Effect of stunning current frequency on carcass downgrading and meat quality of turkey.

The objective of this study was to determine the effect of frequency of a 150 mA water-bath stunning current on turkey hen carcass and meat qualities. Fifty turkey hens were subjected to water-bath stunning with alternating current of various frequencies: 50 Hz (n = 12), 300 Hz (n = 14), 480 Hz (n = 12), and 600 Hz (n = 12); the duration of stunning was 4 s for each bird. Carcass defects such as engorged wing veins, red wing tips, and hemorrhages were recorded. Turkey meat quality traits (M. Pectoralis major) were assessed based on rigor mortis development, color, drip loss, cooking loss, tenderness, and cooking yield of cured products. The data showed that frequencies of 480 Hz and 600 Hz are associated with an increased rate of postmortem pH decline (during bleeding). This effect is most likely due to the occurrence of vigorous wing flapping during the first 3 min poststunning. Under the experimental conditions of the present work, the increase in rate of pH decline after stunning at 480 and 600 Hz did not induce carcass and meat quality defects. However, before any recommendation is given, the influence of stunning frequency on turkey meat quality needs to be evaluated under industrial conditions.

Effect of current frequency during electrical stunning in a water bath on somatosensory evoked responses in turkey's brain.

Somatosensory evoked responses (SEP) in a turkey's brain were determined after water-bath stunning with a 150-mA (constant current) delivered with 50, 300 or 600 Hz, or with 75 mA, delivered with 50-Hz alternating current (AC) in order to evaluate the effectiveness of stunning. Ninety-four BUT 9 turkey hens 12 weeks of age were surgically implanted with EEG recording and left wing nerve stimulating electrodes 4 hours before stunning. They were individually stunned by immersion of the head and upper part of the neck in a water bath for 4 s. Using a 150-mA current, all birds stunned at 50 Hz showed cardiac arrest and a flat EEG immediately after the stun with no SEP recovery. The incidence of cardiac arrest at stunning decreased with increasing current frequency but SEP were lost in all birds. In birds that survived the stun, the duration of SEP abolition was on average 69 and 34 seconds at 300 and 600 Hz, respectively. Stunning with a 75-mA AC, delivered with 50 Hz, induced cardiac arrest in 32 per cent of turkeys. SEP were abolished in only 71 per cent of the birds that survived the stun, with an average duration of SEP of 66 seconds. The results indicate that increasing the frequency of a 150-mA AC current leads to a decreased stunning efficiency. A current of 75 mA per bird is unacceptable since 29 per cent of the birds do not show SEP abolition.

The effect of current frequency during waterbath stunning on the physical recovery and rate and extent of bleed out in turkeys.

Two experiments were carried out to evaluate the influence of the frequency of a sinusoidal stunning current (150 mA, 4 s) on the physical recovery of turkey hens and toms and on the rate and extent of blood loss. In the first experiment, physical recovery of 72 hens and 78 toms was estimated after stunning with one of five different frequencies. The incidence of cardiac arrest after stunning at 50, 300, 480, 550, and 600 Hz was, respectively, 100, 60, 30, 30, and 0% in hens and 53, 38, 0, 0, and 0% in toms. In hens, time to return of corneal reflex and neck tension and the onset of wing flapping decreased as frequency increased. In contrast to hens, about half of the toms stunned at 50 Hz did not show cardiac arrest. In these animals, recovery after 50 Hz was significantly longer than recovery at the four other frequencies. In the second experiment, 50 hens and 53 toms were bled out by a unilateral neck cut 10 s after stunning with one of four different frequencies (50, 300, 480, and 600 Hz). The rate and extent of blood loss within 3 min, relative to live weight, increased as stunning frequency increased. Large differences in the rate and extent of blood loss were observed between turkeys stunned at 50 or 300 Hz, according to the occurrence of cardiac arrest: cardiac activity was associated with significantly higher rate and extent of blood loss in both sexes. Overall, the results suggest that the duration of unconsciousness decreases as stunning frequency increases.

Extracellular K+ dependence of inward rectification kinetics in human left ventricular cardiomyocytes.

BACKGROUND: In human ventricular cells, the inwardly rectifying K+ current (IK1) is very similar to that of other mammalian species, but detailed knowledge about the K+-dependent distribution of open and blocked states during rectification and about the K+-dependent modulation of inactivation on hyperpolarization is currently lacking. METHODS AND RESULTS: We used the whole-cell patch-clamp technique to record IK1 in myocytes isolated from subendocardial layers of left ventricular septum from patients with nonfailing hearts with aortic stenosis and cardiac hypertrophy who were undergoing open-heart surgery. Outward currents were very small at voltages positive to the reversal potential but increased at high external [K+]. Chord conductance measurements and kinetic analyses allowed us to estimate the proportion of channels in the open state and of those showing either slow unblock or instantaneous unblock (the so-called slow or instantaneous "activation") on hyperpolarization: the distribution in the individual states was dependent on external [K+]. The proportion of channels unblocking slowly was greater than that of channels unblocking instantaneously on hyperpolarization from the plateau voltage range. Hence, because of the previously reported link between the presence of highly protonated blocking molecules and slow unblock kinetics, it is suggested that high cellular concentrations of spermine may account for the low outward current density recorded in these cells. The current decrease observed on extended hyperpolarization was significantly relieved by an increase in external [K+]. CONCLUSIONS: The pattern of IK1 current alterations observed in the present model of human ventricular hypertrophy might favor enhanced excitability and underlie ventricular arrhythmias, possibly via increased intracellular polyamine levels.

Cultured neonatal rat cardiomyocytes and 99mTc-sestamibi to assess the direct effects of cardioplegia.

The efficacy of cardioplegia in neonatal myocardial protection is still a matter of debate. 99mTc-sestamibi cellular accumulation reflects sarcolemmal and mitochondrial electrical gradients. It was used to monitor the direct effects of two cardioplegic solutions, modified St Thomas' Hospital and Bretschneider, on normoxic and metabolically-inhibited cultured cells. Cellular accumulation of 99mTc-sestamibi, expressed by the ratio between intra and extra cellular concentrations, was assessed in three different sets of neonatal rat cardiomyocytes. Cells were either treated with different concentrations of modified St Thomas' solution (50, 75, 100%), they were treated or recovering from a treatment with modified St Thomas and Bretschneider solutions at 50% concentrations, or were recovering from treatment with modified St Thomas' and Bretschneider solution at 50% concentrations mixed with metabolic inhibitors. Cardioplegia depressed the tracer accumulation in a concentration-dependent manner. This effect was independent of the type of cardioplegia (120-min uptake, as a percentage of control values, modified St Thomas' 68+/-12 and Bretschneider 59+/-7) and was rapidly reversible. Cardioplegia was unable to prevent the depression of tracer accumulation induced by metabolic inhibitors and even induced a deleterious effect (120-min uptake, as a percentage of control values, metabolic inhibitors 69+/-12, metabolic inhibitors + modified St Thomas 38+/-14, metabolic inhibitors + Bretschneider 43+/-6) during recovery after 30 min of metabolic inhibition. It was concluded that cardioplegia has an apparent detrimental effect on neonatal cardiomyocytes accumulation of 99mTc-sestamibi during recovery from an ischaemic-like insult.

Regional alteration of the transient outward current in human left ventricular septum during compensated hypertrophy.

BACKGROUND: A large calcium-insensitive transient outward current (I(to)) has been recorded in atria, left ventricular (LV) free wall, and right ventricular septal subendocardium of the human heart. Recent studies suggested a major contribution of this current to the electrical heterogeneity of the heart. However, no data have been reported on the distribution of I(to) density within the LV septal wall from compensated human LV hypertrophy. METHODS AND RESULTS: Microelectrode and patch-clamp techniques were used to record action potentials and I(to) in myocytes isolated from superficial (<3 mm deep) and deep (3 to 6 mm deep) layers of LV septum from patients with aortic stenosis and compensated LV hypertrophy. Subendocardial specimens were also obtained from undiseased donor hearts. In none of the superficial subendocardial cells from diseased hearts was a macroscopic I(to) recorded (n=42), whereas in cells from the same location from donor hearts, a typical I(to) was clearly present, with a peak density of 5.88+/-0.78 pA/pF at +60 mV (n=4). However, in deep layers from patients with compensated LV hypertrophy, macroscopic I(to) was present, with a peak density of 10.50+/-2.58 pA/pF at +60 mV (n=4). The absence of I(to) in superficial septal cells from hypertrophied hearts was not due to a divalent cation-related shift of the current kinetics. Instead, extracellular Ca2+ removal induced an I(to)-like current, possibly carried by K+ ions, with a peak density of 30.7+/-2.6 pA/pF at +60 mV (n=29). However, its magnitude, kinetics, and pharmacological characteristics did not allow identification of this current as the usual I(to). CONCLUSIONS: Both topography and pathology can be major modulating factors of the regional distribution of I(to) density in human LV septum. Therefore, they may play a prominent role in determining electrical gradients within this region from which the early depolarization vectors start and the left-to-right activation sequence of the interventricular septum proceeds.