Monitoring great ape heart health through innovative electrocardiogram technology: Training methodologies and welfare implications

Assessing and treating cardiovascular disease (or heart disease) is a growing concern for institutions housing great apes, as it is a major cause of mortality in all four taxa managed in human care. As part of a proactive monitoring plan, zoological managers and veterinarians often elect to perform electrocardiograms (ECGs) on their great ape populations. ECGs noninvasively evaluate cardiac electrical activity, and are thereby capable of providing information regarding heart function. This electrical signature is transcribed as a visual display of waveforms, referred to as telemetry strips, and can detect irregularities in heart rhythm, also known as arrhythmia. While traditional 6- or 12-lead ECGs are recommended periodically as part of a thorough heart performance evaluation, here we discuss the KardiaMobile (KM) device as an additional primate welfare tool. KM is a small, Food and Drug Administration-cleared, clinical-grade mobile ECG monitor that requires only 30 s of pressure to flag heart rate or arrhythmic abnormalities. We detail the training process and applicability to great apes in human care.     

Respiratory changes induced by guanidines and cations in submitochondrial particles

Alkylguanidines inhibit the respiration of submitochondrial particles oxidizing NADH, while hydrophilic guanidines stimulate the rate of oxygen uptake. Regardless of the effect that a guanidine exerts on respiration, all guanidines tested inhibited the stimulatory action of K⁺ on the oxygen uptake of submitochondrial particles. It was found also that octylguanidine modified the Arrhenius plot of respiration of the particles. These findings suggest that alkylguanidines exert their action through the interaction of the alkyl chain with a hydrophobic region in the membrane and also through the interaction of the guanidine moiety with a certain locus in the membrane.The results of studies made on the effect of a wide variety of cations on the respiration of submitochondrial particles may be explained on the assumption that in the inner membrane of the mitochondria exists a negatively charged surface or region with which cations can interact. These results also suggest that the stimulation or inhibition of respiration induced by a given cation depends on the ease with which it can move within this hypothetical negative region.