Alterations in serum creatine kinase and lactate dehydrogenase. Association with abdominal aortic surgery, myocardial infarction and bowel necrosis.

Experimental studies have shown that peripheral serum creatine kinase and lactate dehydrogenase change with bowel infarction. Some clinical reports have suggested that similar changes occur in patients. This prospective study documents the changes in these enzymes associated with acute myocardial infarction, acute bowel necrosis (MES INF), and uncomplicated abdominal aortic reconstruction. Analysis of 15 patients with AMI, 13 patients undergoing major AAS, and eight patients with MES INF has shown that these conditions may be differentiated by analysis of serum CK and LD isoenzymes. The study suggests that in the absence of electrocardiographic changes, a patient with epigastric distress with elevated levels of serum CK and either CK-MB or CK-BB bands present may well have a mesenteric rather than a myocardial infarction. Acute myocardial infarction can be ruled out further through analysis of serum LD1/LD2 ratios.

Changes in serum creatine kinase and lactate dehydrogenase caused by acute perioperative myocardial infarction and by transatrial cardiac surgical procedures.

A prospective clinical study was conducted to ascertain if a patient's postoperative elevation in serum creatine kinase MB isoenzyme coupled with determination of the lactate dehydrogenase1/lactate dehydrogenase2 ratio could differentiate whether atrial or ventricular myocardium was the source of these changes. Animal studies have shown that atrial myocardium is as rich a source of creatine kinase MB as is ventricular myocardium. Atrial myocardium has a lactate dehydrogenase1/lactate dehydrogenase2 ratio less than 1.00, whereas in ventricular myocardium the ratio is greater than 1.00. Sixty-four patients were assigned to six groups on the basis of serial electrocardiograms and vectorcardiograms by a cardiologist who was unaware of their clinical courses. The control group (Group 1) consisted of 16 patients admitted to the coronary care unit who had no electrocardiographic changes. Three surgical groups without electrocardiographic or vectorcardiographic evidence of perioperative myocardial infarction were studied: 10 patients undergoing routine coronary artery bypass procedures (Group 2), six adults undergoing repair of secundum atrial septal defect (Group 3), and 13 patients having mitral valve replacement (Group 4). Two groups of surgical patients who had acute perioperative transmural myocardial infarctions confirmed by serial electrocardiograms and vectorcardiograms were studied: 15 patients (Group 5) who had elective coronary artery bypass procedures and four (Group 6) who had mitral valve replacement. This study suggests that serum creatine kinase MB levels in excess of 50 IU/L on the postoperative day 1 and day 2 samples coupled with serum lactate dehydrogenase1/lactate dehydrogenase2 ratios greater than 1.00 on the postoperative day 2 and day 3 samples support the diagnosis of acute myocardial infarction. Patient groups undergoing procedures necessitating atriotomies had average elevations in serum creatine kinase MB and in the lactate dehydrogenase1/lactate dehydrogenase2 ratio, but these were significantly less than those seen when acute perioperative myocardial infarction had occurred.

Creatine kinase and lactate dehydrogenase in the muscles encountered during median sternotomy and in the myocardium of the cardiac chambers.

The validity of using creatine kinase MB and lactate dehydrogenase serum isoenzymes to confirm the diagnosis of perioperative myocardial infarction in patients who have had cardiac operations has been questioned, since both have been detected in skeletal muscles. Little is known concerning the concentration of either isoenzyme in the muscles routinely encountered during median sternotomy. Since we have previously shown that the dog is an adequate model in which to study creatine kinase and lactate dehydrogenase isoenzymes, eight healthy dogs were placed under general anesthesia and 1 gm blocks were resected from selected muscles (intercostals, rectus abdominis, diaphragm, and sternothyroid) and from the walls of all four cardiac chambers. Each 1 gm block was homogenized individually in Ringer's lactate, centrifuged, and the supernatants were analyzed for total creatine kinase and lactate dehydrogenase activity by spectrophotometry. Isoenzymes were determined by agarose gel electrophoresis. The study shows that the chest wall muscles and atrial myocardium have appreciable quantities of creatine kinase MB. Hence, serum creatine kinase MB bands in the perioperative period can be generated by manipulation of chest wall muscles and the atrial wall as well as by infarction of the ventricular myocardium.

An analysis of creatine phosphokinase in the mucosa and the muscularis of the gastrointestinal tract.

Previous work has shown that mesenteric infarction causes elevation of total serum creatine phosphokinase (CPK) and each of its three isoenzymes. The exact origin of the CPK has not been determined. Little is known about the actual tissue distribution of CPK in bowel. Experiments were performed to confirm the expectation that CPK was present in the bowel wall and to determine its concentration and the distribution of CPK isoenzymes in the muscularis and mucosa, respectively. Multiple segments were resected from the esophagus, stomach, duodenum, jejunum, ileum, and the proximal and distal colon of normal dogs. The mucosa (MUC) was separated from the seromuscular (MSL) tissue in each of the segments and 1-g samples were analyzed individually for total CPK activity by spectrophotometric analysis and for isoenzyme distribution by agarose gel electrophoresis. The results show that all three isoenzymes of CPK are present throughout the GI tract and that the majority of CPK found is in the MSL. Hence, elevations in serum CPK associated with injuries to the GI tract suggest seromuscular injury. While no isoenzyme is located specifically in the bowel, certain associations were seen. CPK-MM, presumably from striated muscles, was most prevalent in the esophagus. In other portions of the bowel all three isoenzymes were present almost equally. In the mucosa the levels of CPK-MM and CPK-BB always exceeded the level of CPK-MB. Knowledge of the distribution of CPK and its isoenzymes in bowel provides a framework for studying and interpreting serum levels of CPK during bowel injury.

Elevated levels of peripheral serum creatine phosphokinase with strangulated small bowel obstruction.

Experimental arterial bowel infarction can cause elevations in levels of peripheral serum creatine phosphokinase (CPK), lactic dehydrogenase (LDH), and their isoenzymes. To test whether these changes would occur in strangulated small bowel infarctions, 18 dogs were placed under general anesthesia and randomized to one of three categories: laparotomy alone, simple mechanical small bowel obstruction, or strangulated small bowel infarction induced by incarcerating bowel in a surgically created ventral hernia. Serum samples were drawn for 48 hours postoperatively. Total CPK and LDH activity were determined by automated spectrophotometry; isoenzyme levels were determined by agarose gel electrophoresis. Levels of peripheral serum CPK and each of its isoenzymes became significantly elevated in the dogs with strangulated infarction. Such elevations did not occur with LDH. The findings suggest that changes in peripheral serum CPK could prove helpful in evaluating bowel viability in cases of intestinal obstruction.

Changes in peripheral serum creatine phosphokinase (CPK) and lactic dehydrogenase (LDH) in acute experimental colonic infarction.

No satisfactory laboratory test for the early diagnosis of bowel infarction exists at this time. We have delineated changes in serum CPK levels after acute superior mesenteric artery infarction; whether or not comparable changes occur with inferior mesenteric artery infarction has not yet been determined. Furthermore, the changes in LDH associated with acute bowel infarction have not been documented. To determine the changes in serum CPK and LDH in acute colonic infarction, laparotomies were performed on dogs after peripheral baseline blood samples were drawn and each subject was randomly placed in one of three groups: laparotomy alone, acute colonic obstruction, and acute colonic infarction by ligation of the inferior mesenteric artery. The marginal artery of the colon was ligated at the peritoneal reflection and at the cecum to interrupt arterial collaterals. Blood samples were taken from each subject at intervals of three hours for 48 hours after injury. Serum from each sample was analyzed for total CPK and LDH by automated spectrophotometry. Isoenzymes were determined by agarose gel electrophoresis. Necropsies were conducted on all the dogs to confirm that the intended condition had been produced and that no intercurrent disease was present. The data support the conclusion that total CPK, total LDH and their isoenzymes become elevated in the peripheral serum after colonic infarction. The maximal elevations were all seen within the first 12 hours after acute colonic infarction. Total LDH and LDH(3), the most prevalent isoenzyme of LDH in bowel, do not become elevated in the serum to as high a level as CPK, but the combination of serum elevations in both enzyme systems may prove to be of diagnostic significance.

Changes in serum total creatine phosphokinase (CPK) and its isoenzymes caused by experimental ligation of the superior mesenteric artery.

The changes in serum total CPK and its isoenzymes have not been delineated in acute mesenteric infarction. As measurement of serum CPK levels could conceivably be a useful diagnostic test for bowel infarction, this experiment was performed to assess changes in serum CPK levels in bowel infarction in dogs, using sham operation and talc peritonitis as controls. Laparotomies were performed in 20 dogs, and each was as signed randomly to one of three groups: those having laparotomy (LAP), talc peritonitis (PER), and superior mesenteric artery infarction (MAI). Mixed venous blood samples were obtained from all subjects for 30 hours after surgery. All animals were killed, and complete autopsies were performed. Confirmation of infarction and determination of its extent were obtained through both gross and microscopic examination of the gut in canines subjected to arterial infarction. Total serum CPK levels were determined by spectrophotometric analysis. Agarose gel electrophoresis was used to determine the levels of each of the isoenzymes. Significant elevations of CPK and CPK-MM occurred nine hours after injury. CPK-BB reached maximum elevation by six hours, while CPK-MB did not reach its maximum until 24 hours after injury. From data in the study we conclude that total CPK and its isoenzymes become elevated in the serum of canines subjected to experimental superior mesenteric artery infarction. That CPK-BB elevations peak in the first 12 hours after injury and CPK-MB in the second 12 hours after injury may be of particular diagnostic significance.