摘要:

The study is part of a series of investigations performed with the ultimate goal of obtaining an objective evaluation of the ethical aspects and the narcotic efficiency of CO2inhalation used as pre‐slaughter anaesthesia for swine. Six Yorkshire swine were exposed twice to 80% CO2for I min during simultaneous recording of the EEGs from the frontal neocortex, the dorsal hippocampus, and the amygdaloid region via permanently implanted electrodes. In five of the animals myoclonic jerks started at 28 ± 1 s of CO2exposure and lasted for 6 ± 2 s. Neocortical slow wave (delta) activity and increased amplitude of the hippocampal theta (5–7 Hz) waves (i.e. EEG changes seen during the second stage of barbiturate anaesthesia) had developed before the brief period of myoclonic jerks. After this period the EEG activity gradually declined, resulting in neocortical EEG silence at the end of the exposure. This apparent isoelectricity lasted for on average 1 min. The return of the neocortical EEG activity exhibited a pattern reverse to its disappearance, but was much prolonged in comparison to the EEG extinction. Pre‐exposure newortical EEG pattern was not regained until 3–5 min postexposure. In eight out of 11 experiments the CO2inhalation also induced hippocampal EEG silence lasting for on average 30 s. EEG flattening was further obtained when recording from the amygdaloid nuclear complex and the adjacent pyriform cortex. The observed changes in the neocortical and hippocampal EEGs suggest that the present swine were unconscious already when they exhibited motor reactions. This does not exclude the possibility that CO2‐independent stress/arousal factors present in a slaughterhouse environment may facilitate the development of motor phenomena similar to seizures, with the result that such reactions become manifest before the neocortical EEG exhibits an anaesthesia pattern. The duration of the observed EEG silence implies that, from the ethical point of view, exsanguination might safely be performed within 1 min after the moment when the animal is removed from the high concentration CO2. However, the slow return to a pre‐exposure neocortical EEG pattern suggests that the swine remains unconscious for at least a

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08104.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

The time course and intensity of miosis accompanying endotoxin (ET) fever was studied in goats concomitant with radio‐immunoassay of plasma PGE metabolites. The i.v. injection of ET (E. colilipopolysaccharide; 0.25 μg kg‐1) induced a biphasic miosis correlated in time with the biphasic febrile response. Plasma PGE metabolites rose from an undetectable level to a mean of 2 nmol l‐1during the early fever phase, but fell to an undetectable level during the second fever phase in spite of persisting pronounced miosis. Like light‐induced pupillary constriction, the ET miosis was antagonized by corneal application of atropine. A corresponding miotic response to ET was obtained also in the sheep. It is concluded that ET‐induced miosis requires cholinergic nerve conduction, and that its direct cause is not systemic liberation of PGE. It is suggested that rather some nervous or humoral stimulus developing in conjunction with ET fever acts upon the same brain stem locus as that mediating the pupillary li

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08105.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

The aim of this study was to evaluate the role of cardiopulmonary receptors with vagal afferents in the reflex control of sympathetic nerve activity during mechanical ventilation with positive end‐expiratory pressure (PEEP). Experiments were performed on 17 chloralose‐anaesthetized rats. Changes in renal sympathetic nerve activity (RSNA), heart rate and mean arterial pressure were studied at zero end‐expiratory pressure (ZEEP) and at 5 and 10 cm H2O PEEP inintact animals(n = 8), aftersino‐aortic denervation(n = 17) and aftersino‐aortic denervation plus vagotomy(n = 10). In the intact animals, 10 cm H2O PEEP induced a significant increase in RSNA (+ 66%) and heart rate(+10%)while the mean arterial pressure did not change significantly. Sino‐aortic denervation increased baseline levels of RSNA, heart rate and mean arterial pressure. After sino‐aortic denervation, 10 cm H2O PEEP still induced a significant increase in RSNA (+ 22 %) and heart rate in 13 animals. In four animals, 10 cm H2O PEEP elicited adepressor reflexwith a significant decrease in both RSNA (— 32%) and heart rate. Bilateral vagotomy after sino‐aortic denervation at ZEEP significantly increased RNSA (+15%) and heart rate, indicating an ongoing tonic inhibitory influence on RSNA from vagal afferents in sino‐aortic denervated rats. The PEEP did not induce any significant change in RSNA or heart rate after sino‐aortic denervation plus vagotomy. The results indicate that cardiopulmonary receptors with vagal afferents contribute to the reflex excitation of the sympathetic nervous system during mechanical ventilation with PEEP. Under certain circumstances, PEEP may also trigger powerful depressor reflexes, mediat

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08106.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

The participation of the afferent arterioles (AA) in RBF autoregulation was studied in two groups of rats (groups A and B) by measurement of the afferent arteriolar diameters (dAA) by the microsphere method at control pressure (groups A and B), at the lower pressure limit of RBF autoregulation (group A) and at a perfusion pressure half‐way between these pressures (intermediate pressure) (group B). The RBF was autoregulated from 109 ± 7 (control pressure) to 80 ± 7 mmHg (lower pressure limit) in group A, and from 101±4 (control pressure) to 77± 3 mmHg in group B. In group A,dAAwas significantly lower (17.2 ±0.3 μm) at control pressure than at the lower pressure limit of RBF autoregulation (20.3 ± 0.03 μm) (P0.005). In group B,dAAwas 17.3 ± 0.3 μm at control pressure and 17.1±0.4 μm at the intermediate pressure (89 ± 3 mmHg) (P>0.10). The results indicate that dilation of the afferent arterioles occurs only in the lower part of the autoregulatory pressure range. Possibly, RBF autoregulation at minor pressure reductions is achieved by dilation of the interlobular artery. Participation of the glomerular hilar branches of the afferent arterioles in RBF autoregulation cann

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08107.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Substance P (SP)‐ and calcitonin gene‐related peptide (CGRP)‐immunoreactivity (‐IR) were localized by immunohistochemistry in the same nerve cell bodies in the trigeminal ganglia as well as in nerve terminals of the dental pulp. The distributions of SP‐ and CGRP‐IR nerves were identical in the dental pulp and mainly associated with blood vessels. The level of CGRP‐IR in the dental pulp, as measured by radio‐immunoassay (RIA), was 1.4±0.2 pmol g‐1 wet wt, which is in the same range as that found for substance P. Local intra‐arterial infusion of synthetic CGRP and substance P produced vasodilatation in the dental pulp as measured by both laser Doppler flowmetry and an1251 clearance technique. The CGRP was effective as a vasodilator when infused in the femtomole per minute range, and SP in the picomole range. The effect of CGRP (50 fmol min‐1) was 10 times larger when given after SP (15 pmol min‐1) than before it. Since the two peptides coexist in the same neurons, it is suggested that they both contribute to the vasodilatation seen upon antidromic stimu

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08108.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

In pentobarbital‐chloralose‐anaesthetized rats, pretreated with hexamethonium and atropine the mechanism by which substance P (SP) causes tachycardia was analysed. Substance P, when infused i.v. at doses between 0.49 nmol and 1.52 nmol elicited a marked, dose‐dependent tachycardia, which was reduced to less than half by propranolol, 0.1 mg kg‐1. Furthermore, the SP‐induced tachycardia was reduced to about 1/10 of control by guanethidine. Further, the tachycardia, which could also be elicited in pithed rats, was antagonized by the SP‐receptor blocker Spantide, but these results must be taken with care since Spantide itself caused a pronounced and long‐lasting depressor response. It is hypothesized that SP causes tachycardia by exciting specific receptors on the stellate ganglia, which leads to an activation of adrenergic fibres to t

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08109.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

The aim of the study was to examine sympathetic nerve activity, heart rate and blood pressure during naloxone‐precipitated withdrawal reactions in morphinedependent rats. In two groups of rats, one group conscious and the other anaesthetized with chloralose, renal sympathetic nerve activity (rSNA), heart rate (HR) and mean arterial blood pressure (MAP) were recorded before and during naloxone‐precipitated abstinence. The conscious rats showed a biphasic pattern in the withdrawal responses. Initially, after small doses of naloxone, rSNA and HR increased and increased somatomotor activity including ‘wet‐dog’ shakes were observed. However, upon further administration of naloxone, rSNA and HR promptly decreased while MAP increased. As rSNA was lowered, the withdrawal behaviour of the rats was markedly diminished and the animals rested calmly in the cages. In contrast, the anaesthetized group reacted with an immediate decrease in rSNA after the lowest dose of naloxone, followed by an increase in MAP and HR after higher doses of naloxone, although rSNA was still decreased. In both groups, rSNA remained below pre‐naloxone control levels when the increased MAP was lowered to the pre‐naloxone level with sodium nitroprusside, indicating a central origin of the sympathetic inhibition. It is concluded that naloxone elicits a biphasic rSNA response in the conscious, morphinedependent rat. This includes an initial increase upon low naloxone doses followed by a pronounced inhibition of rSNA after higher doses. In chloralose‐anaesthetized rats, rSNA declined already after low doses of naloxone. It is suggested that there might be a tonic, excitatory input on rSNA, mediated by the activation of opiate receptors by high levels of circulating morphine in the addicted animal. Naloxone will therefore decrease the tonic sympathetic nerve activit

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08110.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Oxytocin is known to increase plasma levels of insulin, glucagon and glucose in dogs. Plasma levels of vasopressin rise during stressful conditions. Since vasopressin counteracts several oxytocin‐induced effects, it was decided to study how vasopressin influences the oxytocin‐induced elevation of plasma levels of insulin, glucagon and glucose. Therefore oxytocin at 0.11 (which gives rise to physiological plasma concentrations) was infused i.v. for 10 min into fasted, conscious dogs either alone or in combination with 0.033 or 0.17 nmol kg‐1h‐1of L‐vasopressin. Accordingly, 1.1 nmol kg‐1h‐1of oxytocin was infused alone or in combination with 0.67 or 1.7 nmol kg‐1h‐1of L‐vasopressin. Repeated blood samples were drawn during and after the infusions and insulin and glucagon levels were determined by radio‐immunoassay. Plasma levels of insulin increased three‐ and six‐fold in response to 0.11 and 1.1 nmol kg‐1h‐1of oxytocin, respectively, and the elevations were inhibited by L‐vasopressin. Slight (1.5–fold) increases in plasma levels of glucagon were observed following 0.11 and 1.1 nmol kg‐1h‐1of oxytocin, although the effect was significant only after the latter dose. Concomitant infusion with L‐vasopressin did not markedly influence the effect caused by oxytocin. Small, insignificant increases in blood glucose levels were induced by both doses of oxytocin. These effects were not affected by concomitant infusions of L‐vasopressin. The insulin levels rose before glucose levels suggesting that oxytocin stimulates the release of insulin without a previous rise in glucose levels. In conclusion, it has been shown that vasopressin, in amounts which give rise to physiological plasma concentrations, inhibits oxytocin‐induced effects on insulin levels, and that oxytocin stimulates the release of insulin via a mechanism which is indepe

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08111.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

The effects of craniotomy and/or histamine treatment upon brain microvascular permeability was studied in Wistar rats. Extravasation of circulating Na‐fluorescein (MW 376) and of FITCalbumin (MW69,000) was observed through a cranial window using intravital fluorescence microscopy. Simple exposureofthe pial microvessels induced formation of discrete spots of fluorescent material around venules, but not around arterioles or capillaries. The average number of leaky spots to Na‐fluorescein and to FITC‐albumin was 4.3 and 1.8 per 10mm2, respectively, 35 min after exposure. Pretreatment of the rats with either indomethacin (a cyclo‐oxygenase inhibitor) or promethazine (a histamine H1‐receptor blocker) did not reduce the number of leaky sites, whereas pretreatment with a combinationofthe two drugs had a significant protective effect. Administration of histamine (10–4M)to the exposed brain surface for 5 min increased the number of leaky sites to Na‐fluorescein and FITCalbumin 3.2 and 3.6 times, respectively. It is concluded that exposure of the brain surface induces release of histamine and cyclo‐oxygenase metabolites, and that these inflammatory mediators elicit formation of leaky sites i

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08112.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY

摘要:

Thyrotropin‐releasing hormone (TRH) has previously been found to have a potent respiratory stimulant effect following intracerebroventricular administration. One part of the respiratory response, the shortening of inspiratory time, seems to be elicited from the raphe obscurus in the medulla. The prominent tachypnoea however is not elicited after local injections in the medullary region. In the present paper a micro‐injection technique was employed to study respiratory actions of TRH in lightly anaesthetized rats kept in a whole body plethysmograph. Thyrotropin‐releasing hormone in a dose of 100 ng per 0.5 μl was found to induce an immediate tachypnoea after injections into the region of the interpeduncular nucleus of the midbrain. No effects on systemic circulation were seen. More rostral or dorsal sites of injection were without effect. The localization of the sites responsible for respiratory stimulation corresponds to the reticular activating system where electrical stimulation induces hyperventilation in cats. The tachypnoea might be closely related to the well known arousal effects

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1987.tb08113.x

出版商:Blackwell Publishing Ltd    

年代:1987

数据来源: WILEY