hr, and pressure, flow, and resistance were measured serially. The kidneys were randomly assigned to a perfusate group (G): G1=MPS, G2=MPS+TFP, G3=MPS+AL, and G4=MPS+TFP+AL. Kidneys were implanted separately into a single recipient dog. Flow, resistance, and urine output were measured serially for 4 hr. Blood and urine samples and kidney biopsies were then obtained. All measurements were standardized to 100 g of kidney weight. RESULTS: HBD kidneys functioned better than NHBD kidneys in all groups, as expected. Although perfusate G1 was the most effective solution for HBD kidneys, the TFP additive (perfusate G2) more effectively reversed the vasospastic effects of ischemia/reperfusion for NHBD than the MPS solution (G1) with or without other additives. In HBD kidneys, the addition of AL resulted in the best creatinine clearance; however, AL was less effective than MPS alone in NHBD kidneys. TFP+AL together were completely ineffective in preserving renal function, regardless of whether the kidneys were from HBD or NHBD. CONCLUSIONS: MPS+TFP more effectively protected renal function against reperfusion injury in the NHBD than MPS alone, AL, or AL+TFP. AL exerts a salutary effect on creatinine clearance in HBD but not in the NHBD. The TFP and AL combination should not be used together with the MPS in machine preservation of kidneys.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10075581&dopt=Abstract

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Intestinal ischemia/reperfusion provokes a local inflammatory response leading to a systemic inflammatory state. In this study we aimed to assess the effects of intestinal ischemia/reperfusion injury on anastomotic healing in the left colon with an intact vascular supply. A total of 94 Wistar albino rats were divided into three groups: sham-operated control (group I, n = 25), 30 minutes of intestinal ischemia/reperfusion (group II, n = 40), and 7-day allopurinol pretreatment and intestinal ischemia/reperfusion (group III, n = 29). After the reperfusion experiment, a segmental left colon resection and anastomosis were done. On postoperative days 3 and 7 anastomotic bursting pressure, anastomotic and operative complications, and intraabdominal adhesions were assessed. Mortality rates were 1/25, 16/40, and 4/29 for groups I, II, and III, respectively (p = 0.001). There was no difference among the groups for wound and anastomotic healing parameters evaluated by macroscopic criteria. On postoperative day 7 the mean bursting pressures were 220.3 +/- 18.5, 162.0 +/- 21.0, and 213.9 +/- 24.7 for groups I, II, and II, respectively (p = 0.000). Significantly dense adhesions were found in group II (p = 0.000). Allopurinol pretreatment prevented the effects of ischemia/reperfusion on anastomotic healing of the left colon. Intestinal/ischemia reperfusion causes impairment of anastomotic healing of the left colon. In addition to remote organ effects, reperfusion injury may affect anastomotic healing in the viscera with an intact vascular supply.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10865046&dopt=Abstract












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