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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.

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 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.

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 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.