Application of chaos theory to a model biological system: evidence of self-organization in the intrinsic cardiac nervous system.
The neutral organization that determines the specific beat-to-beat pattern of cardiac behavior is expected to be demonstrated in the independent regulation of the RR intervals (chronotropy) and the corresponding QT subintervals (inotropy), as the former defines the rate of contraction and the latter has a linear negative correlation with the peak pressure inside the contracting ventricular muscles. The neurons of the isolated cardiac nervous system, many of which are located in the fat-pads of the heart, exhibit the same types of mechanical and chemical receptors and the same types of cholinergic and noradrenergic effectors as those found in the neural superstructure. In the surgically isolated and perfused rabbit heart we studied the responses of the QT and RR intervals evoked by block of coronary blood flow. We found that if we separated each RR cycle into QT and RR-QT components, then the dynamics of variation for each subinterval series often had the same fractional number of degrees of freedom (i.e., chaotic dimensions), a finding which suggests they are both regulated by the same underlying system. The ischemia/anoxia evoked transient dimensional increases and separations between the two subinterval series that, after the temporary divergence, reconverged to having the same lower value. The dimensional fluctuations occurred repeatedly and preceded or coincided with alterations in the magnitude and sign of the slope of QT vs RR-QT. We interpret the dimensional fluctuations of the two subinterval series as correlates of adaptation-dependent self-organization and reorganization in the underlying intrinsic cardiac nervous system during accumulating ischemia/anoxia. Such attempts at functional reorganization in this simple neurocardiac system may explain the transient dimensional changes in the RR intervals that precedes by 24 hrs the occurrences of fatal ventricular fibrillation in high-risk cardiac patients.
Skinner
J E
JE
Totts Gap Institute, Bangor PA 18013, USA.
Wolf
S G
SG
Kresh
J Y
JY
Izrailtyan
I
I
Armour
J A
JA
Huang
M H
MH
D000465:Algorithms; D000818:Animals; D003326:Coronary Circulation / Q000502:physiology; D004285:Dogs; D004562:Electrocardiography; D006321:Heart / Q000294:innervation*; D006339:Heart Rate; D066298:In Vitro Techniques; D008297:Male; D008839:Microelectrodes; D008954:Models, Biological; D009200:Myocardial Contraction / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology; D017711:Nonlinear Dynamics; D011817:Rabbits