4′-Chlorodiazepam, a translocator protein (18 kDa) antagonist, improves cardiac functional recovery during postischemia reperfusion in rats

2010 ◽  
Vol 235 (4) ◽  
pp. 478-486 ◽  
Author(s):  
Junjie Xiao ◽  
Dandan Liang ◽  
Hong Zhang ◽  
Ying Liu ◽  
Fajie Li ◽  
...  
Keyword(s):  
Heart Rate ◽  
Flow Rate ◽  
Functional Recovery ◽  
Coronary Flow ◽  
Ventricular Arrhythmias ◽  
Left Ventricular ◽  
Translocator Protein ◽  
Oxidative Enzymes ◽  
Mptp Opening ◽  
Translocator Protein 18 Kda

Inhibition of translocator protein (18 kDa) (TSPO) can effectively prevent reperfusion-induced arrhythmias and improve postischemic contractile performance. Mitochondrial permeability transition pore (mPTP) opening, mediated mainly through oxidative stress during ischemia/reperfusion (I/R), is a key event in reperfusion injury. 4′-Chlorodiazepam is a widely used TSPO antagonist. However, whether 4′-chlorodiazepam can improve cardiac functional recovery during postischemia reperfusion by affecting oxidative enzymes, reducing reactive oxygen species (ROS) and thereby inhibiting mPTP opening is still unknown. Cardiac function including heart rate, coronary flow rate, left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), maximal time derivatives of pressure (±d P/d t max) and the severity of ventricular arrhythmias were analyzed in isolated rat hearts during I/R. mPTP opening, ROS and oxidative enzyme activities were measured with fluorometric or spectrophotometric techniques. 4′-Chlorodiazepam did not affect heart rate and coronary flow rate, but abolished the increase in LVEDP, accelerated the recovery of LVDP and ±d P/d t max, and reduced the severity of ventricular arrhythmias. The mPTP opening probability was reduced by 4′-chlorodiazepam, accompanied by a reduction in ROS level. In addition, the activities of mitochondrial electron transport chain complex I and complex III were increased, while those of xanthine oxidase and NADPH oxidase were reduced. Therefore, 4′-chlorodiazepam may improve cardiac functional recovery during reperfusion, potentially by affecting the activities of oxidative enzymes, reducing ROS and thereby inhibiting mPTP opening. The present study presents evidence that 4′-chlorodiazepam could be a novel adjunct to reperfusion.

Effect of Salidroside on Cardiac Functional Recovery

2013 ◽  
Vol 798-799 ◽  
pp. 1030-1032
Author(s):  
Yan Zhang ◽  
Zhong Hua Zheng ◽  
Yue Peng Wang ◽  
Guo Liang Peng ◽  
Liu Hang Wang
Keyword(s):  
Flow Rate ◽  
Functional Recovery ◽  
Rat Heart ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Cardioprotective Effect ◽  
Decrease Rate ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Isolated Rat

To investigate the cardioprotective effect of salidroside to rat heart subjected to 8-hour hypothermic storage and 2-hour normothermic reperfusion. Isolated rat hearts were perfused with Langendorff model; after 30 minutes of baseline, the hearts were arrested and stored by St. Thomas solution (STS) without (STS group) or with different concentration salidroside at 4 °C for 8 hours, then reperfused for 2 hours. Compared with STS group, both middle and high dosage in STS greatly improved the recovery of left ventricular developed pressure (LVDP), maximum LVDP increase and decrease rate (±dp/dt), coronary flow rate (CF). Our study demonstrated that the salidroside was beneficial to improving cardiac functional recovery.

scholarly journals The Association between Coronary Flow Rate and Impaired Heart Rate Recovery in Patient with Metabolic Syndrome

2013 ◽  
Vol 62 (18) ◽  
pp. C188-C189
Author(s):  
Yusuf İzzettin Alihanoğlu ◽  
İsmail Doğu Kilic ◽  
Harun Evrengul ◽  
Bekir Serhat Yıldız ◽  
İhsan Alur ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Heart Rate ◽  
Flow Rate ◽  
Coronary Flow ◽  
Heart Rate Recovery

Left ventricular heat production measured by coronary flow and temperature gradient

1961 ◽  
Vol 16 (5) ◽  
pp. 883-890 ◽  
Author(s):  
William A. Neill ◽  
Herbert J. Levine ◽  
Richard J. Wagman ◽  
Joseph V. Messer ◽  
Norman Krasnow ◽  
...  
Keyword(s):  
Temperature Gradient ◽  
Flow Rate ◽  
Heat Production ◽  
Coronary Flow ◽  
Coronary Circulation ◽  
Heat Removal ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Coronary Perfusion

The study of energetics of the left ventricular myocardium, normally based on its oxygen consumption and mechanical work performance, can be extended by determining its heat production as well. By considering all forms of energy input and output of the left ventricle, calculations were made of left ventricular net heat production under a variety of hemodynamic conditions. One of the mechanisms for removal of the heat produced is provided by the coronary blood, which is warmed in transit through the myocardium. Direct measurements of the rate of heat removal by the coronary circulation were made from coronary flow rate and veno-arterial temperature gradient. The fraction of left ventricular net heat production which is removed by the coronary perfusion is proportional to coronary flow rate. The fraction at a given flow rate is sufficiently reproducible to permit estimation of total heat produced from the portion measured in the coronary circulation. Certain of the theoretical applications of heat data may require more accuracy than appears feasible by this method. Which of the applications discussed will prove practical remains to be determined. Submitted on February 13, 1961

Coronary constriction due to neuropeptide Y: alleviation with cyclooxygenase blockers

1989 ◽  
Vol 257 (3) ◽  
pp. H927-H934
Author(s):  
S. E. Martin ◽  
R. E. Patterson
Keyword(s):  
Heart Rate ◽  
Neuropeptide Y ◽  
Coronary Flow ◽  
Sympathetic Nerves ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Base Line ◽  
Coronary Resistance ◽  
Initial Decrease ◽  
Group A

Intra-arterial administration of neuropeptide Y (NPY), a peptide endogenous to sympathetic nerves, increases coronary vascular resistance by 30-40%. To test whether blockade of prostaglandin synthesis altered the severity of the NPY-induced coronary vasoconstriction, dogs (n = 25) were anesthetized and instrumented to record hemodynamic parameters. In control animals (n = 11) paired infusions of NPY (42 nmol/3 min) were given at 0 and 120 min. NPY produced similar increases in coronary resistance by 10 min, 31 +/- 7% (mean +/- SD) with the first dose vs. 32 +/- 12% with the second dose. The increases in resistance were due to an initial decrease in coronary flow (10 +/- 6%) followed by a prolonged increase in aortic pressure (15-20% over 20 min). Each infusion of NPY decreased heart rate (-10 +/- 7%) but did not alter left ventricular dP/dt. The effects of NPY lasted 40–60 min. In a separate group, a cyclooxygenase inhibitor (COI), indomethacin (n = 6) or ibuprofen (n = 8), was given 1 h before the second dose of NPY. The increases in coronary resistance were blunted significantly after cyclooxygenase blockade from a predrug value of 36 +/- 13 to 19 +/- 12%. In these treated animals, the decrease (-12 +/- 6%) in coronary blood flow seen with the first dose of NPY was prevented (4 +/- 14%) during the second dose (P less than 0.05). Of the two drugs, ibuprofen appeared to restore coronary flow more than did indomethacin. Neither drug affected the base line or the NPY-elicited changes in aortic pressure, heart rate, dP/dt, or myocardial oxygen demands.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial temperature variation: effect on regional function and coronary flow in dogs

1987 ◽  
Vol 252 (2) ◽  
pp. H448-H455 ◽  
Author(s):  
M. N. D'Ambra ◽  
P. Magrassi ◽  
E. Lowenstein ◽  
S. Kyo ◽  
W. G. Austen ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Flow Probe ◽  
Precise Control ◽  
Anesthetized Dogs ◽  
Regional Temperature ◽  
Myocardial Temperature ◽  
Right Heart Bypass

Incremental changes in the temperature (28–42.5 degrees C) of the anterior left ventricular wall in a canine, working, beating right heart bypass preparation (constant preload, afterload, and heart rate) were produced to measure the effect of regional temperature on myocardial function and blood flow. Circumferential-axis segment lengths were measured with sonomicrometry in both the temperature-varied, left-anterior descending coronary artery (LAD)-supplied myocardium and the normothermic (38 degrees C) circumflex-supplied myocardium. Fast thermistors (time constant less than 0.25 s) continuously monitored midmyocardial temperature in both areas. A Silastic loop with heat exchanger, thermistors, strain gauge, and flow probe was inserted into the LAD and allowed precise control of regional myocardial temperature. Nine-micron microspheres injected into left atrium were used to evaluate coronary flow and distribution. In six anesthetized dogs, relative to normothermic control (38 degrees C), regional systolic shortening decreased 42.2 +/- 10% at 41 degrees C and increased 23.3 +/- 6% at 31 degrees C. There was no significant change in coronary blood flow or distribution at the three temperatures. Pressure-length areas varied inversely with myocardial temperature. These data demonstrate that there is a reversible inverse relationship between midwall T and ventricular function when heart rate, preload, and after-load are controlled.

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.

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