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Biomedical subjects

B Lisander

Publications and source records attributed to B Lisander.

At least 55 records · Page 3Linked to original sources
PubMed1985

Epidural fentanyl counteracts sympathetic gastric inhibition.

Postoperative paralytic ileus is in part mediated by the sympathetic gastrointestino-gastrointestinal (GI-GI) reflex. The modulation of this reflex by epidural fentanyl (50 micrograms) was studied in chloralose-anesthetized, ventilated cats. The vagi were cut in the neck but could be efferently stimulated. Gastric volume, arterial pressure and heart rate were followed and the GI-GI reflex was elicited by intestinal distension, mesenteric afferent nerve stimulation or heating or capsaicin administered intra-arterially to an intestinal loop. Epidural fentanyl enhanced the gastric contraction response to efferent vagal stimulation and considerably counter-acted the GI-GI reflex inhibition of vagally induced tone. These effects were reversed by epidural naloxone (10 micrograms). In contrast, 50 micrograms of fentanyl i.v. only enhanced the effect of vagal stimulation but had no influence on the inhibitory GI-GI reflex responses. Apparently, epidural fentanyl may inhibit the GI-GI reflex by a spinal point of action.

Animals↗
PubMed1984

Atropine-sensitive gastric smooth muscle excitation by mucosal nociceptive stimulation--the involvement of an axon reflex?

Experiments were performed in chloralosed cats where gastric motility was recorded by the "volume method". Mucosal and serosal nociceptive stimulations were accomplished by local heating to 45-52 degrees C. Heating generally elicited gastric relaxations, mainly due to activation of extrinsic inhibitory reflexes, but mucosal heating sometimes caused contractile responses which were resistant to nicotinic and adrenergic blockade. The contractions were, however, blocked by atropine and, further, could not be demonstrated after degeneration of splanchnic afferents. On the basis of these and earlier results it is suggested that the gastric contractions induced by mucosal nociceptive stimulation are due to axon reflexes, conveyed by splanchnic afferents that, possibly via release of substance P, make non-nicotinic reflex contacts with intramural excitatory cholinergic neurons.

Animals↗
PubMed1982

Gastric atropine-sensitive excitation by peripheral vagal stimulation after hexamethonium. Antidromic activation of afferents?

Experiments were performed in chloralosed cats with ligated adrenals with recording of arterial blood pressure, heat rate and gastric volume, the latter with a balloon method. Electric activation of the peripheral cut vagus at low and high intensity induced gastric excitatory and relaxatory responses, respectively. Hexamethonium blocked the stimulation-bound bradycardia but now high intensities induced excitatory gastric responses, resistant to alpha- and beta-adrenergic blocking agents and naloxone but sensitive to atropine. Heating of the intact vagus, to selectively activate thin afferents, resulted in gastric inhibition, due to vago-vagal reflex activation. When the nerve had been proximally cut, local nerve heating induced excitatory gastric responses, with the same pharmacological characteristics as those caused by electric nerve stimulation. The observations suggest that the hexamethonium-resistant gastric excitatory responses to peripheral vagal stimulation are due to antidromic activation of thin afferents which are proposed to function in axon reflexes affecting gastric motility.

Animals↗
PubMed1982

Hexamethonium-resistant gastric contractions by stimulation of the vagal nuclei. An antidromic activation of vagal afferents?

Experiments were performed in chloralosed cats, laparotomized with ligated adrenals and spinalized in the cervical region. Blood pressure, heart rate and gastric motility were monitored. Stimulations were performed in two brain stem regions, viz. a "control region" including the nucleus ambiguous and a "dorsal region" approximately corresponding to the dorsal vagal nucleus and the solitarius complex. From both regions were regularly elicited gastric motor responses that were either excitatory, biphasic or inhibitory in direction, and always associated with prompt bradycardia and hypotension. After hexamethonium blockade of the "conventional" efferent vagal excitatory and relaxatory fibres to the stomach, stimulation of the control region no longer augmented gastric motility, while gastric contractions which could be abolished by atropine or vagotomy were produced from the dorsal region. The bradycardia and hypotension responses from both regions were also blocked by hexamethonium and then stimulations often led to delayed pressor responses, resistant to both vagotomy and atropine. The present results, together with previous findings (Delbro et al. 1981, 1982) suggest that the hexamethonium-resistant gastric contractions, elicited by stimulation of the mentioned dorsal region of the brain stem, are due to antidromic activation of afferent gastric vagal fibres with excitatory collaterals to intramural cholinergic neurons.

Afferent Pathways↗
PubMed1980

Non-ganglionic cholinergic excitatory pathways in the sympathetic supply to the feline stomach. An efferent system or afferents with excitatory axon collaterals?

Experiments were performed on chloralosed, adrenalectomized cats, paralysed with gallamine and artificially ventilated. Gastric motility was recorded by the balloon method. Efferent stimulation of the cut greater splanchnic nerve, well proximal to the celiac ganglion, could either increase or decrease gastric tone. The excitatory responses called for higher stimulation intensities than the inhibitory ones but were as a rule observed at lower frequencies only (1-4 Hz). They could be abolished by atropine but were not prevented by bilateral vagotomy, hexamethonium nor guanethidine. The latter two drugs rather reversed inhibitory responses to excitatory ones which exhibited a hyperbolic frequency-response relationship with maximal effects already at 2-4 Hz. Heating of a nerve trunk selectively activates thin afferents of the delta group and C-class. Heating of the greater splanchnic nerve caused an increase in gastric motility which, like that caused by electric stimulation, was not prevented by hexamethonium nor guanethidine; nor was it eliminated by cutting the nerve centrally, nor by vagotomy, while it was abolished by atropine. These results suggest that the excitatory gastric responses to efferent splanchnic nerve stimulation are due to antidromic activation of thin afferent fibres. Their functional significance remains obscure but their peripheral arborizations may convey 'axon reflexes' influencing gastrointestinal motility.

Afferent Pathways↗
PubMed1979

The role of cardiac receptors in clonidine-induced vagal bradycardia.

In chloralosed, spinalized and beta-blocked cats, clonidine, 10 microgram/kg i.v. caused a vagally mediated bradycardia which was further analysed with particular attention to cardiopulmonary receptors. Cardiovascular deafferentiation, with preservation of vagal cardiac efferents, abolished the bradycardia. However, in animals with arterial baroreceptors denervated but with vagal cardiopulmonary pathways intact, clonidine decreased heart rate simultaneously with an increase in left atrial pressure to an extent known to activate cardiac receptors with unmyelinated vagal efferents. Clonidine somewhat enhanced the bradycardia to efferent vagal stimulation and also had a slight positive chronotropic effect on the non-innervated heart. The reflex bradycardia from electrical stimulation of unmyelinated cardiac afferents was augmented by the drug but not more than could be accounted for by the changed neuroeffector sensitivity. The data suggest that clonidine can reflexly augment vagal tone on the heart by an increased activity in vagal cardiac afferents, secondary to the drug's peripheral vasoconstrictor action, whereas no evidence for any central facilitation of these reflexes has been found.

Animals↗
PubMed1978

Baroreceptor-induced decrease in muscle blood flow upon propranolol administration.

The acute effects of propranolol, 1 mg/kg i.v., were studied in chloralosed, vagotomized cats. The vascularly isolated but innervated calf muscles were perfused from another animal. In one group of experiments, the carotid baroreceptors were exposed to ambient arterial pressure. Here, propranolol caused a fall in heart rate and an increase in resistance of the isolated muscle bed. In other experiments, the carotid sinuses were perfused at a constant pressure. In these animals, no increase in muscle flow resistance was observed after the drug. It is concluded that the increase in total peripheral resistance, seen initially upon propranolol administration, may be reflexly induced via the baroreceptors.

Animals↗
PubMed1977

The interrelation between hypothalamically induced changes in sympathetic discharge to the gastrointestinal and cardiovascular systems.

In chloralose-anesthetized, adrenalectomized cats, the sympathetically conveyed effects of topical hypothalamic stimulations on gastric volume, blood pressure and heart rate were systematically explored. The vagal nerves were cut but could be kept active by graded efferent stimulation. In the absence of such vagal activity, hypothalamic stimulation had no appreciable influence on gastric volume, even though the stomach maintained considerable myogenic tone. When, however, a vagal excitatory activity was present, hypothalamic stimulation could markedly affect gastric tone, indicating that the sympathetic fibres exert their inhibitory influence on the stomach via its cholinergic intramural neurons. Hypothalamic stimulations that induced reductions in pressure or heart rate also usually caused an enhancement of gastric tone. Similarly, pressor responses were associated with decreases in gastric volume whereas stimulation-induced tachycardia was not linked to any particular type of gastric response. Thus, the hypothalamic sympathoinhibitory influences on the cardiovascular system seem closely connected to a supression of the sympathetic outflow to the stomach. There is, on the other hand, no regular association between hypothalamic sympathoexcitatory influences on the cardiovascular and gastrointestinal systems; in fact, there is in many areas even a suppression of sympathetic discharge to the stomach in association with cardiovascular stimulation.

Adrenalectomy↗
PubMed1977

Cardiac receptors activated during the hypothalamic defence reaction.

The increases of arterial blood pressure, cardiac inotropy and venous return seen during the hypothalamic defence reaction are likely to lead to concomitant excitation of left ventricular receptors with nonmedullated afferents. The integrated efferent pattern of response resulting from the central interaction between the defence reaction and influences from the mentioned cardiac receptors was recently analyzed. These two, essentially opposing influences on the circulation were then seen to interact in such a way as to produce an optimal cardiovascular response with respect to increases in cardiac output and blood supply to the skeletal muscles. However, direct electrophysiological recordings from nonmedullated cardiac efferents during defence area stimulation have hitherto been lacking. The present experiments, performed on chloralose-anesthetized cats and utilizing electrophysiological recordings, clearly demonstrate that the left ventricular receptors are activated by the cardiovascular readjustments induced by the defence reaction. Defence area stimulation increased the activity of these receptors, which work within a very narrow, low frequency range, from 1.1 +/- 0.3 imp/s to 2.7 +/- 0.7 imp/s associated with rises in systolic blood pressure (afterload) and heart rate. Normally such a receptor activation would induce considerable bradycardia and sympathetic inhibition, but particularly the reflex bradycardia is centrally supressed by a concomitant defence area activation. The marked bradycardia often seen immediately upon interruption of the defence area stimulation is, however, probably to a great extent initiated from the excited ventricular receptors.

Animals↗
PubMed1977

Apnoea and bradycardia from submersion in "chronically" decerebrated cats.

In "chronically" but not in acutely decerebrated cats, submersion of the head caused apnoea and marked bradycardia, associated with a maintained or slightly raised arterial pressure. Since these reflex adjustments, though very reproducible, occurred with a varying latency and could be induced also by nasal injection of water, they appeared to be, at lest in part, elicited from the upper respiratory passages. Thus, a terrestrial mammal, reputed to shun any form of immersion, can exhibit adjustments during head submersion, similar to those in habitually diving species. This response pattern is basically organized at the lower brainstem level.

Animals↗
PubMed1976

Interaction between the hypothalamic defence reaction and cardiac ventricular receptor reflexes.

The interference with regard to the cardiovascular and gastric motility responses which follows stimulation of the hypothalamic defence area (D.A.) and a simultaneous afferent input from cardiac ventricular receptors was analysed in chloralose-anesthetized cats. In spinalized animals with only the vagal efferent innervation of autonomic effectors from supraspinal structures intact, a D.A. stimulation increased the heart rate to the same level irrespective whether the cardiac receptor afferents were stimulated or not. This suggests that the vagal component of the reflex bradycardia of cardiac receptor origin was completely suppressed by the D.A. stimulation. The reflex gastric relaxation to cardiac receptor activation, mediated via vagal efferent non-adrenergic fibres, was similarly completely blocked by D.A. stimulation. In contrast, the reflex inhibition of the sympathetic outflow to the heart and vessels from cardiac receptors was still effective during a D.A. stimulation, a phenomenon which seems compatible with a simple summation of excitatory D.A. and inhibitory cardiac receptor influences on the sympathetic neurons. The modifying influence from ventricular receptors on D.A. responses closely resembles that exerted by the arterial baroreceptors. The two reflex mechanisms thus work in concert and synergistically with the hypothalamic influences to produce maximal cardiac output and skeletal muscle perfusion without undue increases of pressure load on the pump during a defence reaction.

Animals↗
PubMed1975

CNS site of antiarrhythmic action of diphenylhydantoin (DPH) in the cat.

Diphenylhydantoin (DPH) is known to be a potent anticonvulsant agent, useful in treating and preventing grand mal seizures. More recently, DPH was reported also to be a potent antiarrhythmic agent acting by means of a depressant action on the heart. The present experiments demonstrated that DPH has also a potent antiarrhythmic action when administered to the CNS. The posterolateral hypothalamus was stimulated in cats to evoke cardiac arrhythmias of varying severity both during and after stimulation. In general, it was found that the post-stimulus arrhythmias were obtained more readily than those during stimulation. The mean effective dose of DPH required to prevent the arrhythmias via the i.v. route was 11.9 mg/kg, and that via the vertebral artery route and via the fourth ventricular route was only 1.9--1.4 and 1.4 mg/kg, respectively. These results suggest that though DPH has identifiable antiarrhythmic action on the heart itself it has a strong antiarrhythmic effect via the central nervous system as well.

Animals↗
PubMed1975

The hypothalamus and vagally mediated gastric relaxation.

Experiments, with recording of gastric volume, were performed in chloralosed cats. Topical hypothalamic stimulations produced vagally mediated increases in volume by two mechanisms. One type of response, due to central inhibition of vagal excitatory tone was induced from the defence area and eliminated by atropine or vagotomy. The other type of response, far less commonly encountered, remained after atropine and spinal cord section, but was abolished by vagotomy. The latter type was not induced from any well defined hypothalamic region, and had a high stimulation threshold. While sham feeding in conscious cats with esophagostomy and gastrostomy induced prompt, marked and longlasting gastric volume increases in connection with swallowing, such responses were not evoked as "anticipatory" reaction to food intake;The relaxations could be prevented by vagotomy but not by guanethidine nor atropine. It is concluded that the vagally mediated relaxation in connection with sham feeding occurs mainly from activation of mechanoreceptors and that the hypothalamic control over the vagal relaxatory fibres is probably minor.

Animals↗
PubMed1975

Integrated somatomotor, cardiovascular and gastrointestinal adjustments induced from the cerebellar fastigial nucleus.

Behavioural, cardiovascular and gastric responses induced by fastigial stimulation were observed in conscious cats with gastric fistulas, indwelling fastigial electrodes and arterial catheters. Fastigial stimulation elicited oral behaviours, e.g. grooming and chewing, together with tachycardia and pressor responses, while gastric motility was unaffected in most cases as was gastric hydrochloric secretion. In subsequent experiments on the anesthetized animals it was found that the same fastigial area could suppress the intestino-gastric inhibitory reflex. Fastigial influences on small intestinal motility were investigated in anesthetized cats, well recovered from surgical isolation of intestinal loops whose motility could therefore be recorded without laparotomy. Fastigial stimulation either depressed or did not influence ileal motility before laparotomy but after this procedure excitatory responses were uniformly recorded. This reversal is explained by a fastigial suppression of inhibitory intestinal reflexes, elicited by the laparotomy.

Animals↗