Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.10.1 (ERK)
 95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following renal ischemia under protection, the perfusion of the tubular system increases concomitant to the rise of GFR. The transport into urine of enzymes entering the tubular lumen due to ischemic injury is dependent on tubular flow. Thus, we examined if in the early postischemic phase urinary enzyme determinations can contribute to the evaluation of the ischemic injury despite the interference of a changing tubular washout. Canine kidneys were perfused with different protective solutions and subsequently rendered ischemic. From the beginning of reperfusion the endogenous creatinine clearance, the urine minute volume and the urinary LDH-concentration were determined. The urinary LDH-concentration allowed only a rough assessment of renal ischemic damage. The adjustment of the urinary LDH amounts to the GFR resulted in a better graduation according to the ischemic stress. With such a standardized LDH parameter the urinary LDH release was somewhat lower on the average when L-aspartate was added to the HTK solution in place of chloride. In conclusion, during the early postischemic recovery after renal protection the examination of the urinary enzyme release may be a useful diagnostic means for the assessment of the extent of the ischemic injury if an appropriate frame of reference is applied.
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PMID:Urinary LDH-release for evaluation of postischemic renal function. 265 82

We have employed a retroviral vector, ZN(Smu/S gamma 2b)tk1, as a substrate for detecting the presence of immunoglobulin heavy chain constant region (CH) gene switch (S) recombination activity in murine pre-B cells. ZN(Smu/S gamma 2b)tk1 contains a neomycin (neo) resistance gene in addition to the herpes simplex virus thymidine kinase (Htk) gene which is positioned between murine Smu and S gamma 2b sequences. Stable acquisition of the ZN(Smu/S gamma 2b)tk1 vector was selected in G-418 and switch region recombination within these proviruses was selected by resistance to the drug bromodeoxyuridine (BUdR). Fluctuation analyses of ZN(Smu/S gamma 2b)tk1 infected 18-8tk- and 38B9tk- pre-B lines revealed Htk gene inactivations with apparent frequencies of 5 X 10(-5) and 1 X 10(-5) events/cell/generation, respectively, while G-418 resistant Ltk- fibroblasts lost the HTK phenotype at an apparent rate of 4 X 10(-8). Southern blot analysis demonstrated that switch recombination caused the deletion of the Htk gene in all pre-B clones examined while the loss of Htk in Ltk- clones was not mediated by S region recombination. In 21 out of 24 pre-B clones, the recombinations involved the tandemly repetitive portions of the Smu and S gamma 2b sequences. These results demonstrate that the CH gene S region segments inserted into ZN(Smu/S gamma 2b)tk1 are sufficient for B-cell-specific recombination/deletion within the S region tandem repeats.
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PMID:Immunoglobulin heavy chain switch region recombination within a retroviral vector in murine pre-B cells. 303 95

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

Kidneys were perfused either with Euro-Collins-solution or with HTK-solution of Bretschneider. The perfusion pressure as well as the perfusion flow were measured during a six-minute perfusion. The perfusion resistance was higher in Euro-Collins-kidneys than during HTK-perfusion. The venous outflow of the kidney as well as the ureteral outflow was measured during each minute of the perfusion and has analysed for osmolality, and for sodium and potassium concentrations. In Euro-Collins-kidneys a complete "equilibration" of the extracellular space was not achieved, while during HTK-perfusion concentrations in the venous as in the tubular outflow, similar to those in the HTK-solution itself, could be reached. At the end of the different perfusions, tissue was analysed for biochemical parameters such as ATP, ADP, AMP and lactate as well as for morphological features. Lactate had increased and ATP had decreased during perfusion with Euro-Collins-solution, while ATP had not changed and lactate had decreased during perfusion with HTK-solution. Normal glomerular, tubular and dilated vascular structures can be seen after HTK-perfusion, while a glomerular and vascular contraction takes place during Euro-Collins-perfusion.
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PMID:Short-term perfusion and "equilibration" of canine kidneys with protective solutions. 310 3

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 first clinical use of Bretschneider's HTK-solution for in-situ-protection of the kidney in mild hypothermia is reported. By means of this protective method renal surgery can be performed in a bloodless field without permanent loss of renal function. After initial protective perfusion of the kidney no repeated perfusions or additional surface cooling must be done. There are no systemic side effects when the HTK-solution is applied appropriately.
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PMID:[Clinical use of the Bretschneider HTK cardioplegic solution for in situ protection of the kidney]. 312 52

A prospective consecutive study was undertaken to compare the hemodynamic effect of two cardioplegic solutions in CABG patients after bypass, and in relation to aorta occlusion time with the support of a automatic datalogging database. A total of 249 patients were randomized. One group received Bretschneider cardioplegic HTK solution (132 patients, group I) the other group received St. Thomas cardioplegic solution (117 patients, group II). The data was divided in four periods of aortic clamp time: less than or equal to 40 min (group I 26 patients, group II 32 patients); 41-60 min (group I 49 patients, group II 47 patients); 61-80 min (group I 30 patients, group II 29 patients); and greater than 80 minutes (group I 27 pts, group II 9 patients). Anesthesia regime and therapeutic drugs and infusions were given in both groups in similar dosages. Within both groups HR, CO, PAP, PCWP increased after bypass in relation to prebypass values. SVR decreased in both groups by 30%, MAP and PVR decreased only in group I. Between group I and II differences were found in the CI (3.0 vs. 3.3 l/min/m2), MAP (70 vs. 76 mmHg), PMAR (18 vs. 16 mHg), and SVR (827 vs. 954 dyn.sec.cm-5). In significantly more of the patients in group I, sinus rhythm started spontaneously after the release of the aorta clamp (39.5% vs. 20.4%, p less than 0.005). Patients in group I needed temporarily a pacemaker after bypass in 6.3% cases (in 1.1% of patients in group II,). There was no relation of the hemodynamic data in relation to aorta occlusion time within the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical effect of Bretschneider-HTK and St. Thomas cardioplegia on hemodynamic performance after bypass measured using an automatic datalogging database system. 314 85

Long-term preservation of dog hearts was performed over 24 h using Bretschneider-HTK cardioplegia and cold storage. Preservation was assessed in terms of conservation of myocardial tissue levels of high-energy phosphates (HEP) and functional outcome after cardiac transplantation. Serial left ventricular biopsies were taken and analysed for ATP, ADP, AMP, adenosine, inosine, hypoxanthine, xanthine and creatine phosphate. Myocardial structure was studied by electron microscopical examination of a similar biopsy specimen. Cardiac performance was measured before and after cardiac transplantation. Several techniques of cardioplegic arrest were studied: single dose cardioplegia, multidose cardioplegia and continuous perfusion with the cardioplegic solution. In all groups, the hearts were stored at 0.5 degree C for 24 h. In the group of single dose Bretschneider-HTK cardioplegia, myocardial ATP content after 24 h of cold storage was only 25% of control. The total sum of nucleotides at that time interval was however 65% of the control value. Reperfusion of these hearts using a support dog (whole blood reperfusion) did not result in any recovery of ATP. Creatinine phosphate however showed an overshoot. Accumulated nucleosides were washed out. The hearts showed electrical activity but were severely arrhythmic. Contractility was poor. In the group of multidose Bretschneider-HTK cardioplegia, HEP preservation was better than after single dose cardioplegia. ATP content was about 50% of control. The total sum of nucleotides was 85% of control. Ultrastructural assessment of the myocytes revealed only slight ischaemic damage to the mitochondria. Reperfusion on cardiopulmonary bypass after cardiac transplantation did not show any restoration of ATP, but a steady catabolism of HEP. The nucleosides adenosine and inosine were not washed out upon reperfusion. After cardiac transplantation, none of these hearts could be weaned from cardiopulmonary bypass due to irreversible low cardiac output. Histological examination demonstrated irreversible myocardial tissue damage. In the group of continuous cold Bretschneider cardioplegia, HEP content was completely preserved throughout the 24 h of perfusion. Ultrastructure of the myocytes was normal. Reperfusion of the transplanted hearts showed a mild breakdown of ATP to 70% of control values accompanied by a slight accumulation of nucleosides. Haemodynamic recovery however was perfect and none of the hearts needed positive inotropic support. Myocytes after reperfusion had a normal subcellular appearance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Energy state of the myocardium during long-term cold storage and subsequent reperfusion. 327 28


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