Dear Farzad,

According to the following, I believe that you can use it as biomarker:

Rev Esp Cardiol. 2001 May;54(5):580-91.

[Troponine T as possible myocardial injury marker. Its application in myocardial stunning and silent ischemia].

[Article in Spanish]

Capdevila C1, Portolés M, Hernándiz A, Pallarés V, Cosín J.

Author information

Abstract

INTRODUCTION AND OBJECTIVES:

The need for more specific, more sensitive and earlier biochemical markers of acute myocardial infarction, has led to the development of alternative methods to CK-MB). The aim of this work is to assess the usefulness of TnT measurement, in comparison with other markers for detecting transitory ischemic processes without necrosis in some experimental models.

METHODS:

The plasma levels of Troponine T, CK, CK-MB and adenosine were assessed as markers of ischemic myocardial injury. Two protocols were used: in Series I and II very brief (2 min ischemia with 3-min reperfusion) repeated (20 episodes) ischemias were induced, while Series III involved a single 15-min ischemia with a 60-min reperfusion. In Series I the coronary occlusor was placed close to the anterior descending coronary artery (AD); in Series II and III it was placed distally in the AD. Blood samples were taken from the peripheral vein (PVB) and corresponding coronary segment vein; in a basal situation, during ischemia, upon reperfusion, after 24 hours, and after 5 and 10 days. The plasma levels of adenosine, troponine T, CK and CK-MB as well as general and regional function parameters were measured.

RESULTS:

In Series I we observed hypokinesis that lasted 10 days, reaching its maximum on days 4-5. In Series II and III regional function was restored by 24 hours. CK and CK-MB showed similar behaviour; they rose significantly when the chest was opened (p < 0.05) reaching the highest value at 24 hours in all the series. Adenosine rose significantly only during reperfusion (p < 0.05). Troponine T increased after ischemia but not before, remained high for 5 days in all series (PVB).

CONCLUSIONS:

Troponine T rises in absence of necrosis, preferably when the ischemia is longer.

Good luck,

Rafik

The test may be tried, but then used a technique called "ultra-sensitive". Ensure also that the antibody used in the kit recognizes well the dog troponine

Both Troponin levels in terms of acute response and aHBDH (alpha-hydroxibutyrate dehydrogenase) in terms of long term response can be used. Another option is Creatine phospho kinase (CPK) as an intermediate marker, so to say.

Heart sonography is also a procedure that can give you some useful results too.

What is the context of your study? More details can give us a bit more understanding and thus useful suggestions.

Best,

Ivan

If you suspect myocytes injury it should work. You should measure it about 8 hours after the medicine has been given (it will be interesting to see measurments through a longer time period).

Bupivacaine, like lidocaine and the other class I antiarrhythmic drugs, blocks the sodium channels, this block being more slowly reversible. The disturbance of sodium channels throughout the heart leads to a decreased conduction speed throughout the conduction system, thus explaining possible acute conduction disturbances originating below the bundle of His. Sztark et al.demonstrated that mitochondrial adenosine triphosphate (ATP) synthesis was decreased by bupivacaine in isolated rat heart mitochondria because it acted as an un-coupler between oxygen consumption and phosphorylation of adenosine diphosphate and as an inhibitor of respiration. Consequently, the decrease in cellular ATP resulted in an increased rate of anaerobic glycolysis, which may result in the accumulation of lactic acid and inorganic phosphates from hydrolysis of phosphate esters, cumulating in reduced intracellular pH. Finally, the myocardial cell membrane is injured and intracellular molecules such as cardiac enzymes are released to the blood stream, unless the condition is reversed. Not only does bupivacaine decrease cellular ATP from a molecular biological point of view, but it also decreases coronary blood flow and myocardial oxygen consumption in preparation of isolated perfused guinea pig heart. Therefore, an increased rate of anaerobic glycolysis may be accelerated and the myocardial membrane injury may be incrementally aggravated.

Based on the above data, bupivacaine may induce direct myocardial injury and also release cardiac enzymes in to the blood stream. So Troponin measurement  in Bupivacaine induced cardiac toxicity can be useful, at least theoretically.

You can find more about this on "Bupivacaine Induced Cardiac Toxicity Mimicking an Acute Non-ST Segment Elevation Myocardial Infarction" by Ho Yoel Ryu et al., at Yonsei Med J. 2007 Apr 30; 48(2): 331–336.

Thank you all for your kind answers.