Effect of befol on the electric threshold of ventricular fibrillation

Befol (20 mg/kg) rises electric threshold of ventricular fibrillation in cats. This effect is most pronounced in ischemized myocardium. It is shown that not only tricyclic but also monocyclic antidepressants exhibit antifibrillatory activity. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 123, No. 3, pp. 305–307, March, 1997     

Effect of peridural heart block on the threshold of ventricular fibrillation in dogs

The threshold of ventricular fibrillation in animals with an intact heart and myocardial infarction was determined by injection of trimecaine into the peridural space at the T₁-T₂ level. The threshold of fibrillation was shown to be increased under these circumstances on account both of the resorptive action of trimecaine and the blockade of the sympathetic nerves to the heart.Laboratory of Clinical and Experimental Cardiology, I. P. Pavlov Institute of Physiology, Academy of Sciences of the USSR, Leningrad. (Presented by Academician V. N. Chernigovskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 9, pp. 277–279, September, 1978.     

Effect of posterior hypothalamic stimulation on neocortical electrical activity in the chronic premesencephalic cat

Chronic experiments were carried out on 19 adult cats after preliminary division of the brain stem at the level of the anterior border of the superior colliculus. High-frequency electrical stimulation of the posterior hypothalamus of these animals caused desynchronization of electrical activity in different parts of the neocortex. The influence of the posterior hypothalamus was predominantly on activity in the frontal zones of the neocortex. It is postulated on the basis of these results that the posterior hypothalamus has an activating effect on the neocortex through the thalamic nuclei.Translated from Neirofiziologiya, Vol. 8, No. 1, pp. 47–53, January–February, 1976.     

Activation of the retrotrapezoid nucleus by posterior hypothalamic stimulation

The retrotrapezoid nucleus (RTN) contains chemically defined neurons (ccRTN neurons) that provide a pH-regulated excitatory drive to the central respiratory pattern generator. Here we test whether ccRTN neurons respond to stimulation of the perifornical hypothalamus (PeF), a region that regulates breathing during sleep, stress and exercise. PeF stimulation with gabazine increased blood pressure, phrenic nerve discharge (PND) and the firing rate of ccRTN neurons in isoflurane-anaesthetized rats. Gabazine produced an approximately parallel upward shift of the steady-state relationship between ccRTN neuron firing rate and end-tidal CO₂, and a similar shift of the relationship between PND and end-tidal CO₂. The central respiratory modulation of ccRTN neurons persisted after gabazine without a change in pattern. Morphine administration typically abolished PND and reduced the discharge rate of most ccRTN neurons (by 25% on average). After morphine administration, PeF stimulation activated the ccRTN neurons normally but PND activation and the central respiratory modulation of the ccRTN neurons were severely attenuated. In the same rat preparation, most (58%) ccRTN neurons expressed c-Fos after exposure to hypercapnic hyperoxia (6–7% end-tidal CO₂; 3.5 h; no hypothalamic stimulation) and 62% expressed c-Fos under hypocapnia (∼3% end-tidal CO₂) after PeF stimulation. Under baseline conditions (∼3% end-tidal CO₂, hyperoxia, no PeF stimulation) few (11%) ccRTN neurons expressed c-Fos. In summary, most ccRTN neurons are excited by posterior hypothalamic stimulation while retaining their normal response to CNS acidification. ccRTN neurons probably contribute both to the chemical drive of breathing and to the feed-forward control of breathing associated with emotions and or locomotion.     

家兔心肌缺血范围对缺血早期室颤阈的影响

观察30只家兔在心率固定情况下，改变缺血范围对心肌缺血早期室颤阈（VFT）、颈动脉血压和血浆去甲肾上腺素含量的影响以及切断双侧迷走神经后，于上述情况下VFT的变化，结果表明改变心肌缺血范围可影响VFT值；但与心率、血压、血浆去甲肾上腺素水平以及迷走神经状态无关 ，提示心肌缺血早期的室颤和缺血范围有关。     

Effect of KLN-93 on ventricular fibrillation induced by reperfusion and electrical stimulation in cats

In experiments devoted to modeling of reperfusion ventricular fibrillation and determination of the electric threshold of fibrillation, a protective effect of KLN-93 (a para-aminobenzoic acid ester derivative) is compared with that of lidocaine. It is shown that KLN-93 in doses stopping reperfusion fibrillation is 2-4-fold less toxic than the isoeffective doses of lidocaine. In a dose of 0,4 mg/kg (2.5% LD₅₀) KLN-93 increases the fibrillation threshold 4.5-fold, while isotoxic dose of lidocaine increases this parameters apparoximately 2-fold. These data suggest that KLN-93 is an effective antifibrillatory agent. Translated fromByulleten' Eksperimental'noi i Meditsiny, Vol. 124, No. 8, pp. 135–137, August, 1997     

钾对再灌流早期室颤阈变化的影响

本实验在69只家兔上比较观察了高钾动脉血、血浆和正常动脉血对局部缺血心肌再灌流早期室颤阈(VFT)变化的影响。实验结果表明,缺血心肌用正常动脉血再灌流可使其VFT在灌流1分内迅速下降,然后逐渐回升。其中氧的恢复和钾的改变对VFT下降程度影响不同。缺血后用血浆再灌流,其VFT下降程度与缺血后用正常动脉血再灌流相比无显著性差异;而用高钾动脉血再灌流比用正常动脉血再灌流VFT下降程度轻(P<0.05)。本实验结果提示,在再灌流心律失常产生中缺血时所积累的钾的突然冲洗和再分布可能起更重要的作用。     

Effect of posterior hypothalamic knife cuts on the baroreflex and hemorrhage-induced hormonal responses

We made posterior hypothalamic knife cuts in rats to transect the fibers of the medial forebrain bundle (MFB) at the level of the mammillary body. The role of the MFB in the baroreflex and hemorrhage-induced hormonal responses was then examined in the unanesthetized, freely moving condition. The slopes for the relationship between changes in pulse interval and mean arterial pressure (MAP) in the posterior-cut group were significantly steeper than those in the sham-cut group both when there were phenylephrine-induced increases in MAP (1.13 +/- 0.07 vs 0.86 +/- 0.10 msec/mmHg) and nitroprusside-induced decreases in MAP (1.16 +/- 0.10 vs 0.77 +/- 0.05 msec/mmHg). This result indicates that posterior cuts elevated baroreflex sensitivity when MAP was increased or decreased. The resting MAP was not changed, but the resting heart rate (HR) was lowered by the posterior cuts. Furthermore, the posterior cuts augmented hypotensive hemorrhage-induced bradycardia. Hypotensive hemorrhage (16-17 ml/kg) caused elevation of the plasma catecholamine, ACTH and vasopressin (AVP) levels, but the posterior cuts attenuated these hormonal responses. These results indicate that the fibers in the MFB have a tonic inhibitory effect on the baroreflex in the resting condition, and play a stimulatory role in hemorrhage-induced catecholamine, ACTH and AVP responses.     

Effect of stimulation of the hypothalamic and amygdalar motivation centers on vestibular nystagmus

Chronic experiments on rabbits with electrodes implanted into hypothalamic and amygdalar structures showed that weak electrical stimulation of the food center of the lateral hypothalamus, giving a food response to preliminary testing, induces marked facilitation of vestibular (especially rotatory) nystagmus, whereas stimulation of the ventromedial hypothalamic nucleus inhibits it. The effect of amygdalar stimulation was manifested more often as facilitation, but sometimes as inhibition of the nystagmus. The results are evidence of the modulating influence of the hypothalamic and amygdalar motivation centers on the vestibular system.     

Effect of tactile stimulation pulse characteristics on sensation threshold and power consumption

The psychophysical responses of human subjects to vibratory tactile stimulation of the skin were investigated experimentally. The parameters, of the waveform important to the minimization of power consumed by the tactile array of electromechanical vibrators and the maximization of the skin sensitivity to the stimulus were explored to develop optimum stimulation. Parameters investigated included the amplitude, frequency, and duty cycle of the current waveform used to drive the vibrators as well as the number of pulses per stimulating burst and the recovery time between bursts. Graphical techniques were used to determine, the optimal combination of the parameters which gave a stimulus that excited the skin to above tactile threshold while maintaining at a relative minimum the power required for the stimulus. The optimal stimulation waveform contains a burst of 10 rectangular pulses of 4% duty cycle separated by a period of nonstimulation of 2 s. Such a waveform can elicit a sensitivity of 29.4 mA⁻¹ consuming only 55 μW of power.     

Effect of ventromedial hypothalamic stimulation on blood flow of brown adipose tissue in rats

The changes in regional blood flows to the rat's interscapular brown adipose tissue and several other tissues during electrical stimulation of the ventromedial hypothalamus (VMH) were studied using radioactively labelled microspheres. Measurement of blood flow was carried out, along with monitoring heart rate, under anesthesia and at thermoneutrality. During VMH stimulation the heart rate was clearly augmented and cardiac output increased about 45%. Regional blood flows were significantly increased in response to VMH stimulation in interscapular brown adipose tissue, adrenal glands, diaphragm and gastrocnemius muscles. The response of interscapular brown adipose tissue was the most prominent (approx. fiftyfold increase). Blood flows tended to decrease in spleen, lungs and kidneys during VMH stimulation, but did not change in liver or in other visceral organs. These observations suggest that the VMH is concerned with the regulation of regional blood flow to brown adipose tissue and contributes to thermogenesis in this tissue.     

Protection against ventricular fibrillation via cholinergic receptor stimulation and the generation of nitric oxide

AbstractImplantable cardiac vagal nerve stimulators are a promising treatment for ventricular arrhythmia in patients with heart failure. Animal studies suggest the anti‐fibrillatory effect may be nitric oxide (NO) dependent, although the exact site of action is controversial. We investigated whether a stable analogue of acetylcholine could raise ventricular fibrillation threshold (VFT), and whether this was dependent on NO generation and/or muscarinic/nicotinic receptor stimulation. VFT was determined in Langendorff perfused rat hearts by burst pacing until sustained VF was induced. Carbamylcholine (CCh, 200 nmol l^–1, n = 9) significantly (P < 0.05) reduced heart rate from 292 ± 8 to 224 ± 6 b.p.m. Independent of this heart rate change, CCh caused a significant increase in VFT (control 1.5 ± 0.3 mA, CCh 2.4 ± 0.4 mA, wash 1.1 ± 0.2 mA) and flattened the restitution curve (n = 6) derived from optically mapped action potentials. The effect of CCh on VFT was abolished by a muscarinic (atropine, 0.1 μmol l⁻¹, n = 6) or a nicotinic receptor antagonist (mecamylamine, 10 μmol l⁻¹, n = 6). CCh significantly increased NOx content in coronary effluent (n = 8), but not in the presence of mecamylamine (n = 8). The neuronal nitric oxide synthase inhibitor AAAN (N‐(4S)‐4‐amino‐5‐[aminoethyl]aminopentyl‐N′‐nitroguanidine; 10 μmol l⁻¹, n = 6) or soluble guanylate cyclase (sGC) inhibitor ODQ (1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one; 10 μmol l⁻¹, n = 6) prevented the rise in VFT with CCh. The NO donor sodium nitrprusside (10 μmol l^–1, n = 8) mimicked the action of CCh on VFT, an effect that was also blocked by atropine (n = 10). These data demonstrate a protective effect of CCh on VFT that depends upon both muscarinic and nicotinic receptor stimulation, where the generation of NO is likely to be via a neuronal nNOS/sGC‐dependent pathway.