BACKGROUND: Ischemic preconditioning enhances the tolerance of myocardium against ischemia/reperfusion injury, with the enhancement of the recovery of post-ischemic myocardial function. This study was disigned to assess whether the protective effect of ischemic preconditioning could provide one additional hour of myocardial preservation in four hour myocardial ischemia in a rate heart. MATERIAL AND METHOD: Fourty four Spargue-Dawley rats, weighing 300-450gm, were divided into four groups. Group 1(n=7) and group 3 (n=12) were subjected to 30 minutes of aerobic Langendorff perfusion without ischemic preconditioning and then preserved in saline solution at 2-4 degree C for 4 hours and 5 respectively. Group 2 (n=7) and group 4 (n=18) were perfused in the same way for 20 minutes, followed by 3 minutes of global mormothermic ischemia and 10 minutes of perfusion and then preserved in the same cold saline solution for 4 hours and 5 hours respectively. Heart rate, left ventricular developed pressure (LVDP), and coronary flow were measured at 15 minutes during perfusion as baseline. Spontaneous defibrillation time was measured after reperfusion. Heart rate, LVDP, and coronary flow were also recorded at 15 minutes, 30 minutes, and 45 minutes during reperfusion. Samples of the apical left ventricular wall were studied using a transmission electron microscope. Time of spontaneous defibrillation (TSD) was significantly longer in group 4 than in group 1 (p<0.001), and TSD in group 1 was significantly longer in comparision to that of group 2 (p<0.05). Heart rate at 45 minutes was significantly higher in group 1 than in group 4 (p<0.05). Heart rate at 15 min was significantly higher in group 2 than in group 1(p<0.001) and in group 4 than in group 3 (p<0.05). Left ventricular developed pressure (LVDP) at 30 minutes and 45 minutes was higher in group 1 than in group 4 (p<0.01), LVDP at 45 minutes was higher in group 4 than in group 3 (p<0.05). Rate-pressure product (RPP) at 30 minutes and 45 minutes was higher in group 1 than in group 4 (p<0.05). RPP at 15 minutes was higher in group 2 than in group 1 (p<0.01). RPP at 30 minutes and 45 minutes was higher in group 4 than in group 3 (p<0.05). Group 2 showed relatively less sarcoplasmic edema and less nuclear chromatin clearance than group 1. Group 4 showed less myocardial cell damage than group 3, group 4 showed less myocardial cell damage than group 3, group 4 showed more myocardial cell edema than group 1. CONCLUSION: Ischemic preconditioning enhanced the recovery of postischemic myocardial function after 4 hours and 5 hours preservation. However, it was not demonstrated that ischemic preconditioning could definitely provide one additional hour of myocardial preservation in four hour myocardial ischemia in a rat heart.
Animals ; Chromatin ; Edema ; Heart Rate ; Heart* ; Ischemia ; Ischemic Preconditioning* ; Myocardial Ischemia ; Myocardium ; Perfusion ; Rats* ; Reperfusion ; Sodium Chloride

No abstract available.
Rectovaginal Fistula*

BACKGROUND: The aim of this study is to define the cardioprotective effects (functional and metabolic) of newly developed DelNido cardioplegic solution (containing plasma solution, mannitol, magnesium and lidocaine). MATERIAL AND METHOD: This study assessed the function of rat hearts after itermittent infusion of DelNido cardioplegia with different preserving methods(Air or Icebox) for 2hours and perfusing the hearts on a Langendorff apparatus. Heart rate, left ventricular developed pressure (LVDP) and coronary flow, were measured at pre-ischemic, post-reperfusion 15min, 30min and 45min. Coronary flow was standardized to dry heart weight. Each weight was weighted to calculate water content. Creatine kinase-MB isoenzyme release was measured and ultrastructural assessment was done with electron microscopes. DelNido group was better than St, Thomas group and Icebox group was better than Room-air group. CONCLUSION: DelNido cardioplegia have better myocardial protective effects than St. Thomas cardioplegia when they were preserved in the Room-air. But we can not tell the difference between Delnido cardiplegia with Air preserving method and St. Thomas cardioplegia with Icebox.
Animals ; Cardioplegic Solutions ; Creatine ; Heart ; Heart Arrest, Induced* ; Heart Rate ; Magnesium ; Mannitol ; Plasma ; Rats ; Water

No abstract available.
Extracellular Space* ; Ischemia* ; Myocytes, Cardiac*

Three cases of Dupuytrens contracture which developed in hands were reported along with review of literatures. Partial fasciectomy was done as the choice of treatment for them to improve impairment of function of the hands. No attributable causes for the developement of the disease were found.
Dupuytren Contracture ; Hand

This experimental studies was to investigate the location of PNS and CNS labeled neurons following injection of 2% WGA-HRP and pseudorabies virus (PRV), beta-galactosidase inserted Bartha strain, into the epididymis of rats. After survival times 4~5 days following injection of 2% WGA-HRP and PRV-Ba-Gal, the rats were perfused, and their brain, spinal cord, sympathetic ganglia and spinal ganglia were frozen sectioned (30 mm). These sections were stained by HRP histochemical and beta-galactosidase histochemical staining methods, and observed with light microscope. The results were as follows : 1. The WGA-HRP labeled sympathetic ganglia projecting to the epididymis were observed in pelvic ganglion and L1-6 lumbar sympathetic ganglia. 2. The WGA-HRP labeled spinal ganglia projecting to the epididymis were observed in L1-6 spinal ganglia. 3. The beta-galactosidase labeled neurons projecting to the epididymis were observed in lamina VII of cervical segments. In thoracic segments, beta-galactosidase labeled neurons were observed in dorsomedial part of lamina I, II and III. Dense labeled neurons were observed in intermediolateral n. and dorsal commissural n.. In lumbar segment, labeled neurons were observed in lamina III, IV, V, dorsal commisural n. and superficial dorsal horn. 4. In the medulla oblongata, beta-galactosidase labeled neurons projecting to the epididymis were observed in the trigeminal spinal n., A1 noradrenalin cells/C1 adrenalin cells/caudoventrolateral reticular n., rostroventrolateral reticular n., area postrema, n. tractus solitarius, raphe obscurus n., raphe pallidus n., raphe magnus n., parapyra-midal n., lateral reticular n. and lateral paragigantocellular reticular n.. 5. In the pons, labeled neurons were observed in Kolliker-Fuse n., locus coeruleus, subcoeruleus n. and A5 noradrenalin cells. 6. In midbrain, labeled neurons were observed in periaqueductal gray substance, retrorubral n., substantia nigra and dorsal raphe n.. 7. In the diencephalon, labeled neurons were observed in paraventricular hypothalamic n., lateral hypothalamic nucleus., medial preoptic n. and retrochiasmatic n.. These results suggest that WGA-HRP labeled neurons of the spinal cord projecting to the rat epididymis might be the first-order neurons related to the viscero-somatic sensory and sympathetic postganglionic neurons, and beta-galactosidase labeled neurons of the brain and spinal cord may be the second and third-order neurons response to the movement of vascular smooth muscle in epididymis. These beta-galactosidase labeled neurons may be central autonomic center related to the integration and modulation of reflex control linked to the sensory and motor system monitoring the internal environment. These observations provide evidence for previously unknown projections from epididymis to spinal cord and brain which may be play an important neuroanatomical basic evidence in the regulation of epididymal function.
Animals ; Area Postrema ; beta-Galactosidase ; Brain ; Diencephalon ; Epididymis* ; Ganglia, Spinal ; Ganglia, Sympathetic ; Ganglion Cysts ; Herpesvirus 1, Suid* ; Horns ; Hypothalamic Area, Lateral ; Locus Coeruleus ; Male ; Medulla Oblongata ; Mesencephalon ; Muscle, Smooth, Vascular ; Neural Pathways* ; Neurons ; Periaqueductal Gray ; Pons ; Pseudorabies* ; Rats* ; Reflex ; Spinal Cord ; Substantia Nigra ; Wheat Germ Agglutinin-Horseradish Peroxidase Conjugate*

No abstract available.
Humans ; Intensive Care*

24-hour ambulatory ECG monitoring has been examined for the evaluation of heart rate and longest pause in 34 patients with chronic atrial fibrillation (20 patients treated with digoxin and 14 patients without treatment). Following results were obtained: 1. In 34 patients, the mean of average heart rates was 75.7±13.8/minute, fastest heart rates 148.0±32.4/minute, slowest heart rates 48.1±8.4/minute, difference between fastest and slowest heart rates in individual patients 99.9±29.0/minute and longest pauses 2.95±1.06seconds. The longest pauses of more than 4.0 seconds occurred in 4 of the 34 patients and made an exception of comparison groups. 2. In 27 of the 34 patients, ventricular premature contractures were developed and in 11 of 27, mainly occurred less than 100/24 hours and aberrant conduction occurred in all patients. 3. In 20 patients treated with digoxin (0.25 mg/day), the mean of average heart rates was 78.4±13.7/minute, fastest heart rates 152.5±33.1/minute, slowest heart rates 48.9±8.5/minute, difference between fastest and slowest heart rates in individual patients 103.6±31.7/minute and longest pauses 2.55±0.50 seconds. 4. In 10 patients without treatment, the mean of average heart rates was 78.0±10.7/minute, fastest heart rates 154.5±26.8/minute, slowest heart rates 50.6±7.1/minute, difference between fastest and slowest heart rates in individual patients 103.9±22.2/minute and longest pauses 2.66±0.39 seconds. 5. The difference of heart rates and longest pauses between patients with treatment and without treatment were statistically not significant (P>0.05). In summary, authors seemed to consider that 24-hour ambulatory ECG was useful and safe method for clinical evaluation of patients with chronic atrial fibrillation.
Atrial Fibrillation* ; Contracture ; Digoxin ; Electrocardiography* ; Heart Rate ; Humans ; Methods

No abstract available.
Heart Septal Defects, Ventricular*

BACKGROUND: The Histidine-Tryptophan-Ketoglutarate (HTK) solution has been shown to provide the excellent myocardial protection as a cardioplegia. The HTK solution has relatively low potassium as an arresting agent of myocardium, and low sodium content, and high concentration of histidine biological buffer which confer a buffering capacity superior to that of blood. Since HTK solution has an excellent myocardial protective ability, it is reported to protect myocardium from ischemia for a considerable time (120 minutes) with the single infusion of HTK solution as a cardioplegia. The purpose of this study is to evaluate the cardioprotective effect of HTK solution on myocardium when the ischemia is exceeding 120 minutes at two different temperature (10 to 12degrees C, 22 to 24degrees C) using the Langendorff apparatus. MATERIAL AND METHOD: Hearts from Sprague-Dawley rat, weighing 300 to 340 g, were perfused with Krebs-Henseleit solution at a perfusion pressure of 100 cm H2O. After the stabilization, the heart rate, left ventricular developed pressure (LVDP), and coronary flow were measured. Single dose of HTK solution was infused into the ascending aorta of isolated rat heart and hearts were preserved at four different conditions. In group 1 (n=10), hearts were preserved at deep hypothermia (10~12degrees C) for 2 hours, in group 2 (n=10), hearts were preserved at moderate hypothermia (22~24degrees C) for 2 hours, in group 3 (n=10), hearts were preserved at deep hypothermia for 3 hours, and in group 4 (n=10), hearts were preserved at moderate hypothermia for 3 hours. After the completion of the preservation, the heart rate, left ventricular developed pressure, and coronary flow were measured at 15 minutes, 30 minutes, and 45 minutes after the initiation of reperfusion to assess the cardiac function. Biopsies were also done and mitochondrial scores were counted in two cases of each group for ultrastructural assessment. RESULT: The present study showed that the change of heart rate was not different between group 1 and group 2, and group 1 and group 3. The heart rate was significantly decreased at 15 minutes in group 4 compared to that of group 1 (p<0.05 by ANCOVA). The heart rate was recovered at 30 minutes and 45 minutes in group 4 with no significant difference compared to that of group 1. The decrease of LVDP was significant at 15 minutes, 30 minutes and 45 minutes in group 4 compared to that of group 1 (p<0.001 by ANCOVA). Coronary flow was significantly decreased at 15 minutes, 30 minutes, and 45 minutes in group 4 compared to that of group 1 (p<0.001 by ANCOVA). In ultrastructural assessment, the mean myocardial mitochondrial scores in group 1, group 2, group 3, and group 4 were 1.02+/-0.29, 1.52+/-0.26, 1.56+/-0.45, 2.22+/-0.44 respectively. CONCLUSION: The HTK solution provided excellent myocardial protection regardless of myocardial temperature for 2 hours. But, when ischemic time exceeded 2 hours, the myocardial hemodynamic function and ultrastructural changes were significantly deteriorated at moderate hypotherma (22~24degrees C). This indicates that it is recommended to decrease myocardial temperature when myocardial ischemic time exceeds 2 hours with single infusion of HTK solution as a cardioplegia.
Animals ; Aorta ; Biopsy ; Cardioplegic Solutions ; Heart Arrest, Induced ; Heart Rate ; Heart* ; Hemodynamics ; Histidine ; Hypothermia ; Ischemia ; Myocardium ; Organ Preservation ; Perfusion ; Potassium ; Rats* ; Rats, Sprague-Dawley ; Reperfusion ; Sodium