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)

The ability of urokinase to salvage experimental flaps after a secondary ischemic insult was investigated in a rat model. Unilateral abdominal island skin flaps based on the superficial inferior epigastric vessels were raised and subjected to either 4 or 6 hours of primary ischemia followed by 12 hours of reperfusion and varying lengths of secondary ischemia. At the conclusion of secondary ischemia, the flaps were perfused with either lactated Ringer's solution or urokinase. One group of flaps served as a control and received no postischemic perfusion washout. The secondary critical ischemia time at which 50% of the flaps failed clinically was greater for flaps perfused with urokinase. Furthermore, the survival rates for all flaps perfused with urokinase were significantly greater than either control flaps or flaps perfused with lactated Ringer's solution (p < 0.05). Flap survival decreased significantly in all groups with increasing primary and/or secondary ischemia time (p < 0.05).
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PMID:Use of urokinase during secondary ischemia in experimental skin flaps. 819 93

To investigate the mechanism of myocardial; tunning, a Langendorff model of rat hearts (n = 18) underwent 15 min ischemia with coronary flow at 0.2 ml/min and 10 min reperfusion with Ringer's solution of 1.06 mmol/L Mg2+. Histological exam revealed no myocardial necrosis. However, the recovery of pressure product (RPP) was only 77% compared with control period. The myocardial Ca2+ content and water content were significantly increased (P < 0.01, vs control hearts). Pretreatment with high concentration of Mg2+ (2.4 mmol/L) improved the recovery of postischemic ventricular function, attenuated the Ca2+ overload and myocardial edema. The results indicated that a brief period of low-flow ischemia could produce a postischemic ventricular dysfunction-the myocardial stunning. Calcium overload and myocardial edema might be two pathogenic factors. An increased Mg2+ had a protective effects on postischemic ventricular dysfunction, which may involve the following mechanisms: reduced Ca2+ overload and attenuated myocardial edema.
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PMID:[Pathogenic factors of postischemic ventricular dysfunction and effects of magnesium]. 828 88

This study was aimed at examining the vulnerability of the liver to oxygen-free radicals upon reoxygenation after prolonged ischemia. Livers from male Wistar rats were first flushed with Ringer's and Euro-Collins solutions. After ischemic storage in Krebs-Henseleit solution at 37 degrees C for 60 min and in Euro-Collins solution at 4 degrees C for another 60 min, they were then persufflated with either gaseous O2 or N2 for 30 min at 37 degrees C, and rinsed again with Ringer's solution. Enzyme concentrations and calcium ion activities were measured in the effluent rinsing solution after passage through the liver. Treatment with superoxide dismutase (SOD) or allopurinol resulted in a significant reduction of tissue injury, determined by the enzyme loss, calcium uptake, and lipid peroxidation upon persufflation with O2. Allopurinol also improved the tissue levels of ATP and the sum of adenine nucleotides after aerobic persufflation, whereas SOD did not. Notwithstanding, neither treatment had any effect on anoxic persufflation with N2. Thus, we conclude that the postischemic liver is susceptible to oxygen-induced free radical injury and that allopurinol and SOD promote specific antioxidative protection of the liver, with the exclusion of side effects related to substrates or perfusion modalities.
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PMID:The effects of allopurinol and SOD on lipid peroxidation and energy metabolism in the liver after ischemia in an aerobic/anaerobic persufflation. 840 Jun 77

Posttraumatic ischemia appears to be largely responsible for the extension of lesions in acute injury of the spinal cord. In the present study, we have evaluated the putative improvement of axonal function by the calcium channel blocker nimodipine after acute trauma of the spinal cord. Three techniques were used: (1) spinal cord blood flow (SCBF) using a scanographic technique with stable xenon, (2) somatosensory evoked potentials (SEPs), and (3) magnetic resonance imaging (MRI). Thirteen baboons were used in this study. Acute trauma was achieved by compression of the spinal cord at level L1 by applying pressure for 5 sec with an inflated balloon catheter injected with Ringer's solution. Following the injury, one group (n = 5) received a saline infusion (placebo) for seven days, and a second group (n = 8) received a nimodipine infusion (0.04 mg/kg/h) during the same period of time. SCBF and SEP were first recorded prior to trauma. SCBF, SEPs, and MRI were then recorded on the day of the injury and eight days prior to histologic examination of the spinal cord. In these studies nimodipine significantly improved SCBF. The decrease in SCBF observed at day one and day eight following trauma was significantly reduced in the treated group. Two baboons in the treated group also showed improvement of axonal function as assessed by SEP. No significant difference was observed with MRI, however, histologic study revealed that the lesions were significantly smaller in the treated group. Based on these observations we conclude that a week of nimodipine treatment following spinal cord injury enhances SCBF, limits the size of the spinal cord lesion, and perhaps improves functional recovery.
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PMID:Effects of nimodipine on posttraumatic spinal cord ischemia in baboons. 841 Dec 20

The conversion from xanthine dehydrogenase (XD) to xanthine oxidase (XO) and the effect of trifluoperazine (TFP), a calmodulin inhibitor, on the conversion were examined during the normothermic ischemia of the rat small intestine. Rat jejunums were stored in lactated Ringer's solution (LR) at 37 degrees C for various hours after intravascular flushing with LR. The extents of the conversion from XD to XO (%XO) constituted 21.1% +/- 3.0%, 36.2% +/- 7.0%, 63.2% +/- 8.1%, and 88.2% +/- 8.6% after 0, 2, 4, and 6 hours of the preservation, respectively (control group). The preservation without the intravascular flushing showed significant increase in the %XO (99.5% +/- 6.0%) only after 6 hours compared with those in the control group (P < .05). When the intestines were stored in LR containing 50 mg/L of TFP at 37 degrees C, or stored in LR at 37 degrees C after the intraperitoneal pretreatment with 10 mg/kg of TFP 1 hour before laparotomy showed significant decrease in the extents of the conversion after 4 hours (P < .005) and 6 hours (P < .025) of the preservation, compared with those in the control group. When the dose of TFP for the pretreatment was increased to 50 mg/kg, the suppressive effect on the conversion was found even after 2 hours (P < .025) as well as after 4 hours (P < .005) and 6 hours (P < .025) of the preservation. These results suggest that TFP could be effective on reducing the XO-mediated postischemic reperfusion injury by means of inhibiting the conversion during ischemia of the rat small intestine.
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PMID:Conversion of xanthine dehydrogenase to xanthine oxidase during ischemia of the rat small intestine and the effect of trifluoperazine on the conversion. 848 75

Pharmacologic manipulation of free flaps to enhance tolerance to ischemia has become a subject of great interest in the research literature. In an effort to improve survival, perfusion washout of experimental free flaps was performed following an episode of primary ischemia. The perfusates utilized were lactated Ringer's solution (LR), University of Wisconsin solution (UW), a high-molecular-weight medium used in organ preservation, and urokinase, a thrombolytic agent. Seventy-five rats were used in this study and divided into groups of 5 each. A 3 x 6-cm abdominal free flap based on the superficial inferior epigastric vessels was raised in each rat. The free flaps were subjected to either 12 or 18 hr of primary ischemia. Following the period of ischemia, perfusion washout was performed with either LR, UW solution, or urokinase at increasing concentrations alone or in combination with UW solution. Urokinase was first evaluated as a perfusate alone at increasing concentrations. In the 12-hr ischemia group, free-flap survival was shown to increase from 0 percent in the LR-perfused flaps to 20 percent, 60 percent, and 80 percent in flaps perfused with 12,500, 25,000, and 100,000 U of urokinase, respectively (p < 0.05). A similar increase in survival was demonstrated in the 18-hr ischemia group, where 0 percent, 20 percent, and 40 percent of flaps survived following perfusion with 12,500, 25,000, and 100,000 U of urokinase, respectively (p < 0.05). Urokinase was then perfused along with UW solution to evaluate the combined effect on flap survival.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The additive beneficial effect of UW solution and urokinase on experimental microvascular free-flap survival. 851 98

Intestinal barrier function is compromised following severe hemorrhage which may allow bacterial translocation (BT) to occur and subsequently initiate a systemic response leading to multiple system organ failure (MSOF). This study compared BT following hemorrhage and resuscitation with lactated Ringer's solution (LR) or diaspirin crosslinked hemoglobin solution (DCLHb). Rats (250-350 grams) were hemorrhaged to a base deficit of 15 +/- 2 mmol/L and immediately resuscitated with either 3:1 LR or 1:1 DCLHb based on shed blood volume. Four hours following resuscitation, the mesenteric lymph node complex was harvested, homogenized and plated onto MacConkey and Columbia CNA agar culture media. Facultative anaerobic and obligate aerobic bacteria were identified 48 hours later in 11/22 (50%) LR-treated rats and in 4/21 (19%) DCLHb-treated rats (p < or = 0.05). Following resuscitation, base excess (BE) and central venous oxygen saturation (SvO2) were not only restored to baseline but were significantly greater (p < or = 0.05) in DCLHb-treated rats than in LR-treated rats. In a separate group of rats subjected to the same hemorrhage and resuscitation protocol, mean arterial pressure in DCLHb-treated rats, but not LR-treated rats, was restored to baseline by 15 minutes and remained at or above baseline for up to 4 hrs. Twenty-four hour survival was 50% in LR-treated rats and 77% in DCLHb-treated rats (p > 0.05). These data suggest that DCLHb is superior to LR in restoring tissue oxygen delivery, as judged by BE and SvO2. Furthermore, since DCLHb restores oxygen delivery and attenuates BT, early resuscitation with DCLHb may limit gut ischemia and subsequent gut barrier failure and hence prevent the development of sepsis, MSOF and subsequent death.
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PMID:Diaspirin crosslinked hemoglobin (DCLHb) attenuates bacterial translocation in rats. 855 39

This study evaluated the effect of systemic infusion of hypertonic mannitol on renal hemodynamics (aortic pressure [P]-renal blood flow [RBF] relationship, glomerular filtration rate [GFR], and effective renal plasma flow [ERPF]) during 50% reduction of left kidney blood flow. Conditioned mongrel dogs anesthetized with halothane were hydrated by continuous infusion of lactated Ringer's solution containing creatinine to measure GFR and p-aminohippurate (PAH), to measure ERPF. The left kidney was exposed and two hydraulic occluders were placed, one around the aorta just above the renal arteries and the other around the left renal artery. Experimental design consisted of measuring P near the left renal artery, RBF by electromagnetic flowmeter, and ERPF and GFR by clearance methods in both kidneys in response to stepwise reduction in the aortic pressure by aortic occlusion before and after 50% reduction in the left kidney blood flow. The P-RBF relationship, GFR, and ERPF thus obtained were compared with those obtained during systemic intravenous infusion of 20% mannitol for a period of 1 h. We found that 1) a transient increase occurred in RBF with step reduction of P from 80 to 60 mm Hg under control conditions; 2) reducing the RBF by 50% changed the shape of the P-RBF relationship from a convex to the P axis to a linear form with a marked shift toward the P axis; 3) infusion of mannitol, during reduced RBF, caused a significant shift of the P-RBF curve toward the RBF axis and returned the linear P-RBF relationship toward normal, but had no effect on altered yield pressure; and 4) infusion of hypertonic mannitol had slightly increased GFR and ERPF in the right (unconstricted) kidney. However, hypertonic mannitol significantly increased GFR and ERPF values in the left (constricted) kidney suggesting a beneficial effect of mannitol on ischemic kidney. The results are consistent with the hypothesis that infusion of hypertonic mannitol to ischemic kidney increases RBF, presumably by decreasing the intrarenal vascular resistance. We speculate that this compensatory response may be mediated either 1) by stimulating the release of a vasodilator substance (e.g., prostaglandins), or 2) by washing out interstitial sodium, thereby reducing the sensitivity of the renal vasculature to ischemia-induced stimulation of renin-angiotensin system.
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PMID:Effects of hyperosmotic mannitol infusion on hemodynamics of dog kidney. 861 Aug 95

Recent observations showed an improvement of hepatic macro- and microhemodynamics as well as survival rates after warm ischemia of the liver following treatment with N-acetylcysteine (NAC). In this study we assessed the influence of NAC on the hepatic microcirculation after orthotopic liver transplantation (OLT) using intravital fluorescence microscopy. OLT with simultaneous arterialization was performed in 16 male Lewis rats following cold storage in University of Wisconsin solution for 24 hr. Within the experimental group (n = 8) donors received NAC (400 mg/kg) 25 min before hepatectomy. In addition, high-dose treatment of recipients with NAC (400 mg/kg) was started with reperfusion. Control animals (n = 8) received an equivalent amount of Ringer's solution. Intravital fluorescence microscopy was performed 30-90 min after reperfusion assessing acinar and sinusoidal perfusion, leukocyte-endothelium interaction, and phagocytic activity. Treatment with NAC reduced the number of nonperfused sinusoid from 52.4 +/- 0.8% to 15.7 +/- 0.5% (p = 0.0001) (mean +/- SEM). Furthermore, we achieved a significant reduction of leukocytes adhering to sinusoidal endothelium (per mm2 liver surface) from 351.9 +/- 13.0 in controls to 83.6 +/- 4.2 in the experimental group (P = 0.0001). In postsinusoidal venules, treatment with NAC decreased the number of sticking leukocytes (per mm2 endothelium) from 1098.5 +/- 59.6 to 425.9 +/- 37.7 (P = 0.0001). Moreover, bile flow was significantly increased after therapy with NAC (4.3 +/- 1.2 vs. 2.2 +/- 0.7 ml/90 min x 100g liver) (P < 0.05). Phagocytic activity was not influenced by application of NAC. We conclude that high-dose therapy with NAC in OLT attenuates manifestations of microvascular perfusion failure early after reperfusion and should be considered as a means to reduce reperfusion injury.
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PMID:Impact of N-acetylcysteine on the hepatic microcirculation after orthotopic liver transplantation. 862 4

The effects of NBP on concentrations of some purine metabolites in extracellular fluid of rat striatum during global ischemia and reperfusion were studied. Global ischemia was produced by the four-vessel occlusion method. Push-pull cannula was implanted stereotaxically into the striatum of rat and was perfused with Ringer's solution at a flow rate of 2.5 microliters.min-1. The level of adenosine(Ade), inosine(Ino), hypoxanthine(Hyp) and xanthine(Xan) in perfusates were measured with HPLC connected with a UV detector. The results indicate that the levels of ade, ino, hyp and xan were significantly increased (about 3-5 times of initial value) during cerebral ischemia and reperfusion. NBP at the dose of 20 or 40 mg.kg-1 given intra-peritoneally 20 min before ischemia was shown to depress the increase of ade, ino, hyp and xan during ischemia and reperfusion dose dependently. But no change in the level of purine metabolites was found in sham operated rats. It has been known that harmful free radicals were produced when xan and uric acid were formed by xanthine oxidase during reperfusion. This might be important for the development of ischemic injuries. Our findings suggest that the effect of NBP might be beneficial for protection against post-ischemic neuronal damage.
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PMID:[Effect of dl-3-n-butylphthalide (NBP) on purine metabolites in striatum extracellular fluid in four-vessel occlusion rats]. 876 58


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