Ten-hour preservation of guinea pig isolated hearts perfused at low flow with air-saturated Lifor solution at 26°C: comparison to ViaSpan solution

2007 ◽  
Vol 293 (1) ◽  
pp. H895-H901 ◽  
Author(s):  
David F. Stowe ◽  
Amadou K. S. Camara ◽  
James S. Heisner ◽  
Mohammed Aldakkak ◽  
David R. Harder
Keyword(s):  
Heart Rate ◽  
Guinea Pig ◽  
Coronary Flow ◽  
Room Temperature ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Control Flow ◽  
Rate Of Change ◽  
Low Flow ◽  
Isolated Hearts

There is no suitable solution to preserve hearts for longer than 5 h between donor explant and recipient implant. Lifor is a fully artificial preservation medium containing both a nonprotein oxygen and nutrient carrier (nanoparticles) and cellular nutrients, including amino acids and sugars. We proposed that recirculated Lifor solution would satisfactorily preserve guinea pig isolated hearts perfused at low flow with no added O2at room temperature for 10 h. Hearts were isolated from 21 guinea pigs and perfused with Krebs-Ringer (KR) solution (97% O2and 3% CO2) at 37°C. Heart rate, inflow and outflow O2tension, coronary flow, left ventricular pressure (LVP), and maximal and minimal rate of change in LVP (dLVP/d t) were measured. After baseline measurements, hearts were perfused with recirculated Lifor or ViaSpan equilibrated with room air at 15% of control flow at 26°C for 10 h. Hearts were then perfused at 100% flow with KR for 2 h at 37°C. A time control (untreated) group was perfused only with KR solution for 15 h. Lifor arrested and protected hearts against diastolic contracture and maintained a low O2extraction. Compared with time controls, Lifor led to a higher developed LVP and coronary flow; %O2extraction and cardiac efficiency were similar between these two groups. Hearts similarly treated with ViaSpan exhibited diastolic contracture and lower %O2extraction during treatment and, upon reperfusion with KR, exhibited continued diastolic contracture, no return of heart rate or contractility, low coronary flow, low %O2extraction, and marked infarction. For long-term cardiac protection, a suitable preservation solution recirculated at low flow and room temperature without supplemental O2would reduce the support apparatus required for transport. Lifor was far superior to ViaSpan in meeting these requirements.

Improved Contractility and Coronary Flow in Isolated Hearts after 1-Day Hypothermic Preservation with Isoflurane Is Not Dependent on KATPChannel Activation 

1998 ◽  
Vol 88 (1) ◽  
pp. 233-244 ◽  
Author(s):  
David F. Stowe ◽  
Satoshi Fujita ◽  
Zeljko J. Bosnjak
Keyword(s):  
Coronary Flow ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Low Flow ◽  
Control Group ◽  
Protective Effects ◽  
Isolated Hearts ◽  
Time Control ◽  
O2 Extraction

Background Isoflurane protects against reperfusion injury in isolated hearts when given before, during, and initially after hypoxia or ischemia and aids in preconditioning hearts if given before ischemia. The aims of the current study were to determine if isoflurane is cardioprotective during 1-day, severe hypothermic perfusion and if a mechanism of protection is K(ATP) channel activation. Methods Guinea pig hearts (n = 60) were isolated, perfused with Kreb's solution initially at 37 degrees C, and assigned to either a nontreated warm, time control group or one of five cold-treated groups: drug-free cold control, 1.3% isoflurane, 1.3% isoflurane plus glibenclamide (4 microM), 2.6% isoflurane, or 2.6% isoflurane plus glibenclamide. Isoflurane and glibenclamide were given 20 min before hypothermia, during low-flow hypothermia (3.8 degrees C) for 22 h, and for 30 min after rewarming to 37 degrees C. Heart rate, left ventricular pressure, %O2 extraction, and coronary flow were measured continuously, and responses to epinephrine, adenosine, 5-hydroxytryptamine, and nitroprusside were examined before and after hypothermia. Results Each group had similar initial left ventricular pressures, coronary flows, and responses to adenosine, 5-hydroxytryptamine, and nitroprusside. Before hypothermia, isoflurane with or without glibenclamide increased coronary flow while decreasing left ventricular pressure and %O2 extraction. After hypothermia, left ventricular pressure and coronary flow were reduced in all cold groups but least reduced in isoflurane-treated groups. During normothermic perfusion after isoflurane and glibenclamide, left ventricular pressure, coronary flow, %O2 extraction, and flow responses to adenosine, 5-hydroxytryptamine, and nitroprusside were similarly improved in isoflurane and isoflurane-plus-glibenclamide groups over the cold control group but not to levels observed in the warm-time control group. Conclusion Isoflurane, like halothane, given before, during, and initially after hypothermia markedly improved but did not restore cardiac perfusion and function. Protective effects of isoflurane were not concentration dependent and not inhibited by the K(ATP) channel blocker glibenclamide. Volatile anesthetics have novel cardioprotective effects when given during long-term severe hypothermia.

scholarly journals Arrhythmia analysis in Langendorff perfused hearts

2019 ◽  
Author(s):  
Hedvig Takács
Keyword(s):  
Heart Rate ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Observer Agreement ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Isolated Hearts ◽  
Definition Of

In this work, we used the isolated, Langendorff perfused heart model for arrhythmia investigations, and the data of the arrhythmia analysis served for clarifying and characterising the physiology of the model and also, to validate arrhythmia definitions. In our first investigation we examined the relationship between ventricular rhythm and coronary flow autoregulation in Langendorff perfused guinea pig hearts. It is a well-known fact, that heart rate affects coronary flow, but the mechanism is complex, especially in experimental settings. We examined whether ventricular irregularity influences coronary flow independently of heart rate. According to our results, during regular rhythm, left ventricular pressure exceeded perfusion pressure and prevented coronary perfusion at peak systole. However, ventricular irregularity significantly increased the number of beats in which left ventricular pressure remained below perfusion pressure, facilitating coronary perfusion. We found that in isolated hearts, cycle length irregularity increases the slope of the positive linear correlation between mean ventricular rate and coronary flow via producing beats in which left ventricular pressure remains below perfusion pressure. This means that changes in rhythm have the capacity to influence coronary flow independently of heart rate in isolated hearts perfused at constant pressure. In our second investigation we examined whether the arrhythmia definitions of Lambeth Conventions I (LC I) and Lambeth Conventions II (LC II) yield the same qualitative results and whether LC II improves inter-observer agreement. Data obtained with arrhythmia definitions of LC I and LC II were compared within and between two independent observers. Applying ventricular fibrillation (VF) definition of LC II significantly increased VF incidence and reduced VF onset time irrespective of treatment by detecting ‘de novo’ VF episodes. Using LC II reduced the number of ventricular tachycardia (VT) episodes and simultaneously increased the number of VF episodes, and thus, LC II masked the significant antifibrillatory effects of flecainide and the high K+ concentration. When VF incidence was tested, a very strong interobserver agreement was found according to LC I, whereas using VF definition of LC II reduced inter-observer agreement. It is concluded that LC II shifts some tachyarrhythmias from VT to VF class. VF definition of LC II may change the conclusion of pharmacological, physiological and pathophysiological arrhythmia investigations and may reduce inter-observer agreement.

Ketamine Has Stereospecific Effects in the Isolated Perfused Guinea Pig Heart

1995 ◽  
Vol 82 (6) ◽  
pp. 1426-1437. ◽  
Author(s):  
Bernhard M. Graf ◽  
Martin N. Vicenzi ◽  
Eike Martin ◽  
Zeljko J. Bosnjak ◽  
David F. Stowe
Keyword(s):  
Heart Rate ◽  
Guinea Pig ◽  
Opioid Receptors ◽  
Coronary Flow ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Guinea Pig Heart ◽  
Ringer’S Solution ◽  
Cardiac Depression

Background S(+)-Ketamine is judged to produce more potent anesthesia than either the racemate or the R(-) ketamine isomer because of differential activation of specific cerebral receptors. Other than central nervous system effects, the most important side effects of ketamine occur in the cardiovascular system. We examined the direct cardiac effects of the isomers and the racemate of ketamine in the isolated perfused guinea pig heart. Methods Twenty-three guinea pig hearts were perfused by the Langendorff technique with modified 37 degrees C Krebs-Ringer's solution (97% oxygen and 3% carbon dioxide) at a constant perfusion pressure. Eight animals were pretreated with reserpine to deplete hearts of catecholamines. These pretreated hearts were also perfused with Krebs-Ringer's solution containing propranolol, phenoxybenzamine, and atropine to block any remaining effects of catecholamines and of acetylcholine. Five additional hearts were perfused with naloxone to block cardiac opioid receptors. Ten hearts were not treated. All 23 hearts were then exposed to four increasing equimolar concentrations of each isomer and the racemate of ketamine for 10 min. Heart rate, atrioventricular conduction time (AVCT), left ventricular pressure, coronary flow, and inflow and outflow oxygen tensions were measured. Percentage oxygen extraction, oxygen delivery, and oxygen consumption were calculated. Results Both isomers and the racemate caused a concentration-dependent depression of systolic left ventricular pressure and an increase in AVCT. In the untreated hearts, S(+)-ketamine decreased heart rate and left ventricular pressure and, at higher concentrations, oxygen consumption and percentage oxygen extraction significantly less than R(-)-ketamine independent of blocked or unblocked opioid receptors. Racemic ketamine depressed cardiac function to a degree intermediate to that produced by the isomers. Coronary flow and AVCT were equally affected by the isomers and by the racemic mixture. In the catecholamine-depleted hearts both isomers and the racemate caused equipotent depression of all variables. In these hearts cardiac depression was greater, and AVCT, coronary flow, and oxygen delivery were significantly greater than in untreated and opioid receptor-blocked hearts. Conclusions Lesser cardiac depression by the S(+) isomer is attributable to an increased availability of catecholamines, because previous depletion of catecholamine stores and autonomic blockade completely inhibited these differences. The inability of cardiac tissue to reuptake released catecholamines into neuronal or extraneuronal sites during exposure to ketamine is stereoselective and caused predominantly by the S(+) isomer. Cardiac opioid receptors are apparently not involved in this phenomenon.

The effect of isoproterenol on isolated muskrat and guinea pig hearts

1986 ◽  
Vol 64 (12) ◽  
pp. 2674-2677 ◽  
Author(s):  
Thomas A. McKean
Keyword(s):  
Heart Rate ◽  
Guinea Pig ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Adrenergic Stimulation ◽  
Potential Predator ◽  
Opposing Effects ◽  
Sympathetic Effect ◽  
Stimulation Of

Isoproterenol, a β-adrenergic agonist, was given by bolus injection to Langendorff-perfused muskrat and guinea pig hearts. Bolus content ranged from 18 to 29 200 pmol. The hearts responded by increasing left ventricular pressure, heart rate, and release of lactate. The drug threshold was similar for the hearts of the two species but the magnitude of the response differed both at threshold and at saturation doses. The increase in left ventricular pressure and heart rate was greater in guinea pig hearts compared with muskrat hearts. Lactate release was stimulated earlier and increased more in muskrat hearts compared with guinea pig hearts. The weak β-adrenergic stimulation of heart rate and left ventricular pressure in the muskrat may be of benefit when the animal dives to escape a potential predator. Under these conditions of fear, exercise, hypoxia, and diving there would be opposing effects of sympathetic versus vagal stimulation of the myocardium. The sympathetic effect would be to increase myocardial oxygen consumption while the vagal effect would be to reduce it. In the diving mammal the vagal effect predominates and this may be augmented by a blunted rate and pressure response to β-stimulation.

scholarly journals Ten hour preservation of guinea pig isolated hearts perfused at low flow with air‐saturated Lifor® solution at room temperature

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
David F Stowe ◽  
James S Heisner ◽  
Amadou KS Camara ◽  
Mohammed Aldakkak ◽  
David R Harder
Keyword(s):  
Guinea Pig ◽  
Room Temperature ◽  
Low Flow ◽  
Isolated Hearts

Adding Bupivacaine to High-potassium Cardioplegia Improves Function and Reduces Cellular Damage of Rat Isolated Hearts after Prolonged, Cold Storage

2006 ◽  
Vol 105 (4) ◽  
pp. 746-752 ◽  
Author(s):  
James D. Ross ◽  
Richard Ripper ◽  
William R. Law ◽  
Malek Massad ◽  
Patricia Murphy ◽  
...  
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Control Group ◽  
Prolonged Storage ◽  
Mean Values ◽  
Isolated Hearts ◽  
Lactate Dehydrogenase Release ◽  
Positive Rate

Background Bupivacaine retards myocardial acidosis during ischemia. The authors measured function of rat isolated hearts after prolonged storage to determine whether bupivacaine improves cardiac protection compared with standard cardioplegia alone. Methods After measuring cardiac function on a Langendorff apparatus, hearts were perfused with cardioplegia alone (controls), cardioplegia containing 500 microm bupivacaine, or cardioplegia containing 2 mm lidocaine; were stored at 4 degrees C for 12 h; and were then reperfused. Heart rate and left ventricular developed pressures were measured for 60 min. Maximum positive rate of change in ventricular pressure, oxygen consumption, and lactate dehydrogenase release were also measured. Results All bupivacaine-treated, four of five lidocaine-treated, and no control hearts beat throughout the 60-min recovery period. Mean values of heart rate, left ventricular developed pressure, maximum positive rate of change in ventricular pressure, rate-pressure product, and efficiency in bupivacaine-treated hearts exceeded those of the control group (P < 0.001 at 60 min for all). Mean values of the lidocaine group were intermediate. Oxygen consumption of the control group exceeded the other groups early in recovery, but not at later times. Lactate dehydrogenase release from the bupivacaine group was less than that from the control group (P < 0.001) but did not differ from baseline. Conclusions Adding bupivacaine to a depolarizing cardioplegia solution reduces cell damage and improves cardiac function after prolonged storage. Metabolic inhibition may contribute to this phenomenon, which is not entirely explained by sodium channel blockade.

Modulation of myocardial function and [Ca2+] sensitivity by moderate hypothermia in guinea pig isolated hearts

1999 ◽  
Vol 277 (6) ◽  
pp. H2321-H2332 ◽  
Author(s):  
David F. Stowe ◽  
Satoshi Fujita ◽  
Jianzhong An ◽  
Richard A. Paulsen ◽  
Srinivasan G. Varadarajan ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Myocardial Function ◽  
Mild Hypothermia ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Moderate Hypothermia ◽  
Isolated Hearts ◽  
Intracellular Ca ◽  
Relationship Of ◽  
The Relationship

Cardiac hypothermia alters contractility and intracellular Ca2+ concentration ([Ca2+]i) homeostasis. We examined how left ventricular pressure (LVP) is altered as a function of cytosolic [Ca2+]iover a range of extracellular CaCl2 concentration ([CaCl2]e) during perfusion of isolated, paced guinea pig hearts at 37°C, 27°C, and 17°C. Transmural LV phasic [Ca2+] was measured using the Ca2+ indicator indo 1 and calibrated (in nM) after correction was made for autofluorescence, temperature, and noncytosolic Ca2+. Noncytosolic [Ca2+]i, cytosolic diastolic and systolic [Ca2+]i, phasic [Ca2+]i, and systolic Ca2+ released per beat (area Ca2+) were plotted as a function of 0.3–4.5 mM [CaCl2]e, and indexes of contractility [LVP, maximal rates of LVP development (+dLVP/d t) and relaxation (−dLVP/d t), and the integral of the LVP curve per beat (LVParea)] were plotted as a function of [Ca2+]i. Hypothermia increased systolic [Ca2+]iand slightly changed systolic LVP but increased diastolic LVP and [Ca2+]i. The relationship of diastolic and noncytosolic [Ca2+] to [CaCl2]ewas shifted upward at 17°C and 27°C, whereas that of phasic [Ca2+]ito [CaCl2]ewas shifted upward at 17°C but not at 27°C. The relationships of phasic [Ca2+]ito developed LVP, +dLVP/d t, and LVParea were progressively reduced by hypothermia so that maximal Ca2+-activated LVP decreased and hearts were desensitized to Ca2+. Thus mild hypothermia modestly increases diastolic and noncytosolic Ca2+ with little effect on systolic Ca2+ or released (area) Ca2+, whereas moderate hypothermia markedly increases diastolic, noncytosolic, peak systolic, and released Ca2+ and results in reduced maximal Ca2+-activated LVP and myocardial sensitivity to systolic Ca2+.

Statistical analysis of effect of anoxia on rate of change of ventricular pressure

1982 ◽  
Vol 53 (3) ◽  
pp. 726-730 ◽  
Author(s):  
C. George ◽  
M. T. Kopetzky
Keyword(s):  
Heart Rate ◽  
Analysis Of Variance ◽  
Repeated Measures ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Aortic Flow ◽  
Ventricular Pressure ◽  
Ventricular Contractility ◽  
Sprague Dawley

Hearts from 32 male Sprague-Dawley rats were studied to determine effects of anoxia on ventricular contractility. Maximum rate of ventricular pressure changes with time (Pmax) were obtained from simultaneous recordings of right and left ventricular pressure curves. Peak aortic flow and heart rate were measured. Anoxia was produced by 100% N2 respiration. Statistical models were repeated-measures analysis of variance and randomized block factorial analysis of variance. Alpha was 0.05. Heart rate during anoxia was significantly lower than during the 1st min of recovery. Heart rate during both these periods was significantly lower than in preanoxia or the remainder of recovery. Peak aortic flow was not significantly altered. In left ventricles positive Pmax was significantly higher than negative Pmax. In right ventricles positive and negative Pmax were not significantly different. Left ventricular Pmax was significantly depressed during anoxia, whereas right ventricular Pmax was not. Significant differences in pressure developed per mass of tissue was a possible source of variation in right (0.12 +/- 0.002 mmHg/mg) and left (0.16 +/- 0.009 mmHg/mg) ventricular contractile maintenance.

Calcium effect on performance of the heart

1962 ◽  
Vol 202 (4) ◽  
pp. 643-648 ◽  
Author(s):  
H. Feinberg ◽  
E. Boyd ◽  
L. N. Katz
Keyword(s):  
Heart Rate ◽  
Left Ventricle ◽  
Coronary Flow ◽  
Pressure Rise ◽  
Indirect Evidence ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Venous Circulation

Calcium, as the 10% gluconate, was rapidly infused into the venous circulation of the dog "coronary flow" preparation. It was also infused into the aortic circulation perfusing the heart of the "isovolumic" preparation, in which an otherwise empty, beating left ventricle was filled with a known volume of fluid contained within a slack latex balloon. In the coronary flow preparation, calcium was found to: a) increase heart rate, b) leave aortic blood pressure unchanged, c) increase the velocity of the left ventricular pressure rise, d) decrease the circumference of the left ventricle, and e) increase the coronary flow and myocardial oxygen consumption per beat in relation to the existing mean aortic pressure. In the isovolumic preparation calcium increased the peak ventricular pressure at a given balloon volume, but had no effect on the ratio relating myocardial O2 consumption to heart rate and left ventricular pressure developed. In both preparations O2 extraction was decreased. In addition, indirect evidence for the Fenn effect in the contraction of the intact heart is presented.

Sevoflurane Mimics Ischemic Preconditioning Effects on Coronary Flow and Nitric Oxide Release in Isolated Hearts 

1999 ◽  
Vol 91 (3) ◽  
pp. 701-701 ◽  
Author(s):  
Enis Novalija ◽  
Satoshi Fujita ◽  
John P. Kampine ◽  
David F. Stowe
Keyword(s):  
Nitric Oxide ◽  
Ischemic Preconditioning ◽  
Coronary Flow ◽  
Ischemia Reperfusion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Global Ischemia ◽  
Ventricular Pressure ◽  
Nitric Oxide Release ◽  
Isolated Hearts

Background Like ischemic preconditioning, certain volatile anesthetics have been shown to reduce the magnitude of ischemia/ reperfusion injury via activation of K+ adenosine triphosphate (ATP)-sensitive (K(ATP)) channels. The purpose of this study was (1) to determine if ischemic preconditioning (IPC) and sevoflurane preconditioning (SPC) increase nitric oxide release and improve coronary vascular function, as well as mechanical and electrical function, if given for only brief intervals before global ischemia of isolated hearts; and (2) to determine if K(ATP) channel antagonism by glibenclamide (GLB) blunts the cardioprotective effects of IPC and SPC. Methods Guinea pig hearts were isolated and perfused with Krebs-Ringer's solution at 55 mm Hg and randomly assigned to one of seven groups: (1) two 2-min total coronary occlusions (preconditioning, IPC) interspersed with 5 min of normal perfusion; (2) two 2-min occlusions interspersed with 5 min of perfusion while perfusing with GLB (IPC+GLB); (3) SPC (3.5%) for two 2-min periods; (4) SPC+GLB for two 2-min periods; (5) no treatment before ischemia (control [CON]); (6) CON+GLB; and (7) no ischemia (time control). Six minutes after ending IPC or SPC, hearts of ischemic groups were subjected to 30 min of global ischemia and 75 min of reperfusion. Left-ventricular pressure, coronary flow, and effluent NO concentration ([NO]) were measured. Flow and NO responses to bradykinin, and nitroprusside were tested 20-30 min before ischemia or drug treatment and 30-40 min after reperfusion. Results After ischemia, compared with before (percentage change), left-ventricular pressure and coronary flow, respectively, recovered to a greater extent (P<0.05) after IPC (42%, 77%), and treatment with SPC (45%, 76%) than after CON (30%, 65%), IPC+GLB (24%, 64%), SPC+GLB (20%, 65%), and CON+GLB (28%, 64%). Bradykinin and nitroprusside increased [NO] by 30+/-5 (means +/- SEM) and 29+/-4 nM, respectively, averaged for all groups before ischemia. [NO] increased by 26+/-6 and 27+/-7 nM, respectively, in SPC and IPC groups after ischemia, compared with an average [NO] increase of 8+/-5 nM (P<0.01) after ischemia in CON and each of the three GLB groups. Flow increases to bradykinin and nitroprusside were also greater after SPC and IPC. Conclusions Preconditioning with sevoflurane, like IPC, improves not only postischemic contractility, but also basal flow, bradykinin and nitroprusside-induced increases in flow, and effluent [NO] in isolated hearts. The protective effects of both SPC and IPC are reversed by K(ATP) channel antagonism.

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