scholarly journals Methodology of asystolic donor heart’s condition study in an experiment using small laboratory animals

2021 ◽  
Vol 8 (5) ◽  
pp. 50-56
Author(s):  
Ya. I. Poleschenko ◽  
E. S. Protsak ◽  
D. A. Druzhininsky ◽  
M. M. Galagoudza ◽  
S. M. Minasian ◽  
...  
Keyword(s):  
Body Temperature ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
The State ◽  
Laboratory Animals ◽  
Small Laboratory Animal ◽  
Small Laboratory ◽  
Triphenyltetrazolium Chloride ◽  
Human Body Temperature ◽  
Donor Organs

In transplantation, there has always been an acute problem of the discrepancy between the number of donor organs and the number of recipients, including donor hearts. There are various ways to increase the pool of donor organs, one of them is the use of asystolic or non-heart-beating donors. Due to poor myocardial tolerance of ischemia during the asystole period, as well as because of the difficulties in diagnosing cardiac diseases of the asystolic donor, which can be contraindication to transplantation. Therefore, an in-depth study of the state of the myocardium in asystolic donors is required. Currently, there is no generally accepted protocol for working with asystolic heart donors. This protocol should include methods of heart conditioning and assessing of myocardium state. For its development we need more experimental and preclinical studies. A protocol for such a study is proposed. The modeling of an asystolic donor using rats is described on the basis of experimental work carried out by a team of authors. The article describes the following technical aspects: anesthetic guidance, asystole detection criterion, maintaining the rat body temperature in accordance with the human body temperature during cardiac arrest, surgical aspects of performing the main experimental model. The Langendorff model of isolated cardiac perfusion was chosen as the main model for assessing the state of the myocardium of a small laboratory animal. Intra-left ventricular pressure, volume of coronary blood flow, heart rate and the presence of post-reperfusion arrhythmias were selected as criteria for assessing the state of donor hearts. Assessment of the volume of damage to the donor heart is carried out using triphenyltetrazolium chloride staining of the donor organ. 

scholarly journals ASPIRATION OF BONE MARROW IN LABORATORY ANIMALS

Blood ◽  
1949 ◽  
Vol 4 (5) ◽  
pp. 557-561 ◽  
Author(s):  
R. DOROTHY SUNDBERG ◽  
RUTH E. HODGSON
Keyword(s):  
Bone Marrow ◽  
Guinea Pig ◽  
Present Method ◽  
Laboratory Animal ◽  
Laboratory Animals ◽  
Small Laboratory Animal ◽  
Small Laboratory ◽  
Medial Surface ◽  
Tibial Bone ◽  
Triangular Area

Abstract 1. Methods of aspirating tibial bone marrow from living laboratory animals (rabbit, guinea pig, mouse, and chicken) have been described. No method of aspirating marrow from living mice has been encountered in the literature. 2. The method would probably prove useful in obtaining marrow from the tibia of any small laboratory animal which has a flattened triangular area on the superior medial surface of the tibia. 3. In larger animals (rabbit and chicken), large amounts of marrow can be aspirated. Both smears and sections can be made. 4. The present method, if used in combination with the similar method of aspirating marrow from the ilium, will afford four different sites of aspiration. This should make possible the study of progressive changes in the marrow.

scholarly journals Cardioprotection against Ischemia/Reperfusion by Licochalcone B in Isolated Rat Hearts

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Jichun Han ◽  
Dong Wang ◽  
Bacui Yu ◽  
Yanming Wang ◽  
Huanhuan Ren ◽  
...  
Keyword(s):  
Infarct Size ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Left Ventricular Pressure ◽  
Treated Group ◽  
Left Ventricular ◽  
Control Group ◽  
Myocardial Infarct Size ◽  
Triphenyltetrazolium Chloride

The generation of reactive oxygen species (ROS) is a major cause of heart injury induced by ischemia-reperfusion. The left ventricular developed pressure (LVDP) and the maximum up/down rate of left ventricular pressure (±dp/dtmax⁡) were documented by a physiological recorder. Myocardial infarct size was estimated macroscopically using 2,3,5-triphenyltetrazolium chloride staining. Coronary effluent was analyzed for lactate dehydrogenase (LDH) and creatine kinase (CK) release to assess the degree of cardiac injury. The levels of C-reactive protein (CRP), interleukin-8 (IL-8), tumor necrosis factor-α(TNF-α), and interleukin-6 (IL-6) were analyzed to determine the inflammation status of the myocardial tissue. Cardiomyocyte apoptosis analysis was performed using the In Situ Cell Death Detection Kit, POD. Accordingly, licochalcone B pretreatment improved the heart rate (HR), increased LVDP, and decreased CK and LDH levels in coronary flow. SOD level and GSH/GSSG ratio increased, whereas the levels of MDA, TNF-α, and CRP and activities of IL-8 and IL-6 decreased in licochalcone B-treated groups. The infarct size and cell apoptosis in hearts from licochalcone B-treated group were lower than those in hearts from the I/R control group. Therefore, the cardioprotective effects of licochalcone B may be attributed to its antioxidant, antiapoptotic, and anti-inflammatory activities.

Myocardial function and metabolism in pig hearts after relief from chronic partial coronary stenosis

1994 ◽  
Vol 267 (4) ◽  
pp. H1312-H1319 ◽  
Author(s):  
A. J. Liedtke ◽  
B. Renstrom ◽  
S. H. Nellis ◽  
R. Subramanian
Keyword(s):  
Fatty Acid ◽  
Coronary Stenosis ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Acid Oxidation ◽  
O2 Consumption ◽  
Triphenyltetrazolium Chloride ◽  
Early Recovery ◽  
14Co2 Production ◽  
Metabolic Behavior

Metabolic behavior was compared during acute extracorporeal reperfusion after removal of a chronic 4-day partial coronary stenosis in eight pig hearts (RCS group) and during comparable extracorporeal perfusion in seven chronically prepared hearts (Sham group). Coronary stenosis in RCS hearts was induced in the left anterior descending (LAD) artery by partial inflation of a hydraulic occluder to restrict LAD peak phasic velocity by approximately 50%. Regional mechanical shortening was decreased in RCS compared with Sham hearts after 4 days of chronic coronary stenosis [diminished systolic shortening (P < 0.066) with systolic expansion (P < 0.015)] but was comparable to Sham hearts after relief from stenosis. At analogous workloads (left ventricular pressure and heart rate) during reperfusion, metabolic behavior was distinctive between groups. Specifically, compared with Sham hearts, myocardial O2 consumption was selectively increased in RCS hearts (+ 49 delta %, P < 0.026) as was fatty acid oxidation estimated from 14CO2 production from [U-14C]palmitate (+ 60 delta %, P < 0.061) and exogenous glucose utilization measured from the release of 3H2O from [5-3H]glucose (+ 517 delta %, P < 0.025). At the conclusion of the studies, triphenyltetrazolium chloride staining showed no gross evidence of macroinfarction in RCS or Sham hearts, and there was an essentially unremarkable histological survey of anterior myocardium for microscopic necrosis in either group. The level of O2 consumption and preservation of preferred fatty acid utilization indicate that metabolism remains or regains its aerobic pattern of activity in early recovery immediately after removal of chronic partial coronary stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular responses to beta-stimulation with isoproterenol in deep hypothermia

1996 ◽  
Vol 81 (2) ◽  
pp. 573-577 ◽  
Author(s):  
T. Lauri
Keyword(s):  
Body Temperature ◽  
Left Ventricular Pressure ◽  
Cardiovascular Responses ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Pressure Curve ◽  
Normal Body Temperature ◽  
Normal Body ◽  
Isoproterenol Infusion ◽  
Shivering Thermogenesis

The aim of this study was to investigate the effects of beta-stimulation in deep (25 degrees C) hypothermia. Cardiac catheterization was performed on seven anesthetized beagle dogs. They were cooled between ice bags down to 25 degrees C and received isoproterenol administered intravenously three times: at the normal body temperature (37 degrees C) before cooling, after cooling at 25 degrees C, and after rewarming at 37 degrees C. Circulatory function was measured for every 1 degree C of temperature change. Isoproterenol infusion at 37 degrees C induced cardiac acceleration, including the increases of heart rate, cardiac output, and peak first derivative of the left ventricular pressure curve. Systemic vascular and mean outflow resistances and mean aortic pressure decreased. During cooling, shivering thermogenesis continued, even down to 25 degrees C. At 25 degrees C, cardiac acceleration after isoproterenol infusion did not exist but relaxation rate increased slightly. Systemic vascular and mean outflow resistances decreased, but left ventricular end-diastolic and filling pressures increased. beta-Stimulation at normal body temperature increases shivering thermogenesis during cooling. The venous return to the left ventricle at 25 degrees C increased after isoproterenol infusion while systemic vascular resistance decreased, indicating systemic vasodilatation. This increase in preload is probably due to vasoconstriction in pulmonary vessels, which may be mediated by prejunctional beta-adrenoceptors. For cardiac inotrophy, the isoproterenol had no physiologically significant effects at 25 degrees C. After rewarming at 37 degrees C, the effects of isoproterenol were physiologically similar to the effects at the same temperature before cooling.

Regional function, blood flow, and oxygen utilization relations in repetitively occluded-reperfused canine myocardium

1991 ◽  
Vol 261 (2) ◽  
pp. H538-H547 ◽  
Author(s):  
J. Vinten-Johansen ◽  
P. A. Gayheart ◽  
W. E. Johnston ◽  
J. S. Julian ◽  
A. R. Cordell
Keyword(s):  
Blood Flow ◽  
Coronary Occlusion ◽  
Contractile Function ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Segment Length ◽  
Oxygen Utilization ◽  
Triphenyltetrazolium Chloride ◽  
Reperfusion Period ◽  
Length Analysis

Temporary coronary occlusion followed by reperfusion severely reduces contractile function in the involved segment. We tested whether an uncoupling exists between O2 utilization (MVO2) and systolic shortening in the ischemic-reperfused segment subjected to repetitive coronary occlusion and reperfusion. In 10 anesthetized open-chest dogs, left ventricular pressure and segment length (sonomicrometry) relations were measured in the left anterior descending (LAD, ischemic-reperfused) segment and circumflex coronary artery (nonischemic segment). Four 12-min LAD occlusions were each followed by 30 min reperfusion. MVO2 was determined in both segments by transmural blood flow (15 microns microspheres) and regional coronary arterial-venous O2 extraction after each occlusion-reperfusion period. The four occlusion-reperfusion periods did not produce necrosis by staining with triphenyltetrazolium chloride. LAD occlusion produced dyskinesis [control = 16 +/- 3.0% systolic shortening (SS) vs. -8.8 +/- 1.5%, P less than 0.0001]. The first reperfusion restored SS only to 2.3 +/- 2.0%, which progressively deteriorated to -3.9 +/- 1.1% (P less than 0.05) with subsequent occlusion-reperfusion episodes. Relative to the nonischemic segment, MVO2 in the ischemic-reperfused segment decreased by only 18% despite dyskinesis. Pressure-length analysis showed systolic stiffening during reperfusion with displacement of the passive ischemic pressure-length loop to the left. Segment work (integral of each loop) continued to be generated at 34.5% of control levels after the last occlusion-reperfusion event in contrast to the negative SS. We conclude that 1) MVO2 in the ischemic-reperfused segment without necrosis remains elevated despite severe reductions in systolic shortening, and 2) the discrepancy between systolic shortening and MVO2 is partially due to persistent development of segment work.

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