Enteric nervous system with chronic mesenteric ischemia: experimental study

Introduction. The pathology of the enteric ganglia can lead to different diseases (Hirschsprungs, neuronal intestinal dysplasia, ganglioneuromatosis, and Chagasse). Causes of acquired dysganglionosis remained unclear. Some authors hypothesized that pathology of the enteral nervous system may be secondary to intestinal ischemia. Aim. To investigate the intestinal function and histological changes of the colon in rats with chronic ischemia. Materials and methods. A total of 20 Sprague Dawley rats underwent surgery (ligation of the terminal mesenteric vessels next to the descending colon). The appetite of animals were checked, and stool were collected after the procedure. Reoperation was performed after 7 (n = 1), 9 (n = 2), 12 (n = 2), 14 (n = 1), 21 (n = 1), 42 (n = 1), 53 (n = 1), and 62 (n = 1) days. The diameter of the colon and changes of the serosa were visualized. In the experimental group, two samples biopsy was performed (ischemic and normal colon). Results. Functional changes were observed in 90% of rats after the ligation of mesenteric vessels (constipation/impact, softening stool/diarrhea, and hemocolitis). Colonic stenosis of the ischemic area in 30% was detected. 70% animals have the intestinal dilatation above the ischemic segment (partial bowel obstruction). Necrosis of the ischemic colon was observed in 20%. Spontaneous fixation of the omentum to the ischemic segment was found in 40% animals. A microscopically inflamed infiltration of the mucosa in the ischemic zone (70%) and in normal colon (50%) was revealed in the ligation group. The number of the enteric ganglia decreased in the ischemic segment. Conclusion. Functional disorders (colitis and obstruction) and morphological changes (inflammation and ganglion cells pathology) were found in rats with chronic mesenteric ischemia.

Abstract 20355: Cardiac Magnetic Resonance Assessment of Absolute Myocardial Blood Flow and Myocardial Perfusion Reserve Compared With FFR in Patients With Coronary Artery Disease

Background: The diagnostic value of absolute myocardial blood flow (AMBF) obtained by cardiac magnetic resonance (CMR) quantitative measurement remains uncertain. We evaluated the subendocardial, epicardial, transmural AMBF, and myocardial perfusion reserve (MPR) derived from AMBF determined by perfusion CMR. We also assessed the relationship between CMR-derived AMBF and fractional flow reserve (FFR) in patients with coronary artery disease (CAD). Methods and Results: We investigated 38 CAD patients (mean age, 67±10 years; male, 89%, 46 vessels territories) who underwent perfusion CMR both at stress and rest, and invasive coronary angiography. FFR was measured in all vessels with stenosis more than 40% by QCA. FFR<0.8 was considered hemodynamically significant stenosis. Patients with previous revascularization and/or myocardial infarction, and with renal dysfunction were excluded. We perform quantitative analysis of the transmural, subendocardial and epicardial AMBF, and MPR at mid-ventricular level. AMBF distributed in the wide range both subendocardium and subepicardium. At stress, AMBF was significantly increased in all of the subendocardial, epicardial, and transmural layers of the ischemic segment at adenosine-induced hyperemia from rest AMBF. (At rest: subendocardial 245±122 ml/100g/min, epicardial 124 [75-233] ml/100g/min, transmural 172 [102-261] ml/100mg/min. At stress: subendocardial 380 [156-517] ml/100g/min, epicardial 275 [158-502] ml/100g/mintransmural 287 [152-456] ml/100g/min.) There was a significant relationship between transmural AMBF and FFR, transmural MPR and FFR values, with r = 0.33 (p = 0.028), r=0.39 (p=0.007). The transmural MPR<2.47 threshold yielded a sensitivity of 0.92 (95% confidence interval: 0.77 to 0.99) and a specificity of 0.71 (0.44-0.90) to detect coronary ischemia with a FFR <0.8, and an area under the ROC curve (AUC) of 0.77 (0.62 to 0.88) for vessel-based analysis. Subendocardial AMBF and MPR gradually decreased with decreasing FFR at ischemic segment, but it was not significant. Conclusions: The quantitative analysis of transmural AMBF and myocardial MPR on perfusion cardiac magnetic resonance may predicts hemodynamically significant CAD as defined by FFR.

Abstract 13030: Post-systolic Shortening and Early Systolic Lengthening in the Ischemic Segment are Affected by the Contractility in its Adjacent Segment

Background: Post-systolic shortening (PSS) and early systolic lengthening (ESL) are sensitive markers of acute myocardial ischemia and the magnitude of these deformation is considered proportional to the severity of ischemia. Theoretical and mathematical models have suggested these deformation is caused by the difference of contractility between the ischemic and its adjacent normal segments. However, it has not been fully confirmed in an in vivo model yet. The aim of the study was to investigate whether PSS and ESL are affected by the contractility of its adjacent segment in an animal model which underwent left anterior descending coronary artery (LAD) occlusion (ischemic segment) followed by left circumflex coronary artery (LCx) occlusion (adjacent segment). Methods: In 6 open-chest dogs, left ventricular short-axis images with frame rate of over 90 fps (GE Vivid E9) and hemodynamics data were acquired at 3 conditions: (1) at baseline, (2) during LAD occlusion, and (3) during both LAD and LCx occlusion. Circumferential strain was analyzed in the LAD and LCx segments by speckle tracking software. End-systolic strain (ε ES ) and the amplitude of PSS and ESL (ε PSS and ε ESL ) were measured. Results: During LAD occlusion, ε PSS and ε ESL in the LAD segment significantly increased compared with baseline (ε PSS , 1.2 ± 1.1% vs. 9.5 ± 2.7%, p<0.05; ε ESL , 1.3 ± 1.0% vs. 8.5 ± 4.2%, p<0.05). During both LAD and LCx occlusion, ε ES in the LCx segment decreased, and both ε PSS and ε ESL in the LAD segment significantly decreased compared with during LAD occlusion (ε PSS , 9.5 ± 2.7% vs. 2.8 ± 1.3%, p<0.05; ε ESL , 8.5 ± 4.2% vs. 2.3 ± 1.9%, p<0.05) (figure). Conclusions: PSS and ESL diminished with the decrease of contractility in its adjacent segment. This suggests PSS and ESL occur based on the interplay of contraction between ischemic and adjacent segments and do not always reflect the severity of ischemia.

ОСОБЛИВОСТІ РЕМОДЕЛЮВАННЯ СТРУКТУР СЛИЗОВОЇ ОБОЛОНКИ ШЛУНКА ПІСЛЯ РІЗНИХ МЕТОДІВ ХІРУРГІЧНОГО ЛІКУВАННЯ ВИРАЗКОВОЇ ХВОРОБИ ШЛУНКА У ВІДДАЛЕНОМУ ПЕРІОДІ

<p>A morphometric study of operated stomach walls after different methods of surgical treatment of gastric ulcer was performed. It was shown that in the remote period operated stomach wall structure had a tendency to regenerate. The most optimal changes were detected after organsparing method of surgical treatment – selective proximal vagotomy with sighting resection of ischemic segment of the stomach by L. Ya. Kovalchuk.</p>

Limitations of postextrasystolic potentiation in identifying ischemic myocardium

To evaluate the usefulness of postextrasystolic potentiation in differentiating ischemic yet viable myocardium from infarcted myocardium, 20 dogs were chronically instrumented with left ventricular pressure gauges, left circumflex coronary artery flow probes, occluders, pacing wires, and ultrasonic segment-length transducers. Ten dogs had acute (1 h) coronary occlusions followed by reperfusion (4 days) and were then killed. Ten more dogs had more prolonged (1 mo) occlusions and were then killed. Timed premature ventricular contractions were induced, and the postextrasystolic beat was evaluated. In ischemic segments that were hypokinetic, postextrasystolic potentiation of shortening occurred in both groups. In ischemic segments that were akinetic or dyskinetic, potentiation of shortening did not occur in either group. Both groups showed recovery of shortening, and histologically normal myocardium was identified in the region between the segments in all animals. Thus, akinetic and dyskinetic segments did not show postextrasystolic potentiation of shortening, even though the tissue was viable and showed functional recovery. Failure to improve shortening after a premature ventricular beta in an ischemic segment does not necessarily indicate nonviable myocardium.

Time course of regional function after coronary occlusions of 1- to 120-min duration

The purpose of this study was to characterize the degree and duration of functional impairment in previously ischemic tissue following coronary artery occlusions of varying duration. Open-chest dogs with left ventricular pressure transducers and ultrasonic segment length crystals were subjected to coronary artery occlusions of 1 (n = 22), 5 (n = 8), 10 (n = 7), 15 (n = 8), 20 (n = 7), 30 (n = 6), 60 (n = 10), or 120 (n = 8) min and segment length motion was measured during 6 h of reperfusion. Active shortening was replaced by passive lengthening during coronary occlusion and regional myocardial blood flow within the ischemic zone was always less than 0.4 ml . min-1 . g-1. Following reperfusion, the improvement of ischemic segment length function was inversely proportional to the duration of coronary occlusion. Function in previously ischemic segment lengths recovered rapidly after 1- and 5-min coronary occlusions, but after occlusions of 10-20 min, there was slow, though incomplete, return of some degree of active shortening yet no evidence of myocardial infarction. With occlusions exceeding 20 min there was persistence of systolic passive lengthening for 6 h despite the absence of infarction in the segment lengths in which function was being evaluated, although infarcted tissue was present ranging from 16.5 +/- 2.6% of the area of ischemia in dogs with 60-min coronary occlusions to 37.2 +/- 4.6% of the area of ischemia in dogs with 120-min occlusions.