窦性起搏对心室肌纤维自发节律位相重置性质的数值研究

本文应用Beeler-Reuter模型，选取损伤电流I＝23μA，产生自发振荡，施加不同程度的电流脉冲刺激，研究窦性起搏对心室肌纤维自节律位相重置的过程，结果表明：当外加电流脉冲强度小于14时，体现位相奇重置，反之，体现位相偶重置，并给出位相重置函数。     

Cardiovascular ‘reactivity’ to graded splanchnic nerve stimulation in spontaneously hypertensive and normotensive control rats

Cardiovascular ‘reactivity’ to graded splanchnic nerve stimulations was compared in adult spontaneously hypertensive rats (SHR) and normotensive controls (NCR), during abolished adrenal medullary secretion and neurogenic cardiac control and depressed reflex vascular adjustments. Arterial pressure, heart rate and cardiac output were measured, and total peripheral resistance (TPR) and stroke volume (SV) computed before, during and after nerve stimulation. The neurogenic resistance increases in the major gastrointestinal-renal-hepatic circuits expressed themselves as TPR elevations, which were much accentuated in SHR. This reflects an increased w/r₁ of SHR resistance vessels rather than any altered effector sensitivity, since the responses were particularly accentuated at high discharge rates when noradrenaline junction concentrations approach maximal levels. The splanchnic capacitance responses expressed themselves as SV increases, being the most relevant aspect of capacitance control. SV increased less in SHR, mainly reflecting the reduced diastolic compliance of the hypertrophied SHR left ventricle and the consequent rightward shift of its Frank-Starling curve. The results indicate that an elevated resistance may well be maintained by a normal sympathetic discharge in established SHR hypertension. There seems, however, to be an increasing need for accentuated discharge to the capacitance side to maintain proper cardiac filling of the hypertrophied left ventricle.     

Entrainment mapping: Theoretical considerations and practical implementation

Entrainment mapping enables the diagnosis and characterization of reentrant arrhythmias from analysis of the specific interaction between pacing maneuvers and tachycardia. Described 40 years ago, the implementation and interpretation of pacing maneuvers to entrain tachycardias has evolved into an indispensible tool for diagnosis and mapping reentrant cardiac arrhythmias. For complex re‐entry pathways entrainment mapping allows determination of the relation of pacing sites to the re‐entry circuit and discrimination of relevant re‐entry parts from bystander areas. Careful interpretation is needed to recognize misleading findings. The general physiology of re‐entry, and the application, interpretation, limitations, and pitfalls of entrainment maneuvers used for cardiac mapping is reviewed.     

Voltage-gated calcium channels play crucial roles in the glutamate-induced phase shifts of the rat suprachiasmatic circadian clock

The resetting of the circadian clock based on photic cues delivered by the glutamatergic retinohypothalamic tract is an important process helping mammals to function adaptively to the daily light-dark cycle. To see if the photic resetting relies on voltage-gated Ca(2+) channels (VGCCs), we examined the effects of VGCC blockers on the glutamate-induced phase shifts of circadian firing activity rhythms of suprachiasmatic nucleus (SCN) neurons in hypothalamic slices. First, we found that a cocktail of amiloride, nimodipine and omega-conotoxin MVIIC (T-, L- and NPQ-type VGCC antagonists, respectively) completely blocked both phase delays and advances, which were, respectively, induced by glutamate application in early and late night. Next, we discovered that: (i) amiloride and another T-type VGCC antagonist, mibefradil, completely obstructed the delays without affecting the advances; (ii) nimodipine completely blocked the advances while having less impact on delays; and (iii) omega-conotoxin MVIIC blocked largely, if not entirely, both delays and advances. Subsequent whole-cell recordings revealed that T-type Ca(2+) currents in neurons in the ventrolateral, not dorsomedial, region of the SCN were larger during early than late night, whereas L-type Ca(2+) currents did not differ from early to late night in both regions. These results indicate that VGCCs play important roles in glutamate-induced phase shifts, T-type being more important for phase delays and L-type being so for phase advances. Moreover, the results point to the possibility that a nocturnal modulation of T-type Ca(2+) current in retinorecipient neurons is related to the differential involvement of T-type VGCC in phase delays and advances.     

Blood Pressure Regulation during Exercise

This brief review examines five problems concerning arterial blood pressure regulation during exercise. These are:

1. A history and summary of evidence that baroreflexes are, or are not, active during exercise.

2. What might be other “regulators” of blood pressure during exercise? The characteristics of a blood pressure-raising reflex from ischemic and active skeletal muscle (muscle chemoreflex) is reviewed along with a putative role for centrally generated motor command signals (central command).

3. How blood pressure is maintained during exercise. The importance of regional vasoconstriction, particularly in active skeletal muscle, is reviewed.

4. How well matched are cardiac output and total vascular conductance? Does demand for muscle blood flow outstrip cardiac pumping capacity?

5. Reflex control of blood pressure by both baroreflexes and muscle chemoreflexes. The importance of baroreflexes and evidence for resetting is reviewed. A new hypothesis is stated.     

NEURAL CONTROL OF MUSCLE BLOOD FLOW: IMPORTANCE DURING DYNAMIC EXERCISE

1. The present review examines the control of muscle vascular conductance by the sympathetic nervous system during exercise. 2. Evidence for tonic sympathetic neural control of active muscle rests on three findings: (i) directly measured muscle sympathetic nerve traffic is increased; (ii) spillover of noradrenaline from active muscles is also increased; and (iii) withdrawal of sympathetic outflow to active muscle either by acute blockade of its sympathetic nerve supply or by reflex inhibition of sympathetic nervous activity raises muscle vascular conductance via inhibition of tonic vasoconstriction. 3. Loss of tonic sympathetic control of muscle vascular conductance during mild to severe exercise causes marked hypotension despite maintenance of a normal cardiac output. 4. The extent to which active muscle can vasodilate in intact animals appears to have been hidden by tonic vasoconstriction. This vasoconstriction appears to be minimally affected by metabolites in oxidative (red) muscle, but may be inhibited in predominantly glycolytic (white) muscle owing to different spatial distributions of α- and α₂-adrenoceptors in the two muscle types and to the different susceptibilities of the two receptor types to interference by metabolites. 5. The reflexes causing vasoconstriction in active and inactive muscles are unknown. One hypothesis is that a flow-sensitive muscle chemoreflex raises sympathetic outflow to reduce accumulations of muscle metabolites caused by mismatches between muscle blood flow and metabolism, called ‘flow errors’. Another hypothesis is that the arterial baroreflex corrects mismatches between cardiac output and vascular conductance called ‘pressure errors’. This review argues for a dominance of control by the baroreflex based on the following observations: (i) the arterial baroreflex is essential to the normal rise in sympathetic nervous activity and arterial pressure at the onset of exercise; (ii) during submaximal exercise, a functioning arterial baroreflex is required to maintain tonic sympathetic activity and prevent arterial hypotension; and (iii) whereas a muscle chemoreflex may be needed to guard against hypoperfusion of active muscle, the arterial baroreflex must oppose hypotension by initiating sympathetic vasoconstriction to oppose muscle vasodilation.     

Effect of Strength and Timing of Transmembrane Current Pulses on Isolated Ventricular Myocytes

INTRODUCTION: Little is known about how the amplitude and timing of transmembrane current pulses affect transmembrane potential (Vm) and action potential duration (APD) in isolated myocytes. METHODS AND RESULTS: Ten ventricular myocytes were isolated from five rabbit hearts. Each cell was paced at an S1 cycle length of 250 msec, and S2 pulses of 10-msec duration were delivered at various strengths and time intervals. For all S2 strengths (0.2 to 1.5 nA), the magnitude of changes in Vm did not depend on polarity during the plateau, but were larger for depolarizing pulses during phase 3 repolarization. However, the magnitude of changes in APD varied with polarity during the entire action potential for strengths ranging from 0.5 to 1.5 nA. Greater changes in APD occurred for hyperpolarizing pulses during the plateau and depolarizing pulses during phase 3. In addition, we used a cardiac phase variable to quantify the current threshold for regenerative depolarization and repolarization as a function of prestimulus Vm. Regenerative depolarization occurred during phase 3 repolarization, and its current threshold was less than that required for regenerative repolarization that occurred during the plateau. These data were compared to computer simulations in a patch of membrane represented by Luo-Rudy dynamic kinetics, and the results were qualitatively similar, including the higher threshold for regenerative repolarization compared to regenerative depolarization. CONCLUSION: This characterization of the nonlinear response of isolated cells to transmembrane current, including phase resetting, should aid in understanding the mechanisms of defibrillation because shock-induced changes in Vm and APD have been implicated as important factors in determining defibrillation success.     

Unusual Resetting Patterns in Response to Single Atrial Extrastimuli During AV Junctional Reentrant Tachycardia

Unusual Resetting Patterns in AV Junctional Reentry. Introduction : Two unusual resetting patterns were observed in two patients with slow-fast AV junctional reentrant tachycardia (AVJRT) submitted to an electrophysiologic study.
Methods and Results : After AVJRT induction, resetting was evaluated by introducing single extrastimuli at progressively shorter coupling intervals from the high right atrium (HRA) and the proximal coronary sinus (CS). An alteration in the return cycle length duration allowed demonstration of resetting. In the first patient, during an AVJRT with a large excitable gap, properly timed extrastimuli delivered both from the HRA and CS simultaneously reset the tachycardia and advanced the H electrogram of the preceding tachycardia beat. In the second patient, both HRA and CS stimulation apparently failed to reset AVJRT (return cycle length unchanged), but, at critical coupling intervals, the cycle length duration of the tachycardia beat following the return cycle was consistently shortened.
Conclusions : During slow-fast AVJRT, single atrial stimulation from sites remote to the reentrant circuit may result in unusual resetting patterns. Further studies are required to evidence the full spectrum of resetting in AVJRT.     

Structurally reduced distensibility of cardiovascular ‘low-pressure’ compartments in primary hypertension,as studied in spontaneously hypertensive rats (SHR)

Adult male spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) were compared to explore to what extent venous ‘unstressed’ volume, compliance and wall distensibility are structurally altered in primary hypertension. The perfused, maximally vasodilated hindquarters and the entire, completely relaxed cardiovascular system during cardiac arrest were used for comparisons of ‘initial’ volumes and pressure-volume characteristics of the respective low-pressure compartments. In both preparations SHR and WKY showed identical ‘unstressed’ venous volumes, computed by extrapolation to zero pressure from initial volumes and the nearly linear pressure-volume relationships, while venous compliance (Δ/ΔP) was in each case about 20% reduced in SHR. Consequently, the structurally determined wall distensibility of the low-pressure compartment, calculated as the square root of volume compliance/unstressed (or initial) volume, was significantly reduced in SHR; about 10%. Such venous ‘structural resetting’ has important hemodynamic consequences, not least because it reinforces increase of venous return and cardiac filling pressure in SHR, caused by given sympathetic activations. Evidently, not only resistance, cardiac and barostat functions but also the venous capacitance function are structurally reset early in primary hypertension, implying a redesign of the entire cardiovascular system to operate at a higher pressure equilibrium.     

Alpha phase reset contributes to the generation of ERPs

An unresolved question in electroencephalogram (EEG) research is whether event-related potentials (ERPs) are generated by phase-reset or evoked response. We analyzed data of a visual feature detection task and will show 1) phase concentration in the alpha frequency range, 2) ongoing alpha activity prior to stimulus onset, 3) evoked alpha oscillation in the ERP, 4) lack of power increase during phase concentration, 5) decrease in amplitude variance during early evoked components preceding a decrease in power, and 6) the same cortical sources for induced prestimulus power and evoked poststimulus power. Because none of these data provide unequivocal evidence for phase reset, we additionally tested the basic assumption of the evoked model, which is the additivity of the evoked response on the basis of a simulation approach. Our findings suggest that nonadditive processes-typical for a phase reset-are involved in the generation of the ERP. Thus, together with the other findings this study provides unequivocal evidence for phase resetting in the human EEG.