An isothermic flow microcalorimeter system for fluid rates of 1-50 cm3 min -1 has been developed to measure the total heat flow produced by isolated perfused small animal hearts and its rate of change. The heat, which is absorbed by the perfusion fluid flowing through the coronary capillary system, is detected by passing the coronary effluent through a plate heat exchanger mounted in intimate contact with the internal surface of a gradient layer calorimeter. By employing electrical calibration, this heat flow detector gives a precision of +/- 0.2 m W for average effluent rates of about 15 cm3 min-1. The method provides direct comparison of the biologically produced heat flow with electrically generated energy flows. The response time to step changes in heat flow is 1 min to 90% of the total change. Possible systematic errors are analysed and quantified, using a heart bypass flow technique and a thermoelectric differential temperature meter. The accuracy of the measurement of constant heat sources with the complete system over the range of 5-40 mW is +/- 2% for fluid rates up to 40 cm3 min-1. Measurements with small rat hearts have given absolute values between 17 and 36 mW measured with an accuracy of +/- 3%. The rate of total myocardial energy turnover can be studied with the system.

The article describes a method for monitoring the total energy output and oxygen uptake of isolated perfused rat hearts with working left ventricles. Twenty-two unpaced hearts (rates 4-4.5 bs-1) were separately investigated inside a flow micro-calorimeter (one minute for 90% thermal response) at 37 degrees C. They pumped fluid into an artificial arterial system with adjustable linear peripheral resistance and variable volume compliance. After about 20-40 minutes a steady state period was achieved and most of the hearts continued to operate in this state for a further 40-100 minutes. In the steady state the outputs were in the ranges of 30-50 mJ s-1g-1 mechanical power (per gram tissue dry weight) and 100-300 mJ s-1g-1 heat production at an oxygen uptake of between 0.01 and 0.02 cm3 O2 s-1g-1. This resulted in approximately constant cardiac outputs between 2 and 4 cm3 s-1g-1 aortic and coronary fluid and stable mechanical efficiencies between 12 and 20%. The energy balance in steady state under a number of defined arterial loads was also analyzed. The hearts attained reproducible maxima of mechanical efficiency at specific loads. Methods to allocate reference points in the energy scheme are discussed. The yield of biochemical energy from the perfusion fluid (utilized for contraction and heat production) was (on average) 21 J per cm3 oxygen consumption (energy equivalent of oxygen). No obvious correlation between this value and the mechanical efficiency was evident.

A constant temperature perfusion system employing four heat exchangers has been developed in which perfusion fluid is heated from room temperature to 37 +/- 10 -4 degrees C for precision heat flow measurements on isolated working rat hearts. The temperature characteristics have been established and mathematical expressions developed to identify and quantify spurious thermal events. The system is a refinement of existing perfusion systems for metabolic and mechanical investigations which meets the complete requirements of myocardial energetics. It can also be used for experiments which include high precision temperature measurements on isolated working hearts or for thermal investigations on other isolated perfused organs where a highly stabilised temperature base line is required over perfusion flows from 0-100 cm3 min -1.

Total global ischaemia of the normothermic working rat heart caused an initial positive inotropic response characterized by vigorous contractions. After +/- 15 s this response reached a peak whereafter the isotonic contraction amplitude started to decline. After +/- 3.5 min the heart ceased to beat. The low level of high energy phosphates (HEP), determined 3 min after the onset of ischaemia, indicated that these phases of contractility during ischaemia might play a significant role in depleting HEP. This was substantiated by the observation that inhibition of the contractions during ischaemia by low calcium or high potassium solutions resulted in conservation of myocardial adenosine triphosphate (ATP) and creatine phosphate (CP) stores. It also resulted in the prevention of contracture development during ischaemia and improved mechanical recovery during reperfusion. It was therefore concluded that inhibition of contractility immediately after the onset of total global ischaemia of the normothermic working rat heart is of prime importance in mechanical recovery during reperfusion.