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Patellofemoral relationships were analyzed in 11 patients (13 knees) with patellar dislocation and 15 asymptomatic subjects (15 knees) at 0 degree and 20 degrees of flexion. The measurements were made from five consecutive axial images through the patellofemoral joint. The six indices measured were lateral patellar tilt (LPT), lateral patellofemoral angle (LPA), lateral patellar displacement (LPD), patella-lateral condyle index (L/PW), congruence angle (CA), and sulcus angle (SA). The reproducibility of the method was evaluated. The difference between the two study groups was more evident at 0 degree than at 20 degrees of knee flexion. Significant differences were noted between measurements made at different levels of the joint, particularly in the controls. Isometric contraction of the quadriceps muscle lateralized and tilted the patella slightly in both groups. L/PW with and without quadriceps muscle contraction, and LPA with reference to the anterior condyles differentiated between the two study groups most clearly. LPT and LPA with reference to the anterior condyles differentiated the study groups better than LPT and LPA with reference to the posterior condyles. The reproducibility was good except for inter-observer comparison of CA and SA. The use of an imaging plane selected at the midpoint of the patellar articular cartilage increases the sensitivity of the measurements, since it takes into account both the height of the patella and the tendency towards lateralization. These results indicate that patellar tilt is best measured with the LPA index and patellar lateralization with the L/PW index at 0 degree knee flexion. This study should always include isometric contraction of the quadriceps muscle. [ABSTRACT FROM AUTHOR]

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Conservative therapy has been recommended for the treatment of a chronic cuff lesion with relatively good results. However, recent reports about operative treatment of cuff lesions have yielded more favorable results. Although the current literature seems to favor early treatment, there is an ongoing debate about the timing of the operation. During a 16-year period, 415 chronic full-thickness rotator cuff tears were operated on at our institution. The indication for operative treatment was persistent, severe or moderate pain at rest and impairment of shoulder function after initial conservative treatment. At follow-up, the symptoms were assessed by an interview, and all patients were clinically examined. Pain, function, range of active forward flexion, active abduction, strength (manual muscle testing), and patient satisfaction were recorded, and the results were evaluated by the University of California, Los Angeles shoulder rating scale. On the basis of our results, we recommend operative treatment of the rotator cuff for all cases in which the tear is full thickness, regardless of tear size, if patients have any symptoms, especially pain.

Seventeen patients (18 knees) with a history of one or more patellar dislocations underwent Elmslie-Trillat (9 knees [group 1]) or Roux-Goldthwait (9 knees [group 2]) patellar realignment surgery. Anterior knee pain was evaluated with a questionnaire, and lateral patellar displacement and tilt were analyzed by magnetic resonance imaging both pre- and postoperatively. Postoperative evaluations were performed after 44 and 50 months (mean) in groups 1 and 2, respectively. The Elmslie-Trillat procedure provided better subjective relief of anterior knee pain and symptoms. One redislocation occurred in each group. Both procedures relieved excessive patellar lateralization, but the effect on patellar tilt was less marked. In patients who underwent the Roux-Goldthwait operation, a less pronounced correction of tilt and lateralization appeared to correlate with more satisfactory subjective results.

Objective: To evaluate the in vivo production of prostacyclin and thromboxane A2 during the initial phase of experimental fat embolism as assessed, respectively, by determinations of urine 2,3-dinor-6-ketoprostaglandin F1alpha and 11-dehydrothromboxane B2 excretion., Design: Randomized, controlled trial., Setting: Animal laboratory., Subjects: Twenty seven domestic pigs, weighing 24 to 31 kg., Interventions: All pigs were anesthetized and mechanically ventilated during the experiment. Eighteen pigs were subjected to an intracaval infusion of 10% allogeneic bone marrow suspension at a dose of 100 mg/kg over 5 mins. Nine pigs received only bone marrow suspension (fat embolism group). Nine pigs were given an intravenous bolus of aspirin (300 mg) 1 hr before the bone marrow suspension infusion. After the induction of fat embolism, intravenous aspirin was administered at a dose of 150 mg/hr for 2 hrs (aspirin-treated group). Nine pigs were infused with saline (control group)., Measurements and Main Results: In the fat embolism group, cardiac index decreased within 30 mins, while mean arterial pressure remained unchanged. Central venous pressure and pulmonary artery occlusion pressure remained relatively stable over time in the animals with fat embolism. Mean pulmonary arterial pressure and pulmonary vascular resistance increased immediately after the bone marrow suspension infusion from 23 +/- 0.8 (SEM) to 34 +/- 1.3 mm Hg and from 305 +/- 28 to 585 +/- 45 dyne x sec/cm5, respectively; these variables remained increased throughout the study period. Simultaneously, pulmonary shunt in the fat embolism group increased persistently from the baseline of 12.3 +/- 2.8%, and reached its maximum of 26.1 +/- 4.8% at the end of the experiment. Instant and gradual decreases in PaO2 (from 95 +/- 4 to 67 +/- 5 torr [12.6 +/- 0.5 to 8.9 +/- 0.7 kPa]), hemoglobin oxygen saturation (from 97.2 +/- 0.4 to 91.8 +/- 1.8%), and oxygen delivery (from 16.3 +/- 1.0 to 12.6 +/- 0.4 mL/min/kg) were observed in the fat embolism group. In the bone marrow suspension-infused animals, urine 2,3-dinor-6-ketoprostaglandin F1alpha excretion increased transiently from 451 +/- 63 up to 1466 +/- 499 pg/micromol creatinine, while urine 11-dehydrothromboxane B2 excretion increased transiently from 385 +/- 36 up to 2307 +/- 685 pg/micromol creatinine. In the aspirin-treated animals, urinary excretion of these prostanoid metabolites was reduced by 81% and 88%, respectively. The changes in mean pulmonary arterial pressure and PaO2 were ameliorated, and the alterations in pulmonary shunt and SaO2 were abolished in the animals with aspirin treatment., Conclusions: Pulmonary hypertension, increased pulmonary vascular tone, and increased pulmonary shunt are hallmarks of the present fat embolism model. These hemodynamic responses may, at least partly, be related to the changed balance between prostacyclin and thromboxane A2 production.

Objective: To investigate the catalytic activity of phospholipase A2 in serum during the early phase of experimental fat embolism., Design: Randomised controlled experimental study., Setting: Animal laboratory, Finland., Subjects: 18 domestic pigs weighing 25-31 kg., Interventions: Allogeneic bone marrow suspension at a dose of 100 mg/kg was infused intracavally in 9 anaesthetised, mechanically ventilated, and haemodynamically monitored pigs; 9 control pigs received saline., Main Outcome Measures: Central haemodynamics, blood gases, catalytic activity of phospholipase A2., Results: In the fat embolism group, there were significant increases in mean pulmonary arterial pressure (p < 0.001), pulmonary vascular resistance (p < 0.001) and pulmonary shunting (p < 0.05) and simultaneously, systemic oxygenation was significantly impaired. The animals with fat embolism developed gradual fever and leucocytosis, whereas the catalytic activity of phospholipase A2 remained relatively unchanged., Conclusion: In this experimental model the measurement of serum phospholipase A2 activity does not provide a useful tool for the early detection of experimental fat embolism.

Objective: To investigate the acute effects of experimental fat embolism on splanchnic and peripheral perfusion and oxygenation in pigs., Design: Randomized, controlled trial., Setting: Animal laboratory., Subjects: Eighteen domestic pigs, weighing 25 to 31 kg., Interventions: The 18 pigs were randomized to either the fat embolism or control groups. Nine anesthetized and mechanically ventilated pigs were intracavally infused with a 10% allogeneic bone marrow suspension at a dose of 100 mg/kg over 5 mins (the fat embolism group); nine control pigs received normal saline in the same volume and speed (control group)., Measurements and Main Results: Mean pulmonary arterial pressure, pulmonary vascular resistance, and pulmonary shunt increased, and PaO2 decreased immediately after the bone marrow suspension infusion. In the fat embolism animals, oxygen delivery decreased, oxygen content difference widened, and total oxygen consumption remained high, indicating enhanced oxygen extraction. Further, superior mesenteric artery blood flow and mesenteric oxygen delivery decreased, while intramucosal pH in the small bowel was stable. Subcutaneous PO2 decreased in both groups, whereas transcutaneous PO2 decreased only in the animals receiving bone marrow suspension. Skin red cell flux showed no significant changes., Conclusions: The present model of fat embolism results in significant impairment in systemic oxygenation. Despite this fact, the intestinal oxygenation remains unaffected probably due to sufficient compensatory mechanisms. Transcutaneous PO2 measurements may provide a useful index for early detection of fat embolism.

A new questionnaire was used to evaluate subjective symptoms and functional limitations in patellofemoral disorders. The questionnaire was completed independently by four groups of female subjects: controls (N = 17), and subjects with anterior knee pain (N = 16), patellar subluxation (N = 16), and patellar dislocation (N = 19). The questionnaire mean scores for the groups were 100, 83, 68, and 62 points, respectively (p < 0.0001). The items dealing with abnormal painful patellar movements (subluxations) (p < 0.0001), limp (p < 0.0001), pain (p < 0.0001), running (p < 0.0001), climbing stairs (p < 0.0001), and prolonged sitting with the knees flexed (p < 0.0001) differentiated the study groups most clearly. We recommend that these questions be asked when taking a standardized clinical history of an anterior knee pain patient. We also analyzed lateral patellar tilt and displacement by magnetic resonance imaging (MRI) in 28 subjects with patellar subluxation or dislocation. Low questionnaire sum score correlated best with increased lateral patellar tilt measured during quadriceps contraction in 0 degree knee flexion. It seems that a tendency to lateral patellar tilt during quadriceps contraction causes anterior knee pain and can be imaged in knee extension when the patella is not fully supported by femoral condyles.

Background and Methods: Renal cortical and serum carnitine concentrations were studied in seven anesthetized beagle dogs in which acute circulatory collapse was induced by an iv injection of Escherichia coli endotoxin, 0.5 mg/kg given over 15 mins. Four controls received normal saline., Results: The endotoxin injection resulted in cardiac depression, renal hypoperfusion, acidosis with a decrease in urinary output, and hematuria. Arterial and renal venous free carnitine concentrations increased significantly in endotoxemia during the 5-hr experiment, but remained low and unchanged in the controls. Circulating acyl-carnitine concentrations underwent no essential changes in either group. Total, free, and acyl-carnitine concentrations decreased in endotoxic renal tissue., Conclusions: These data suggest that endotoxemia decreases carnitine concentrations in the renal cortex, but increases free carnitine concentrations in the circulation.

Circulatory changes and renal uptake of free fatty acids (FFA), glycerol and triglycerides were studied in ten adult beagle dogs during pentobarbital anesthesia. Six dogs were injected intravenously with E. coli endotoxin 0.5 mg/kg over 15 min and four control dogs received saline. Cardiac depression, hypotension, renal hypoperfusion and acidosis resulted in endotoxin shock. Arterial FFA concentrations increased significantly 2 hours after onset of shock whereas renal venous FFA levels remained rather stationary during the 5-hour study. Arterial and renal venous glycerol levels increased during the first two hours and decreased thereafter. Unchanged triglyceride levels were observed in endotoxin shock. The renal uptake of FFA increased with increasing arterial FFA concentrations. Net renal uptake of glycerol and triglycerides were observed as well. Blood concentrations and renal uptake of fats and glycerol remained relatively stationary in the control animals through the observation period. These data suggest renal ability to consume FFA, glycerol and triglycerides during endotoxin shock.

Renal cortical and medullary tissue pO2 and pCO2 were measured by means of implanted Silastic tonometers during arterial occlusion and graded hemorrhage in dogs. The results of studies of tissue pO2 decay curves after interruption of renal circulation suggest that a mean critical pO2 level for oxygen consumption is 15 millimeters of mercury for the cortex and 13 millimeters of mercury for the medulla. Aerobic oxidative metabolism ceased at a pO2 value of 6 millimeters of mercury in both tissue layers. At this phase, carbon dioxide was produced anaerobically in both tissue layers. In graded hemorrhage, the critical pO2 level for oxygen consumption and the minimum pO2 value for aerobic oxidative metabolism were reached earlier in the cortex than in the medulla, which may contribute to the frequent occurrence of ischemic damage and necrosis in the renal cortex after severe hemorrhagic shock.

Renal cortical tissue gas tensions, systemic oxygen supply and some features of energy metabolism and central hemodynamics were recorded in splenectomized dogs during graded hemorrhage and subsequent reinfusion of shed blood. Renal cortical partial pressure of oxygen and carbon dioxide responded rapidly to changes in blood volume and cardiac output. Lowest cortical partial pressure of oxygen values and highest cortical partial pressure of carbon dioxide levels were achieved at a maximal 50 percent blood loss. The decrease in arterial pressure, blood hemoglobin and hematocrit as well as the increase in blood lactate concentration lagged behind blood loss. Renal cortical partial pressure of oxygen, arterial pressure and cardiac output responded rapidly to reinfusions of withdrawn blood, while the cortical partial pressure of carbon dioxide, heart rate, arterial pH and blood lactate concentration returned to initial levels more slowly. Arterial blood gases remained normal throughout the observation period and did not provide an adequate index of tissue oxygenation. In contrast, the partial pressure of oxygen of the renal cortex proved an excellent and sensitive indicator of renal perfusion during hemorrhagic shock and its management.

Altogether 540 succesful insulin tests were performed on 377 patients after vagotomy, on 316 patients less than three months after the operation (early phase) and on 182 patients between three months and nine years after (late phase). The proportion of positive insulin test responses after vagotomy and antral resection was similar in the selective gastric (SV) and truncal vagotomy (TV) groups (10.7% and 11.8% respectively in the early phase) and remained the same during follow-up (12.5% and 9.3% in the late phase). In the vagotomy and drainage group there were significantly fewer positive test responses in the early phase after SV (15.6%) than after TV (36.4%), but in the late phase the incidence was similar (56.7% and 55.6%). There was a significant rise in the number of positive responses after SV and drainage during follow-up (from 15.6% to 56.7%). Insulin-stimulated peak acid output (I-PAO) was about the same in the vagotomy and drainage group after SV and TV (3.52 and 5.03 mmol/h in the early phase and 4.20 and 4.93 mmol/h in the late phase). Although the number of Hollander positive insulin tests after vagotomy and drainage increased during follow-up, no corresponding changes were seen in I-PAO. There was no evidence of vagal reinnervation.

Changes in arterial plasma levels of atrial natriuretic factor and catecholamine release were studied in 11 beagle dogs during pentobarbital anesthesia. Seven dogs were injected intravenously with Escherichia coli endotoxin, 0.5 mg/kg over 15 min. Four control dogs received only saline solution. The endotoxin injection resulted in cardiac depression,, hemoconcentration, acidosis and renal hypoperfusion. The central venous pressure remained relatively unchanged in both groups during the 2-hour study. The concentrations of epinephrine, norepinephrine and the norepinephrine metabolite 3,4-dihydroxyphenylglycol increased in arterial plasma during the acute hypodynamic endotoxin shock. In the control dogs the levels of these hormones remained very low and constant. Increased circulating levels of atrial natriuretic factor were observed in endotoxin shock with renal hypoperfusion, unchanged central venous pressure and no concomitant tachycardia.

Renal oxygen and lactate metabolism as well as central and renal hemodynamics were investigated in hemorrhagic shock in dogs. The animals were bled progressively until a 40-50% blood loss was achieved. Following a 20-, 40-, 60-, or 80-minute shock phase the shed blood was gradually returned. The effect of acute total ischemia on renal oxygen metabolism was studied during arterial occlusion. The renal cortical and medullary PO2 and PCO2 were recorded by means of implanted Silastic tonometers. The mean baseline cortical PO2 was 35 mmHg and the corresponding medullary PO2 25 mmHg. The renal cortical PO2 responded promptly to hemorrhage and declined in parallel with the cardiac output and renal blood flow. Hypoxia became more severe in the cortex than in the medulla during hemorrhagic shock. The response of both the cortical and the medullary PO2 to blood return increased with prolongation of the preceding shock phase. After one hour of shock, or more, the tissue oxygen tensions exceeded the prehemorrhage levels. Concomitantly, the renal blood flow and oxygen consumption were depressed below the initial values. The results of the studies of tissue PO2 decay curves after renal arterial occlusion suggested that the mean critical PO2 level for oxygen consumption is 15 mmHg for the cortex and 13 mmHg for the medulla. Aerobic oxidative metabolism ceased at a PO2 value of 6 mmHg in both tissue layers. In hemorrhagic shock, the critical PO2 level for oxygen consumption was reached earlier in the cortex than in the medulla. The minimum PO2 for aerobic oxidative metabolism was recorded in the cortex during severe shock, but not in the medulla. Renal lactate uptake remained rather unaffected during graded hemorrhage. The extreme impairment of renal perfusion associated with hemorrhagic shock produced a parallel decrease in the cortical PO2 and lactate utilization. Renal lactate utilization became limited at the cortical PO2 level, which coincided with the critical PO2 measured during the arterial occlusion. Lactate utilization ceased at a cortical PO2 level that was analogous with the minimum PO2 for aerobic oxidative metabolism determined after arterial occlusion. After reinfusion of shed blood renal lactate uptake failed to return to the prehemorrhage level. The renal lactate uptake was inversely related to the arterial pH under baseline conditions whereas after blood return the correlation between these parameters was less significant. The present findings suggest that in hemorrhagic shock renal metabolism may become limited by hypoxia and the susceptibility to the development of hypoxia is greater in the cortex than in the medulla.(ABSTRACT TRUNCATED AT 400 WORDS)

Two multiple trauma patients with total rupture of the pericardium and luxation of the heart into the left pleural cavity after blunt trauma are presented. One of the patients also had rupture of the posterior wall of the left ventricle with abundant bleeding. Both patients had intra-abdominal organ injuries, and emergency laparotomy was the first surgical procedure. The pericardial injury in one patient was diagnosed and treated by immediate thoracolaparotomy, in the other by left thoracotomy within 1 hour after laparotomy: both patients recovered. Awareness of possible pericardial lesions in multiple trauma patients with symptoms of hemodynamic failure is stressed.

Central and renal hemodynamics, renal cortical and medullary oxygen tension, and renal lactate metabolism were investigated in hemorrhagic shock in dogs. During graded hemorrhage, renal tissue PO2 decreased in parallel with renal blood flow, whereas renal lactate uptake remained virtually unchanged. During shock, below a mean arterial pressure (MAP) of 72 mm Hg, renal lactate utilization declined in parallel with tissue PO2. Renal lactate was produced at an MAP of 38 mm Hg. Reinfusion of shed blood increased renal tissue PO2 above its preshock value but did not restore baseline renal oxygen consumption and lactate uptake levels. These results suggest that renal lactate utilization is not limited by oxygen delivery under moderate hemorrhagic hypotension but decreases linearly with renal tissue PO2 during shock.

Renal cortical and medullary tissue oxygen tension, systemic oxygen supply as well as central and renal hemodynamics were investigated in dogs during graded hemorrhage and subsequent reinfusion of shed blood. The measurements of tissue gas tension were carried out by means of implanted Silastic tubes. The baseline renal cortical PO2 was 35 mmHg and the corresponding medullary PO2 25 mmHg. The lowest mean cortical and medullary oxygen tensions--8 and 12 mmHg, respectively--were recorded during the severest hypotension at 40% blood loss. After reinfusions of shed blood the cortical PO2 underwent a transient increase to the original preshock level decreasing slowly thereafter. Concomitantly, the medullary PO2 reached the prehemorrhage value remaining then stationary until the end of the experiment. Arterial blood PO2 was normal throughout the study. Renal venous PO2 fell during the deepest shock but consistently exceeded the corresponding tissue PO2 levels. It is concluded that hemorrhagic hypotension impaired tissue oxygenation of both cortex and medulla, the effect being greatest in the cortex.

Renal hemodynamics and oxygen metabolism were studied in eight adult beagle dogs during shock induced with an iv infusion of Escherichia coli endotoxin. Renal blood flow (RBF) and renal cortical PO2 decreased profoundly during the 15-min endotoxin infusion. RBF increased sharply immediately after cessation of infusion, but soon declined and remained depressed throughout the rest of the 4-h experiment. The renal cortical PO2 remained depressed for approximately 2 h and then gradually increased toward the baseline level. Endotoxin infusion was followed by an increased renal PvO2 and a decreased renal arteriovenous oxygen difference. Renal oxygen consumption declined abruptly during endotoxin infusion, but increased toward the end of the experiment. These results suggest impaired tissue oxygenation and possibly increased oxygen shunting in the kidney during endotoxin shock.

The interrelation between the renal tissue PO2, venous PO2, oxygen consumption, and lactate utilization was investigated in dogs subjected to graded hemorrhage. The cortical PO2 measured by means of an implanted silicone elastomer tube responded immediately to graded hemorrhage. The renal venous PO2 remained at the baseline level when the cortical PO2 declined from the mean initial value of 36 to 15 torr. A further decrease in the cortical PO2 was followed by a sharp fall in the renal venous PO2, oxygen consumption, and lactate uptake. These three variables decreased simultaneously at the same cortical PO2 level. During severe hypoperfusion the renal tissue PO2 decreased progressively despite an increase in the renal arteriovenous oxygen difference. These results suggest that the renal venous PO2 remains unchanged until the tissue PO2 decreases to a level at which renal metabolism becomes limited by oxygen availability.

Repeated insulin tests were carried out on 118 patients after vagotomy and antral resection or vagotomy and drainage. The main indication for operation was gastro-duodenal ulcer. The test was performed in both the early (average 13.7 days after the operation) and late (average 3.3 years) postoperative phase. After vagotomy and antral resection, the proportion of Hollander-positive responses decreased from 21.1% in the early phase to 11.1% in the late phase, but after vagotomy and drainage, it increased from 32.1% to 57.1% (p greater than 0.05 in both). Changes of the test response from negative to positive and vice versa were seen after both types of operations. After vagotomy and antral resection, in tests with a change of the response from positive to negative (14.4%) there was a significant decrease in insulin-stimulated acid secretion. After vagotomy and drainage, there were more changes from negative to positive (28.6%), but no significant differences were seen in acid secretion values. Some tests showed a change from early positive to late positive (Ross & Kay). The significance and possible explanations for the changes are discussed in the light of acid secretion values.

The interrelation between the renal cortical pO2 and renal fractional extraction of arterial lactate was investigated in dogs subjected to gradual haemorrhage up to 45-50% of their blood volume. The cortical pO2, measured by means of an implanted Silastic tube, responded immediately to graded haemorrhage. The renal lactate extraction increased parallel with the arterial lactate concentration when the cortical pO2 declined from the mean initial value of 36 mmHg to 15 mmHg. A further decline of the cortical pO2 was followed by a sharp fall in the renal lactate extraction. A decrease in lactate extraction correlated closely with the cortical pO2 below 15 mmHg during severe hypoperfusion. These results suggest that the changes in the renal lactate utilization are independent of the tissue oxygen tension until the cortical pO2 decreases to the level at which the renal metabolism becomes limited by the availability of oxygen. Below this cortical pO2 the renal lactate extraction decreases in proportion to the developing tissue hypoxia.

Renal metabolism of glucose and lactate was studied in ten adult beagle dogs during pentobarbital anesthesia. Six dogs were submitted to hypodynamic shock by means of an intravenous bolus injection of Escherichia coli endotoxin, 0.5 mg/kg over 15 min. Four dogs received only saline solution and served as controls. Sudden cardiac depression, hypotension and moderate renal hypoperfusion were observed in the endotoxin-injected animals. Acidosis and oliguria also occurred during the 5-hour study. Arterial and renal venous glucose concentration increased transiently during the early phase of endotoxin shock. In the control group glucose levels increased slightly by the end of the experiment. Despite marked hyperlactatemia in the endotoxin group, the arteriovenous lactate difference remained almost unchanged. Renal uptake of lactate and output of glucose were not influenced during the moderate renal hypoperfusion caused by endotoxin.

The efficacy of single doses of intravenously administered indomethacin (50 mg) and metamizole (2.5 g) in the relief of biliary pain were compared in 60 consecutive patients attending the emergency ward of university central hospital. There were no statistically significant differences between the two treatment groups. There was no response in 13.3% in both groups and additional analgecics were required by 20% of the patients in both groups. Intravenous indomethacin is a recommendable alternative for intravenous metamizole in the treatment of biliary pain and the risks for agranulocytosis appear to be lesser than those associated with metamizole.

Renal tissue oxygen tension and lactate metabolism were studied in hemorrhagic shock in dogs. The renal tissue PO2 and oxygen consumption declined in proportion to blood loss and decreasing blood flow. The decrease of tissue PO2 was greater in the cortex than in the medulla. Renal lactate uptake remained constant at the control level until 30% blood loss through an increase of renal arteriovenous lactate difference in direct proportion to arterial lactate concentration. During hemorrhagic shock after 40% blood loss lactate uptake decreased sharply and ceased almost totally. Before shock renal lactate uptake correlated highly significantly with arterial pH whereas after shock the correlation between these parameters was less significant. After reinfusions of shed blood the renal tissue PO2 returned to the prehemorrhage level in both tissue layers despite the reduced renal blood flow. At this phase renal oxygen consumption and lactate uptake failed to reach the control levels. These findings indicate that in moderate hypotension renal lactate uptake is not restricted by the local oxygen supply. During established shock tissue hypoperfusion and hypoxia seem to be responsible for deterioration of renal lactate metabolism.