PROPERTIES OF HEART MUSCLE 181 



flowing through the heart is diminished by a greater internal pressure and 

 a consequent distention of the heart, even when it is beating (Hyde). 



The flow of blood from the coronary veins is temporarily hindered by the 

 contraction of the right auricle, since at this time the mouth of the common 

 sinus is narrowed an effect which is aided also by the valve of Thebesius. 

 But the same temporary stoppage tends to favor dilatation of the heart wall, 

 thereby making the auricular systole that much easier. When the auricles 

 relax the coronary veins empty themselves again, and the elasticity of the 

 ventricular wall, which is important for the prompt closure of the atrio- 

 ventricular valves, can the more readily assert itself (v. Vintschgau, cf. 

 page 166). 



Since the coronary arteries do not anastomose with one another, ligation 

 of one of its branches deprives the corresponding part of the heart wall of its 

 blood supply, and a coagulation necrosis then makes its appearance. In such 

 a region the power of contraction is retained however for at least eleven hours ; 

 and in animals which survived well the operation of tying off a large arterial 

 branch, the frequency and rhythm of the heart beats and the heart sounds 

 were normal throughout for thirty-six to fifty-four hours afterwards (Baum- 

 garten). Small restricted anaemias were in general well borne. 



It is evident that the heart muscle must eventually die, if one of the 

 larger branches of the coronary arteries becomes impassable. What is diffi- 

 cult to explain however is the circumstance that the coordination of the cardiac 

 muscle fibers, upon ligation of a large arterial branch, ceases almost imme- 

 diately (within one hundred to one hundred and twenty seconds) and the 

 heart falls into fibrillary contractions. The same thing happens even -if 

 the ligature is loosed before the inception of these disturbances (Cohnheim 

 and v. Schulthess-Rechberg). Since, however, one often meets with cases 

 where such sudden disturbance of the heart's activity does not follow stoppage 

 of its blood supply, it has been assumed by many that this is traceable to 

 some injury to the ventricular wall. Porter on the contrary has shown that 

 fibrillary contractions appear if the blood flow in an artery is stopped in such 

 a way that no possible injury to the ventricular wall can 'occur, and takes 

 the view therefore that such contractions are caused by scanty nourishment 

 to the heart muscle. That they do not appear in the heart at death from all 

 manner of causes, he explains by saying that the heart is seized with fibrillary 

 contractions only in case it is working against great resistance when the dis- 

 turbance to its nourishment occurs. When the resistance is not great (and 

 is diminishing gradually) the contractility of the heart muscle decreases stead- 

 ily, but gradually, and when finally the heart comes to a standstill the residual 

 contractility remaining in it is no longer sufficient to produce well-defined 

 fibrillary contractions. Whether this explanation is correct in all points can- 

 not be definitely decided at this time. 



The heart muscle can get its nourishment not only through the coronary 

 arteries but also through the veins of Thebesius. From observations on extir- 

 pated hearts, it is seen that the food which can be supplied by these vessels is 

 sufficient to maintain rhythmical contractions for a considerable time. The 

 same is true of artificial perfusion through the coronary veins (Pratt). 



