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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ischemic damage following liver transplantation (LTX) is predominantly located at the endothelial cell level and is a major cause for a disturbance of microcirculation. The present study was designed to test the hypothesis that changes in the quality of organ preservation are correlated with changes in microcirculation: 16 pigs underwent LTX, preservation by Bretschneider's HTK-solution (Histidin, Tryptophan, alpha-Ketoglutarat) complemented by indomethacin (50 mumol/L). Cold ischemia times were 9 hr (n = 8) and 18 hr (n = 8), respectively. Using the H2-clearance technique, hepatic microcirculation was measured before, 30 min, and 20 hr after LTX. Normal tissue perfusion was 107 +/- 16 ml/100 g/min, at 30 min posttransplantation 91 +/- 13 ml/100 g/min in the short-term and 48 +/- 7 ml/100 g/min in the long-term preservation group. Whereas no animal of the long-term preservation group survived longer than 8 hr, all animals of the short-term preservation group survived, and tissue perfusion could be measured 20 hr postoperatively (101 +/- 19 ml/100 g/min). At 30 min postoperatively, all surviving animals had tissue perfusion rates greater than 70, and all nonsurvivors had values below 60 ml/100 g/min. We conclude therefore that the extent of decrease of microcirculation after LTX may be a useful predictor of organ function and survival.
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PMID:Evaluation of preservation damage after porcine liver transplantation by assessment of hepatic microcirculation. 225 66

Imperative indications for organ-sparing surgery of renal tumors are given mainly in existing or imminent restriction of renal function. Organ-sparing excision of renal tumors under in-situ protection with HTK-solution compared with operations without protection have the following advantages: 1. reduced blood loss, 2. longer ischemia, 3. better tissue differentiation with benefit for radicality, 4. shorter hospital stay.
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PMID:["Imperative indication" for organ-preserving kidney tumor surgery]. 226 26

Several functional parameters were applied in an experimental model of ischemia to test the ability to localize the distribution of tubular lesions. Canine kidneys were perfused with protective solutions and rendered ischemic for definite periods. Renal function was determined during a subsequent 3-h reperfusion. The pattern and the extent of renal injury were influenced by varying the duration of ischemia and by modifying the protective solution used. The results suggest that by employing an appropriate selection of parameters it is possible to allocate renal injury to definite sections of the tubules. According to such an evaluation, under protection with HTK-solution, the proximal tubule limits the tolerance of renal ischemia. The thick ascending limb shows some vulnerability that is aggravated by disadvantageous modifications of the protective solution and that may become more pronounced in the course of reperfusion. In contrast, more distal parts of the nephron retain a remarkable reserve transport capacity after a tolerable level of ischemia.
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PMID:Postischemic diagnostic localization of tubular lesions. 231 10

Clinically applied methods of cardioplegia show very different effects on the rapidity of decay of energy-rich phosphates as well as on kind and progression of ultrastructural alterations of the ischemic myocardium. Comparing the methods of cardioplegia according to Kirklin, St. Thomas's Hospital and Bretschneider (solution HTK) with pure ischemia at 25 degrees C (model A) and Kirklin's or St. Thomas's cardioplegia and subsequent 210 min or HTK cardioplegia and 300 min ischemia at 22 degrees C plus 20 min subsequent reperfusion (model B) leads to the following results: Model A: Compared with pure ischemia cardioplegia according to Kirklin and the St. Thomas's Hospital slows down the decay of the left ventricular ATP-concentration by a mean factor of 3 and the progression of structural alterations of the left ventricular subendocardium by a factor of 2. HTK retards the ATP-decay by a factor of 6, the alterations of ultrastructure by a factor of 6.5. St. Thomas's solution, in contrast to all other methods of cardioplegia, at the onset of ischemia already causes a cellular edema of myocytes; the edema increases during ischemia, and at the ATP-concentration of 4 mumol per gram myocardium is more pronounced than with pure ischemia, Kirklin or HTK. After application of Kirklin's solution, in contrast, a cellular edema of capillary endothelia develops during ischemia, which at 4 mumol ATP is more pronounced than with each of the other methods. Model B: After global ischemia until the ATP-concentration of left ventricular myocardium is 4 mumol/g and a subsequent 20 minutes post-ischemic recovery the ultrastructural alterations in principle resemble those occurring during ischemia (model A).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial protection: left ventricular ultrastructure after different forms of cardiac arrest. 244 33

The addition of the disaccharides maltose (10, 20, 30 mM) and sucrose (30, 60 mM) to Bretschneider's organ protective HTK solution was evaluated to improve renal protection by an enhanced glycolytic energy supply. Canine kidneys were perfused for 8 min with either HTK solution or HTK solution containing additional disaccharides. After nephrectomy the kidneys were incubated at 25 degrees C and metabolic parameters were determined at regular intervals. Maltose and sucrose are slowly cleaved during renal ischemia but maltose distinctly faster than sucrose. Maltose increases intraischemic ATP supply. However, 30 mM maltose was no better than 10 mM. 60 mM sucrose was about as effective for glycolysis as 10 mM maltose. However, possibly due to fructose release there was an accelerated decrease of adenine nucleotides with sucrose. Although fructose enters glycolysis it seems to have negative side-effects. Hence, probably neither sucrose nor fructose are appropriate for renal substrate supply during ischemia.
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PMID:Intraischemic metabolic effects of different disaccharides on protected canine kidneys. 251 81

The cardioplegic solution HTK of Bretschneider was used for canine kidney protection. The kidneys were perfused with this solution for 6-10 min prior to the induction of ischemia. The kidneys were left in-situ for 60, 90, 120 and 135 min ischemia time at a temperature of 25-34 degrees C (n = 13). As a control group we used unilateral nephrectomized dogs (n = 9). After unilateral nephrectomy an elevated plasma creatinine in comparison to preoperative values was observed. After 60 and 90 min under HTK-protection the postoperative plasma creatinine was not elevated compared to the control group. After 120 min of ischemia creatinine level was slightly increased to an average of 2.1 mg% on the first and second postoperative day. These experiments indicate the protective effect of the cardioplegic solution for canine kidney preservation in situ.
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PMID:Post-ischemic renal function after kidney protection with the HTK-solution of Bretschneider. 309 46

Protection-methods, for an improvement of ischemic tolerance of the kidney, can be investigated by intraischemic analysis of metabolism and structure. A definite proof for the effectiveness of a protection method is only postischemic function in combination with postischemic structure-regeneration. For this reason postischemic function was chosen for examination of the protective ability of the Euro-Collins-solution and the HTK-solution during a two-hour reperfusion period. We perfused 57 dog kidneys either with the Euro-Collins- or with the HTK-solution prior to ischemia. Ischemia was 7, 60, 90 and 120 min after Euro-Collins-perfusion and 7, 120, 150 and 180 min after HTK-protection. The protected and ischemic kidneys were left in-situ; the mean ischemic temperature was therefore 20-25 degrees C for the shorter ischemic times and 30-34 degrees C for the longer ischemic times. We compared the protected and ischemic kidneys with 14 untreated kidneys (control). Postischemic renal blood flow (RBF) was measured by an electromagnetic flow probe; renal oxygen consumption (V02/min) was calculated by arterio-venous oxygen content difference and the renal blood flow. If urine could be collected, the glomerular filtration rate (GFR) was measured by an endogenous creatinine clearance. In Euro-Collins-protected kidneys after 60-120 min ischemia the RBF was after 15 min of reperfusion between 20 and 100 ml/min/100 g. After 30 min we got values of 100-200 ml/min/100 g. The V02/min, which was in the control kidneys between 5-6 ml/min/100 g, was about 2 ml/min/100 g.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Kidney function parameters following ischemia stress using the Euro-Collins solution or the Bretschneider cardioplegic HTK solution]. 310 96

Energy reserves (TAN) and anaerobic substrates (glucose, glycogen) are lower in renal than in myocardial tissue. Euro-Collins-solution contains nearly 200 mmol/l glucose, while the HTK-solution of Bretschneider contains none. Therefore the influence of glucose on kidney lactate production, on energy reserves (TAN), intrarenal pH and on morphology during the protection of ischemic kidneys was analysed using either Euro-Collins-solution, or modified "Euro-Collins-solution", containing mannitol instead of glucose, or HTK-solution with and without the addition of 5, 10 and 20 mmol/l glucose. Glucose content changed during kidney perfusion with Euro-Collins-solution from about 60 to 800 mumol/gdw. While intrarenal pH decreased from 7.1 to 5.1 in Euro-Collins-kidneys during 420 min of ischemia at 25 degrees C, pH decreased to 6.7 with the modified, mannitol containing "Euro-Collins-solution". In HTK-protected kidneys intrarenal pH decreased with increasing glucose addition to the solution. Although Total Adenine Nucleotides are highest at the end of ischemia with Euro-Collins-solution, structural protection after the same ischemic stress was best in HTK-protected kidneys without glucose addition. We conclude that glucose stimulated lactate production, reduced interstitial pH in the kidney even in combination with a highly buffered solution and that it might cause greater membrane permeability leading to a structural deterioration. Mannitol seemed more appropriate than glucose in this respect, although other substances, which provide energy substrate and prevent structural damage, may exist.
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PMID:Effects of glucose in protected ischemic kidneys. 311 45

In 110 canine kidneys, we examined the time course of energy rich phosphates, lactate, intrarenal ph and renal morphology with Euro-Collins- or with HTK-protection of Bretschneider and compared these findings with unprotected kidneys during complete ischemia at 1 degree C and at 25 degrees C. Both kidney protective solutions prolonged energy-rich phosphate-decline by a factor of 3-4 compared with that of unprotected kidneys. The lactate increase was greater in Euro-Collins-protected kidneys than in HTK-protected and in unprotected kidneys, leading to pH values of 6.5 in Euro-Collins and to 6.4 in unprotected kidneys after 24 hours, in contrast to a pH-value of 7.3 with HTK-protection. This may be the reason for structural deterioration seen in unprotected and in Euro-Collins-protected kidneys after 12, and 48 h of ischemia at 1 degree C, whereas in HTK-protected kidneys a sufficient preservation of structure can be seen. In one human kidney, protected with Euro-Collins-solution, we were able to show that at 1 degree C intrarenal pH and lactate accumulation is similar to the levels in canine kidneys. In Euro-Collins preserved kidneys lactate accumulation at 25 degrees C is even greater than at 1 degree C, leading to inhibition of energy metabolism and to structural deterioration, whereas HTK-solution, because of its high buffer concentration, is able to maintain ischemic metabolism leading to sufficient protection of intrarenal pH and of adenine nucleotides as well as structural protection at 1 degree C and at 25 degrees C.
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PMID:Metabolic, energetic and structural changes in protected and unprotected kidneys at temperatures of 1 degree C and 25 degrees C. 312 49

The influence of temperature (5, 15, 25, and 35 degrees C) on the degree of tissue acidification was examined using 74 canine kidneys with simple ischemia or after protection of the kidneys with Euro-Collins solution or with the HTK-solution of Bretschneider. At an incubation temperature of 5 degrees C, the intrarenal pH value in HTK-protected kidneys is continuously higher than 7.3 during 36 hr of ischemia. In Euro-Collins kidneys the pH value decreases to a pH of 6.4 during this time. In simple ischemic kidneys pH is 6.3 after 36 hr. At 15 degrees C the pH value falls to a lower level in Euro-Collins kidneys than in purely ischemic kidneys, but the pH in HTK-protected kidneys is higher than 6.9 for 24 hr. At 25 degrees C, and especially at 35 degrees C the intrarenal acidosis in Euro-Collins kidneys is much stronger than in unprotected kidneys, and the pH in HTK-protected kidneys does not decrease below 6.7. The lactate production in simple ischemic kidneys and in HTK-protected kidneys is nearly the same (80-100 mumol/gdw), although Euro-Collins kidneys have a steeper increase and reach higher lactate levels (330 mumol/gdw). The HTK solution guarantees satisfactory protection against damaging acidosis over the whole temperature range (5-35 degrees C), but the Euro-Collins solution leads to a stronger and more dangerous acidosis the higher the temperature.
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PMID:Effects of preservation conditions and temperature on tissue acidification in canine kidneys. 399 49


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