To understand the collapse of the heart, first, the heart rate must be well understood. The heart rate in a fish is a combination of the intrinsic heart rate and the extrinsic modulations that act on it, such as excitatory adrenergic stimulations and inhibitory cholinergic stimulations (Nilsson, 1983). With the hypothesis that intrinsic heart rate might be the limiting factor, many have attempted to study the intrinsic cardiac functioning to further the understanding of the mechanical properties of the heart (Reference). However, the experiments were conducted on intact fish where the extent of extrinsic modulation is mostly unknown; therefore, even by blocking the adrenergic and cholinergic receptors we still cannot know the distinct point
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In in situ heart perfusion, the heart is disconnected from any physiological influence, including adrenergic and cholinergic receptors, while it is still intact and protected inside the pericardial cavity and directly infused with physiological saline solution. Considering l the above information, the objective of this study is first, to understand the effects of acute warming on the intrinsic cardiac functioning where all the other environmental are optimum, such oxygen content. Second, to understand the extent of the excitatory adrenergic stimulations on the intrinsic cardiac functioning. These aims were achieved by warming the heart acutely starting at 12 oC. Furthermore, the rate of warming was chosen to be 5oC per hour, so the temperature of the cardiac collapse can be closely monitored and the upper thermal limit at which cardiac arrhythmia takes place (Casselman et al., 2012), cannot go unnoticed. The In situ heart was warmed without any extrinsic modulation until it reached it reached arrhythmia at Tarr. Once an arrhythmia is reached then it was quickly brought down to 5oC below the Tarr, where it was subjected to either intermediate concentration or maximum concentration of adrenaline. Following this intervention, the heart continued to be subjected to the acute warming and any changes in Tarr due to interventions were noted. Our prediction was adrenergic intervention would have a positive chronotropic effect on the heart and with the increase in the concentration of adrenaline, will increase Tarr as
In in situ heart perfusion, the heart is disconnected from any physiological influence, including adrenergic and cholinergic receptors, while it is still intact and protected inside the pericardial cavity and directly infused with physiological saline solution. Considering l the above information, the objective of this study is first, to understand the effects of acute warming on the intrinsic cardiac functioning where all the other environmental are optimum, such oxygen content. Second, to understand the extent of the excitatory adrenergic stimulations on the intrinsic cardiac functioning. These aims were achieved by warming the heart acutely starting at 12 oC. Furthermore, the rate of warming was chosen to be 5oC per hour, so the temperature of the cardiac collapse can be closely monitored and the upper thermal limit at which cardiac arrhythmia takes place (Casselman et al., 2012), cannot go unnoticed. The In situ heart was warmed without any extrinsic modulation until it reached it reached arrhythmia at Tarr. Once an arrhythmia is reached then it was quickly brought down to 5oC below the Tarr, where it was subjected to either intermediate concentration or maximum concentration of adrenaline. Following this intervention, the heart continued to be subjected to the acute warming and any changes in Tarr due to interventions were noted. Our prediction was adrenergic intervention would have a positive chronotropic effect on the heart and with the increase in the concentration of adrenaline, will increase Tarr as