Effects of a Static Magnetic Field on Hemodynamics During Administration of a Cell Membrane Calcium Channel Blocking Agent

We investigated the influence of a 0.2 T static magnetic field (SMF) on the carotid sinus region in rabbits during infusion of a cell membrane calcium channel blocking agent (verapamil). The experiments were carried out under pentobarbital anesthesia. Blood pressure, heart rate, and respiration were also monitored. Contrary to our earlier studies without verapamil (1–4), the SMF had no significant effect on blood pressure and heart rate during verapamil infusion. Changes in calcium membrane channel transport might be participants in SMF effects on sinocarotid baro-receptors.     

Influence of substance P on carotid sinus nerve baro- and chemoreceptor activity in rabbits.

Substance P (SP) is abundant in the carotid sinus nerve (CSN) and has been implicated in baro- and chemoreceptor reflexes. We examined the effect of SP on blood pressure, heart rate, phrenic nerve activity, hindlimb perfusion pressure, and cardiac contractile strength in urethane-anesthetized rabbits with bilaterally cut cervical sympathetic, vagus, and aortic depressor nerves. Retrograde simultaneous injection of SP (0.5-2.7 micrograms/kg in 0.2-0.3 ml saline) into both carotid sinus areas via the internal carotid arteries decreased blood pressure (by 56%), heart rate (by 13%), cardiac contractility (by 25%) and phrenic nerve activity (by 77%). The effect on hindlimb perfusion pressure was variable. There was both a reflex effect and direct hindlimb vasodilation. In another group of rabbits, the carotid sinus areas were vascularly isolated and perfused with SP (0.19 micrograms/min dissolved in Locke's solution) or Locke's solution alone for 5 min. While carotid sinus perfusion pressure was maintained in the range of 80-120 mmHg, mean arterial blood pressure, heart rate, and unit activity from the CSN were recorded. SP increased the activity of 11 of 18 baroreceptor fibers and inhibited all of 20 chemoreceptor fibers. SP decreased mean arterial blood pressure and heart rate, but the changes were less than those obtained with injection of SP into nonisolated carotid sinus arteries because systemic effects of SP, which in some cases counteracted the reflex effects, were eliminated.     

缓冲神经在电针抑制犬急性实验性高血压中的作用

在切除双侧窦神经与主动脉弓神经的慢性犬,血压很快回复至对照水平,但较易波动。在此种犬静脉匀速注射去甲肾上腺素造成高血压状态时,电针“足三里”不再有明显降压作用。在麻醉犬静脉勻速注射去甲肾上腺素时,肾交感冲动随血压上升而受到明显抑制,然后在16分钟内逐渐回升。血压上升时呼出气 CO_2百分比明显升高,伴随动脉血 CO_2分压升高而 O_2分压降低。在切除缓冲神经后再注射去甲肾上腺素时,肾交感冲动未见明显变化。在清醒犬静脉匀速注射去甲肾上腺素时,动脉血 O_2分压也有明显降低,而注射苯肾上腺素时,血 O_2分压很少改变。电针“足三里’对苯肾上腺素性高血压的降压作用不明显。且心得安可阻断电针对去甲肾上腺素性高血压的降压作用。此外,电针能抑制山梗菜碱所致的化学感受性升压反射,此种抑制作用可为静脉注射纳洛酮所阻断。结果表明,去甲肾上腺素除能收缩血管升高血压,增加压力感受性传入冲动外,还能刺激新陈代谢,改变血液气体成分而引起化学感受性升压反射。电针“足三里”主要因能抑制化学感受性反射而能降压,仅有压力感受性传入冲动的增多并不能使电针具有明显降压效应。     

Static Magnetic Field Effects on Sinocarotid Baroreceptors in Rabbits Exposed under Conscious Conditions

This research is an extension of our previous studies, where we showed that sinocarotid baroreceptors react to a static magnetic field (SMF) in unconscious rabbits (1–7).

The objective was to study the cardiovascular effect of SMF on sinocarotid baroreceptors in conscious rabbits. Two groups of experiments with different protocols were carried out in 18 healthy adult male rabbits. The first group included 31 experimental runs. In this group 0.24 T static bar magnets were positioned under rabbits' carotid sinus areas for 30 min. The second group included 20 experimental runs. In this group 0.5 T static bar magnets were positioned under carotid sinus areas for 40 min. We found that SMF significantly decreased blood pressure and heart rate and increased blood pressure variability and microcirculation during its local application to the sinocarotid baroreceptor region. SMF might stabilize cellular membranes, leading to an increase of buffer capacity of the sinocarotid baroreceptors to blood pressure variations.     

刺激肾神经传入纤维的降压反应与颈动脉窦压力感受性反射的相互作用

在麻醉兔,研究了刺激肾神经传入纤维与颈动脉窦压力感受性反射在减压反射中的相互作用。电刺激肾神经传入纤维引起平均动脉压(MAP)下降,下降程度在一定范围有赖于刺激频率。当颈动脉窦被隔离和主动脉神经切断后,随着颈动脉窦内压逐渐升高,刺激肾神经传入纤维引起的减压反应不断减弱。在45至135mmHg 之间的7个颈动脉窦内压(ISP)水平,刺激肾神经传入纤维,并画出刺激前和刺激时的 ISP-MAP 关系曲线。在颈动脉窦内压为75至105mmHg 之间,刺激肾神经传入纤维显著降低 ISP-MAP 关系曲线的斜率和对ISP 的平均动脉压反应范围。这些结果提示:(1)颈动脉窦压力感受器的传入冲动可调制刺激肾神经传入纤维的降压反应,在一定范围内与颈动脉窦内压呈反比;(2)刺激肾神经传入纤维明显减弱颈动脉窦的压力感受性反射。     

颈动脉窦内压的变化速率对反射性降压效应的影响

在成年狗身上制备右侧孤离颈动脉窦,借助灌流装置用饱和氧的任氏液对其进行灌流。灌流压为搏动性的。通过改变每搏泵出量、灌流管道的阻力和弹性来调节灌流压及其变化速率。用多导生理记录仪同步记录股动脉血压、窦内灌流压及其变化速率。本文主要观察窦内压的变化速率对降压反射的影响。在8只狗身上共进行了93次实验。结果表明,在窦内压相同的情况下,灌流压的上升速率愈快,降压效应愈明显,而其下降速率则无显著作用。已有资料证明搏动性窦内压所引起的降压效应较非搏动性压力更为明显。由此可见,狗的颈动脉窦压力感受器不仅对搏动性压力而且对其上升的变化速率也很敏感。     

Effect of gamma-aminobutyric acid and phenibut on the central links of the vascular reflexes with chemo- and mechanoreceptors of the aorto-carotid zone]

Experiments were conducted on decerebrated cats. A depressive effect of gamma-aminobutyruc acid (GABA)--100--200 mg/kg and its phenyl derivative phenibut--20 mg/kg--on depressive reactions of the systemic arterial pressure and on the inhibition of spontaneous bioelectrical activity in the renal nerve occurring in stimulation of the mechanoreceptors of the carotid sinus and of the sinus and depressor nerve afferents (having a mechanoreceptor modality) was demonstrated. Pressor reactions of the systemic arterial pressure and evoked bioelectrical activity were enhanced in the renal nerve in stimulation of chemoreceptors of the carotid sinus following administration of the same GABA and phenibut doses. The data obtained are interpreted from the aspect of a deprimating action of GABA and phenibut in the area of the paramedian reticular nuclei of the medulla oblongata.     

Effects of auricular electrostimulation and naloxone on nociceptive sensitivity in rabbits

Auriculo-acupuncture electrostimulation (AES) (15 H2) decreased the amplitude of somatosensory evoked potential (EP) in response to tooth pulp electrostimulation in 64% of acupuncture-sensitive unanesthetized rabbits and didn't induce the changes of EP in 36% of animals (acupuncture-resistant rabbits). The systemic naloxone (0.2 mg/kg) injection reversed the AES analgetic effect and induced the hyperalgesic one in acupuncture-sensitive rabbits but induced the analgetic effect in acupuncture-resistant animals. It has been suggested that the differences of individual characteristics of endogenous opioid system determined different naloxone action in acupuncture-sensitive and acupuncture-resistant rabbits.     

Exercise training and the arterial baroreflex

To test the hypothesis that endurance training would attenuate the carotid sinus baroreflex in rats, studies were undertaken with 25 nontrained (NT) and 22 trained (T) male Sprague-Dawley rats that were exercised for 11-14 wk. Maximal O2 consumption was significantly increased 10% after training. The left carotid sinus region was functionally isolated in anesthetized animals. Subsequently, static carotid sinus pressure was raised in 20-Torr increments from 95 Torr until a maximal response in systemic arterial pressure and regional blood flows was recorded. Compared with the NT group, baroreflex control of blood pressure and calculated regional resistance of the T animals was less responsive to changes in carotid sinus pressure. Resting blood pressure, heart rate, and changes in peripheral blood flow velocity were similar for the two groups. Peripheral sensitivity to phenylephrine-HCl and hexamethonium bromide were also similar in the T and NT groups. It was concluded that the arterial baroreflex control of blood pressure was attenuated by exercise training. These findings support the concept that the trained individual is at disadvantage during hypotensive episodes and that endurance training will attenuate the sympathetic component of the arterial baroreflex.     

颈动脉窦区注入枸橼酸钠抑制家兔呼吸的机制

向颈总动脉头端注入枸橼酸钠能使大多数家兔发生呼气性呼吸暂停和呼吸频率变慢。此呼吸抑制效应可被地卡因麻醉颈动脉窦区所消除。切断窦神经不能阻断枸橼酸钠对呼吸的抑制。切断迷走神经窦支则使半数以上家兔的呼吸抑制减弱或消失,而在结状神经节上方切断迷走神经能阻断大多数家兔的呼吸抑制。结果提示,迷走神经窦支是颈动脉窦区感受器传入通路之一,向颈动脉窦区注入枸橼酸钠对呼吸的抑制主要是通过迷走神经传入引起的。     

Specific baroreceptor control of vertebral and cardiac sympathetic activity.

The effect of bilateral carotid occlusion (BCO) on the activity of the vertebral and cardiac sympathetic efferent nerves was studied in gallamine-immobilized and artificially ventilated cats under chloralose-urethane anaesthesia. Electrical activity of the vertebral and cardiac nerves (VNA and CNA), their integram, arterial blood pressure and respiration were recorded. BCO led to an increase in VNA persisting throughout the occlusion period, while merely a transient increase took place in CNA. When blood pressure was kept at a constant level or the depressor nerves was transected, CNA responded to BCO with a lasting increase. Electrical stimulation of the central stump of the left depressor nerve inhibited CNA much more than VNA. It is assumed that the selective inhibition of CNA, after a transient increase, arises as a consequence of a rise in blood pressure, i.e. of consecutive aortic baroreceptor excitation.     

Electrical activity of the sympathetic ganglia during the depressor reflex

Tonic activity of neurons of the superior cervical sympathetic ganglion was recorded by the "sucrose gap" method and in the 4th and 5th lumbar sympathetic ganglia with the aid of focal nonpolarizing electrodes in acute experiments on anesthetized cats and rabbits. The preganglionic fibers of the ganglia were left intact. Stimulation of the depressor nerve not only sharply inhibited the tonic activity of the ganglia but also led to the appearance of electropositive potentials of 0.7 ± 0.2 mV in the superior cervical ganglion and 20–250 µV in the lumbar ganglia. The amplitude of this potential was unchanged by atropine (1 · 10^–6M). A similar effect occured without stimulation of the depressor nerve, after division of the preganglionic fibers or blocking of their conduction; it is attributed to the cessation of preganglionic tonic impulses which induce not only spikes, but also many EPSPs in neurons of the ganglion. Their frequency in the lumbar ganglia was 4/sec. Summation of these EPSPs leads to constant electronegativity of the ganglion surface relative to the postganglionic fibers, and its disappearance is recorded as a positive potential. Stimulation of the depressor nerve thus does not induce IPSPs in the ganglion; consequently, the inhibition of synaptic activity observed under these circumstances is located in the CNS and not in the ganglion.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 6, No. 5, pp. 519–524, September–October, 1974.     

刺激家兔腹部迷走神经外周端引起的降压作用

本文对电刺激家兔腹部的迷走神经外周端所引起的降压反应进行了研究。在121只家兔中的实验结果表明:电刺激腹部迷走神经外周端可引起动脉压、小肠和后肢的灌流压同时降低,而心率则无明显变化。这一降压反应发生时,小肠静脉血中的组织胺含量较刺激前明显升高,然后恢复;将小剂量的组织胺 H_1受体阻断剂扑尔敏、非乃根和 H_2受体阻断剂甲氰咪胍(Cimetidine)分别注入肠系膜上动脉均能减弱刺激腹部迷走神经外周端引起的动脉压和小肠灌流压的降低。心得安能削弱此降压反应,而阿托品无效;切断两侧内脏大神经能显著削弱刺激腹部迷走神经外周端引起的降压反应。此残余的降压反应在注入抗组织胺剂后完全消失。由此推论,刺激家兔腹部迷走神经外周端引起的降压反应是通过中枢和外周两方面因素的作用,使血管舒张,外周阻力降低而实现的。     

L-arginine availability determines the duration of acetylcholine-induced systemic vasodilation in vivo

In vitro studies have shown that acetylcholine-induced vasorelaxation is mediated by endothelium-derived relaxing factor/nitric oxide (EDRF/NO). EDRF/NO is synthesized from L-arginine by an enzymatic pathway that is inhibited by L-NG-methylarginine. To assess whether EDRF/NO also mediates the vasodilating action of acetylcholine in vivo, we have investigated the effect of L-arginine and L-NG-methylarginine on the hypotensive response to acetylcholine in the anesthetized guinea pig. L-arginine prolonged the duration of the depressor response to acetylcholine and L-NG-methylarginine decreased it. However, neither L-arginine nor L-NG-methylarginine modified the magnitude of acetylcholine's hypotensive effect unless the blood pressure was previously elevated by infusion with norepinephrine. Thus, de novo synthesis of nitric oxide from L-arginine contributes importantly, but not exclusively, to acetylcholine's hypotensive effect in the guinea pig. Furthermore, the concentration of circulating L-arginine may influence the duration and magnitude of acetylcholine-induced depressor responses under normotensive and hypertensive conditions.     

胍丁胺抑制大鼠颈动脉窦压力感受器活动

在麻醉大鼠隔离灌流颈动脉窦区条件下,记录窦神经传入放电,观察胍丁胺（agmatine,Agm)对动脉压力感受器活动的影响,结果如下：（1）以1mmol/L Agm隔离灌流大鼠颈动脉窦区时,窦内压－窦神经传入放电积分（ISP－ISNA）关系曲线向右下方移位,曲线的最大斜率（PS）降低,窦神经传入放电量最大积分值（PIV）减小,再分别以5,10mmol/L Agm灌流时,机能曲线向右下方移位更为明显,PS及PIV降低更加明显,从而表明Agm抑制压力感受器活动且呈剂量依赖性,（2）α2－肾上腺素受体（α2－adrenoceptor,α-AR）和咪唑啉受体（IR）的阻断剂咪唑克生（0．1mmol/L)可阻断Agm的上述效应。（3）预先灌流α-AR能亨宾（15umol/L)可部分阻断Agm的抑制效应。（4）预先灌流Ca^2 通道激动剂Bay K8644(500mmol/L)亦可取消Agm对窦神经传入放电的影响,以上结果表明,Agm对基动脉窦压力感受器活动有抑制作用,此作用由IR和α-AR介导,并与颈动脉窦压力感受器活动时Ca^2 内流减少有关。     

The effects of dl-sotalol on the urinary osmolarity of anesthetized dogs]

The effect of dl-sotalol (intrarenal perfusion of 19 mg/kg during 30 min) on urinary concentration was studied under pentobarbital anaesthesia in dehydrated dogs. Sotalol infusion decreased urinary osmolality and increased natriuresis and urine flow. This diuretic action was accompanied by the reduction of the renin hypersecretion elicited by water deprivation.     

心房钠泵因子对颈动脉窦压力感受器反射的易化作用

Effects of atriopeptin II (APII) on the carotid sinus baroreflex in anesthetized rats and on the sinus nerve afferent activity in the anesthetized rabbits were investigated. The results were as follows: (1) By perfusing the isolated left carotid sinus with APII (1 microgram/ml) in anesthetized rats (n = 10), the threshold pressure (TP) of the carotid baroreflex did not show any change, while the equilibrium pressure (EP), the saturation pressure (SP) and the operating range (OR) were decreased from 101 +/- 2.8 to 95 +/- 2.0 mmHg (P less than 0.05), 202 +/- 5.2 to 168 +/- 6.1 mmHg (P less than 0.001) and 128 +/- 5.5 to 93 +/- 6.3 mmHg (P less than 0.001), respectively. The function curve of the baroreflex was shifted to the left and downward with a peak slope (PS) increased during perfusing with APII. In contrast, by perfusing the carotid sinus with sodium nitroprusside (NP, 0.5 micrograms/ml), TP and EP remained unchanged, whereas SP and OR were increased from 188 +/- 6.4 to 218 +/- 6.0 mmHg (n = 6, P less than 0.01) and from 107 +/- 6.9 to 132 +/- 7.6 mmHg (P less than 0.05), respectively. The function curve of the baroreflex and its PS were not affected by NP. The sinus nerve afferent activity was quite stable with the perfusion of carotid sinus at constant intrasinus pressure (ISP) in the rabbits (n = 6) and increased during the elevation of ISP.(ABSTRACT TRUNCATED AT 250 WORDS)     

Carotid sinus pressure, blood volume, and vasopressin in the anaesthetized rabbit

Experiments were carried out on anaesthetized rabbits to determine the influence of carotid sinus pressure (CSP) on the changes in the plasma concentration of arginine vasopressin (AVP) that occurred in response to changing blood volume. The aortic depressor nerves were sectioned in all experiments and the vagus nerves remained intact. Both carotid sinuses were perfused at constant controlled pressure. Blood volume was increased (n = 10) or decreased (n = 10) by 10 and 20% of the estimated blood volume. Plasma immunoreactive arginine vasopressin concentration (IR-AVP) was significantly higher at a CSP of 60 mmHg (1 mmHg = 133.322 Pa) than it was at a CSP of 120 mmHg in both groups of animals. Increasing blood volume did not cause any significant change in IR-AVP at either carotid sinus pressure. Haemorrhage of 10% of the blood volume did not change IR-AVP. Haemorrhage of 20% of the blood volume significantly increased IR-AVP at both CSPs; the magnitude of the increase in IR-AVP was not altered by changing the CSP. No interaction was demonstrated between the effects of CSP and blood volume on plasma IR-AVP.     

刺激家兔腹部迷走神经外周端降压效应中枢机制的研究

应用电解损毁和脑室内注射药物的方法研究了刺激家兔腹部迷走神经外周端所致降压效应的中枢机制。结果表明:1.电刺激延脑闩部尾侧1.5—2mm、中线旁开0.25mm、深1—2mm 处主要引起降压反应。2.电解损毁该部位可以使刺激腹部迷走神经外周端所引起的降压效应显著减弱(n=20,P<0.001),但对刺激减压神经所致降压反应无影响。3.在延脑闩部水平电解损毁减压神经纤维在孤束核的主要投射区可以使刺激减压神经所致降压反应显著减弱,而对刺激腹部迷走神经外周端所致降压反应无影响。4.第四脑室注射5,6-双羟色胺的动物较之注射人工脑脊液的动物颈、胸髓5-羟色胺含量明显降低、动物动脉压增高、心率明显增快、刺激减压神经所致降压反应未见减弱,而刺激腹部迷走神经外周端所致降压反应却明显减小。因此,我们认为家兔腹部迷走神经外周端所致降压效应依赖于延脑闩下部的中缝隐核及连合核等结构,而与减压神经的投射部位无关。延脑中缝核至脊髓的下行性5-HT能神经纤维抑制脊髓交感节前神经元的活动,是这个降压效应的中枢机制之一。     

Biological Effect and Inactivation Mechanism of <Emphasis Type="Italic">Bacillus subtilis</Emphasis> Exposed to Pulsed Magnetic Field: Morphology,Membrane Permeability and Intracellular Contents

Biological effect and inactivation mechanism of Bacillus subtilis exposed to pulsed magnetic field (PMF) were investigated. Cell morphology, membrane permeability, release of intracellular proteins and damage of deoxyribonucleic acid (DNA) were monitored. The inactivation effect of PMF treatment on B. subtilis was enhanced with the increase in intensity and pulse number. Scanning electron microscopy (SEM) analysis showed that the PMF treated bacterial cells had rough surfaces and damaged cellular membranes. Flow cytometry measurements showed that the cell membrane permeability increased after the PMF treatment. Leakage of intracellular contents, measured as OD, significantly increased with the increase in PMF intensity and pulsed number. A maximum leakage of cytoplasmic contents was detected at intensity of 3.30 T and 30 pulses. Enterobacterial repetitive intergenic consensus - polymerase chain reaction (ERIC-PCR) fingerprint signaled that the DNA was fragmented after the PMF treatment at the intensity of 3.0 T with 30 pulses and 3.3 T with 10, 20 and 30 pulses. These findings may give clues to the mechanism of bacterial cell death due to the PMF treatment.