Absence Of Overshoot Research Articles

Differential Requirement for de novo RNA Synthesis in the Starved-refed Rat; Inhibition of the Overshoot by 8-Azaguanine after Refeeding

The activities of phosphohexose isomerase, pyruvate kinase, L-α-glycerophosphate dehydrogenase, glucose 6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, malic enzyme, dihydroxyacetone kinase and hexose phosphorylating capacity were measured in ad libitum-fed rats, starved rats, and starved rats refed for 1, 2 and 3 days. The activities of all enzymes measured increased to about twice the level measured in rats adapted to ad libitum feeding on days 2 and 3 of refeeding, except the activity of L-α-glycerophosphate dehydrogenase and the hexose phosphorylating capacity, which after the overshoot at 2 days returned to normal levels 3 days after refeeding. Treatment with 8-azaguanine resulted in high levels of liver glycogen and prevented the overshoot in enzyme activities — but not the increase back to normal levels. Phosphorylase activity was the same in both treated and nontreated rats; thus, increased liver glycogen levels in rats treated with azaguanine could not be explained on the basis of phosphorylase activity. 8-Azaguanine did decrease food intake; however, the overshoot was also observed in pair-fed rats. Therefore, the absence of overshoot in azaguanine-treated rats was not due to a decrease in food intake. The observed overshoot in enzyme activities on day 2 of refeeding was not observed in rats which received the first injection of the antibiotic 12 hours after refeeding. A possible explanation of the data is that the overshoot observed after refeeding is dependent on de novo RNA synthesis which occurs at least 12 hours after refeeding.

Studies on sinocaval conduction

Many studies on the cardiac transmembrane potentials and on the sequence of activation of the heart have been reported. However, there have been only a few reports on the transmembrane potentials of the musculature in the great vessels proximal to the heart and on the excitation conduction from the heart to these vessels. Previously, MASHIBA and coworkers reported that, in the in situ rabbit, the sinus node impulse spreads not only to the atrial muscle but also to the musculature in the vena cava. They called this phenomenon "sinocaval conduction". To extend this observation, in the present paper, the author studied on the sinocaval conduction of the rabbit atriocaval preparation with the microelectrode methods. METHODS In the rabbit, there are three venaec avae which empty into the right atrium by separate ostia: right superior vena cava, left superior vena cava and inferior vena eava. In all experiments, the preparation consisting of atria resected together with three venae cavae (atriocaval preparation) was used (Fig. 1). The preparation was perfused with oxygenated Tyrode solution at a constant temperature (35-37°C) and with a constant flow. As for intracellular electrode, the LING-GERARD type of microelectrode was used which was filled with 3 M KCl solution and had 20-40 Megohm electrical resistance. RESULTS 1 . Shape of the transmembrane action potentials of the musculature in the rabbit venae cavae (Fig. 2 and 3). On the basis of the shape of the observed action potentials, 4 functional regions could be described in the vena caval tissues: I) sinus node, II) sinocaval (SC) areas, 111) superior venae cavae and IV) inferior vena cava. The features of the action potentials in the sinus node are the marked diastolic slow depolarization, the slow rate of rise, the low amplitude and the absence of overshoot.

The role of acetylcholine and cholinesterase in sympathetic ganglia

The effects of applied acetylcholine (ACh) and physostigmine upon waveformsAandB in virus-infected sympathetic ganglia of the rat were studied in vitro with standard electrophysiological techniques. ACh produced a simultaneous and synchronous increase in frequency and decrease in amplitude of both waveforms without changing the original form; the waveforms still appeared as single, simultaneous and synchronous waves or oscillations with a more rapid decay time and consistent overshoot of waveformB. The effects of physostigmine were markedly different from those of ACh. Physostigmine application resulted in an increase of decay time of both waveforms and the absence of overshoot in waveformB. In addition, single waveforms or oscillations were replaced by bursts of activity of long duration. It was concluded that ACh acted at sites represented by Capacitor I and operationA; that physostigmine acted at sites represented by Capacitors I and II and operationsAandB. It was suggested that intrinsic ACh was a constituent of structures represented by Capacitor I and played a role in operationA. Cholinesterase was a constituent of structures represented by Capacitors I and II and played a role in both operationsAandB.