Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats were anesthetized and their lift kidneys were made ischemic for 1 h by clamping of the aorta just above the left renal artery. Mannitol (2.5 g/kg), Dextran 70 (0.6 g/kg), methylprednisolone (50 and 100 mg/kg), and allopurinol (100 mg/kg body weight) were administered before, during, or after the ischemia period in order to test the effect of each of these drugs upon this model of renal injury. At 24 h after the release of the aortic clamp the left kidneys of the drug treated animals wwere perfusion fixed and processed for light and electron microscopy. Dextran administration to animals with ischemic kidneys gave rise to a pronounced vacuolization ("osmotic nephrosis"), in the entire proximal tubule and especially in the pars recta. This was in contrast to dextran administration to rats with nonischemic kidenys, which showed no or very mild "osmotic nephrosis." This demonstrates that ischemia makes rat kidneys more susceptible to the development of "osmotic nephrosis." In controls (no drug treatment) one hour of renal ischemia gave partial necrosis of pars recta of the proximal tubule, while the pars convoluta tubule survived. Mannitol treatment significantly reduced the amount of necrosis of the pars recta, whereas dextran, methylprednisolone, and allopurinol had no or a negative effect on the survival of the cells of the pars recta segment. It is suggested that mannitol protects against the development of necrosis by increasing medullary blood flow in combination with a counteractive influence on the cellular swelling, which is known to occur in ischemia.
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PMID:Effect of mannitol, dextran (macrodex), allopurinol, and methylprednisolone on the morphology of the proximal tubule of the rat kidney made ischemic in vivo. 40 53

In unilateral nephrectomized beagle dogs the remaining kidney was subjected to 2 hrs of ischemia in situ. The ischemic organ was cooled to 22--23 degrees C by initial hypothermic perfusion over a 5-F catheter introduced into the renal artery via the carotid artery. It was then left in the open abdominal wound without any further attempts of cooling. Three perfusates were used: an isoosmolar Dextran solution (Eisenberger), a hyperosmolar, "intracellular" electrolyte solution (Sacks), and a hyperosmolar, "extracellular" electrolyte solution. There was a mean postoperative increase in serum creatinine levels of 0.6 mg-%. By the 3rd p.o. day at latest the serum creatinine was again within normal limits. The inulin and PAH clearances on the 7th and 14th p.o. day showed no significant differences to preoperative determinations. No definite advantage or disadvantage was noted among the three perfusates. All control dogs whose kidneys were made ischemic for 2 hrs without perfusion died due to acute tubular necrosis. Apparently the homogenous cooling and flushing by the initial perfusion is of more importance for good preservation in this situation than the composition of the perfusate.
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PMID:[Short time in-situ preservation of the ischemic kidney by a simple initial hypothermic perfusion with various cold solutions. An animal experimental study]. 115 70

Vascular resistance was determined during hypothermic perfusion of rabbit kidneys after various periods of warm ischemia. Ischemia was induced by clamping of the renal artery, or of the renal artery and vein, in situ. Studies were made after periods of clamping ranging from 0 to 180 min. The perfusing fluid was 5% Dextran of low molecular weight in balanced saline solution (Tis-U-Sol), with addition of 5 mg % Papaverin. When the renal artery was clamped for more than 15 min, vascular resistance increased. Maximal resistance was reached after 60 min of clamping, and was 3 times as high as that value in the control group of kidneys which were not clamped. The vascular resistance attained after 60 min of clamping did not further increase when clamping was maintained for 180 min. When both the renal artery and the renal vein were clamped vascular resistance first increased after 30 min. Maximal resistance was reached after 60 min of clamping, but was only 1/2 of that level seen when the renal artery alone was clamped.
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PMID:Vascular resistance in hypothermically perfused kidneys damaged by warm ischemia. 127 30

The underlying mechanisms of the beneficial therapeutic effects of small-volume resuscitation with hyperosmolar solutions for treatment of hypovolemic shock are still poorly understood. Using the dorsal skinfold chamber model and intravital fluorescence microscopy, we investigated the effects of hyperosmolar saline dextran on ischemia-reperfusion injury in striated skin muscle of awake normovolemic golden hamsters. Test solutions (4 ml/kg body wt i.v.) were administered 2 min before reperfusion after 4 h of pressure-induced ischemia. In animals receiving 0.9% saline (control), we observed a drastic enhancement of leukocyte rolling along and sticking to the endothelium of postcapillary venules 0.5 h after reperfusion. Postischemic leukocyte rolling and sticking were significantly reduced when animals were treated with 7.2% saline alone (HSS), 10% Dextran 60 in 0.9% saline (HDS), or 10% Dextran 60 in 7.2% saline (HHS). In control animals, capillary perfusion was reduced to approximately 60% of preischemic values 0.5 h after reperfusion. Concomitantly, leakage of the macromolecule fluorescein isothiocyanate-dextran (5 mg in 0.1 ml saline i.v., M(r) 150,000) into the perivascular space increased from 0% before ischemia to approximately 12% at 0.5 h reperfusion. In contrast, when animals were treated with HSS, HDS, or HHS before reperfusion, capillary perfusion decreased to a significantly minor extent of approximately 15%, and macromolecular leakage was slightly increased to approximately 5%. Our results suggest that hyperosmolar saline dextran effectively attenuates postischemic microvascular disturbances elicited by ischemia-reperfusion, presumably through reduction of postischemic leukocyte-endothelium interaction and capillary swelling.
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PMID:Attenuation of postischemic microvascular disturbances in striated muscle by hyperosmolar saline dextran. 127 89

Increased vascular permeability is an early and sensitive indicator of ischemic muscle injury, occurring before significant histologic or radionuclide changes are evident. We investigated the effect of iloprost, a stable prostacyclin analog, on microvascular permeability in a rat striated muscle model. In six control and six experimental animals the cremaster muscle was dissected, placed in a closed-flow acrylic chamber, and suffused with a bicarbonate buffer solution. Dextran labeled with fluorescein was injected intravenously as a macromolecular tracer, and microvascular permeability was determined on the basis of clearance of the fluorescent tracer. Two hours of ischemia were followed by 2 hours of reperfusion. In the experimental group iloprost (0.5 microgram/kg/min) was given in a continuous intravenous infusion. Microvascular permeability increased significantly during reperfusion in both control and experimental animals (p less than 0.0001). Treatment with iloprost, however, significantly attenuated this response compared to the control group, 4.8 +/- 0.3 versus 7.3 +/- 0.5 microliters/gm/min, respectively (p less than 0.0001). Iloprost decreases the rise in vascular permeability after ischemia and reperfusion. Experimental clinical use of iloprost under controlled conditions in the treatment of patients with acute skeletal muscle ischemia appears justified.
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PMID:Iloprost attenuates the increased permeability in skeletal muscle after ischemia and reperfusion. 170 Aug 37

Qualitative changes in skeletal muscle injury after ischemia are well known; however, quantitative assessments have not been well documented. We have determined microvascular permeability changes by measuring the clearance of fluorescein-labeled dextran of MW 150,000 (FITC-Dextran-150). The cremaster muscle of anesthetized rats was fashioned as a single layer, splayed on a lucite chamber and suffused with bicarbonate buffer solution at 35 degrees C. Clearance is the product of suffusion rate times the ratio of suffusate to plasma concentrations of FITC-Dx 150. After a 1-hr period of baseline data collection, ischemia was produced by cross-clamping the cremasteric vascular pedicle for periods of 30 min and 2 hr in separate experiments. Clearance of FITC-Dx 150 increased from a control value (mean +/- SE) of 8.3 +/- 2.7 to 29.9 +/- 8.1 microliters/min/g after reperfusion following a 30-min period of ischemia, and from a control value of 36.2 +/- 13.6 to 274 +/- 94.5 after 2 hr of ischemia. The differences were statistically significant (P less than 0.05). Our results show a significant increase in microvascular permeability occurring after only 30 min of ischemia. They also demonstrate a direct relationship between the extent of the permeability change and the duration of the ischemic period.
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PMID:Assessment of ischemia reperfusion injury in skeletal muscle by macromolecular clearance. 243 77

A controlled double-blind evaluation of the effects of Dextran 40 at different concentrations on cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2) and cerebral lactate production (CMRLact) was carried out. We studied 40 patients in coma due to recent head injury. Concentrations of Dextran solution were not significantly related to variations in CBF and metabolic rate over the period of infusion. The lack of effect of the Dextran infusion may be explained by the absence of global brain ischemia in these patients at the time of the study. The very low initial CBF values were a consequence of brain metabolic depression and not a sign of global ischaemia. The rheological benefits of treatment with Dextran 40 in head injured patients should preferably be investigated using techniques which permit detection of local changes in CBF and metabolism.
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PMID:A controlled study of Dextran 40: effect on cerebral blood flow and metabolic rates in acute head trauma. 248 92

We studied the in vivo effects of Daflon 500 mg on transvascular movement of macromolecules induced by bradykinin (BK) and ischemia. The experimental preparation involved the rat cremaster muscle. The muscle was fashioned as a single bag (new procedure), placed in a transparent chamber and superfused with a bicarbonate buffer solution equilibrated with a 5% CO2 95% N2 gas mixture in order to obtain pH 7.40, PCO2 = 40 mmHg, PO2 = 20-40 mmHg and thermostated at 35 degrees C. FITC-Dextran 150 (MW 150,000) was injected i.v. as a macromolecular tracer. BK was added to the buffer solution at the concentration of 2 micrograms/ml five minutes after a control period of 60 minutes. Ischemia was performed during 60 min by a clamp positioned on the main artery of the cremaster muscle. Animals treated with Daflon 500 mg (100 mg/kg) 18 and 2 hours before experiments showed a significant reduction in FITC-Dextran 150 leakage in both BK and ischemia protocols. Leakage of FITC-Dextran 150 started 2-3 min after application of BK in the two animal groups but the response was less important (+ 270%) and the preparation returned to control appearance after 40 min in the treated rats in contrast with control rats (+ 450% and 70 min). The amplitude of FITC-Dextran 150 leakage was identical just one hour after ischemia in the two animal groups, but microvascular permeability returned to basal state in treated animals (30 min), a fact non observed in non treated animals. These data demonstrate the protective effect of Daflon 500 mg on the microvascular muscle network in vivo.
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PMID:Daflon 500 mg depresses bradykinin-ischemia-induced microvascular leakage of FITC dextran in rat cremaster muscle. 248 28

We investigated the effect of progressive normovolemic hemodilution with Dextran 70 on subcutaneous tissue oxygen tension (PscO2) in canine random pattern flaps and in adjacent intact skin. PscO2 was measured polarographically in implanted oxygen-permeable Silastic catheters. The mean PscO2 of 5.7 kPa in intact subcutis at hematocrit (HCT) 40 was maintained or insignificantly improved during hemodilution to a HCT of 14. The mean flap PscO2 of 3.1 kPa at HCT 40 was maintained down to HCT 20. Most flap measuring sites exhibited a PscO2 improvement in an individual HCT range at some point during hemodilution. The increment in PscO2 tended to be relatively greater and to occur at lower Hct values in locations with more severe ischemia initially. Central hemodynamics were characterized by a lowered total peripheral resistance and an increased cardiac output, whereas systemic and pulmonary arterial blood pressures and central venous pressure remained essentially unchanged.
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PMID:Tissue oxygen tension in random pattern skin flaps during normovolemic hemodilution. 266 19

Prolonged ischemia is known to cause severe damage in skeletal muscle and skin as a result of reperfusion failure. Isovolemic hemodilution has been suggested as a modality to reverse microcirculatory disorders by improving flow properties and flow conditions of the blood. The aim of the present study was to investigate whether prophylactic isovolemic hemodilution could improve tissue oxygenation after 4h of pressure induced ischemia in skeletal muscle. In 17 Syrian golden hamsters a dorsal skin fold chamber and two permanent arterial and venous catheters were implanted. Following a recovery period of 48h ischemia was induced for 4h by means of a transparent stamp compressing the tissue within the chamber. In 9 animals (control, hct 43%) measurements of tissue PO2 (platinum multiwire electrode) were performed prior to and 15 min, 2h and 24h after release of ischemia. In 8 animals isovolemic hemodilution with Dextran 60 (hct 29%) was carried out prior to ischemia and measurements of local tissue PO2 were performed as reported for the control group with an additional measurement 30 min after hemodilution. In control animals tissue PO2 decreased significantly (p less than 0.01) from 20.7 +/- 2.4 mmHg prior to ischemia to 8.8 +/- 3.1 mmHg after 15 min of reperfusion; after 24h tissue PO2 was 15.6 +/- 6.1 mmHg. In hemodiluted animals tissue PO2 increased due to hemodilution from 20.9 +/- 1.6 mmHg to 23.5 +/- 2.5 mmHg (p less than 0.05); after 15 min of reperfusion tissue PO2 was 19.8 +/- 6.8 mmHg and remained unchanged for 24h (20.0 +/- 2.5 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tissue oxygenation after prolonged ischemia in skeletal muscle: therapeutic effect of prophylactic isovolemic hemodilution. 278 61


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