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Biomedical subjects

C Y Chai

Publications and source records attributed to C Y Chai.

At least 163 records · Page 9Linked to original sources
PubMed1987

Differential biochemical mechanisms mediate locomotor stimulation effects by caffeine and nicotine in rats.

Effects of caffeine and the interactive effects of caffeine and nicotine on locomotor activity in rats were examined in the present study. Other than confirming previous reports that both drugs enhanced locomotion, we have also found that their effects on activity were additive. Meanwhile, results of various biochemical measures have revealed that at the minimum effective doses of caffeine and nicotine which facilitated locomotor activity, only one biochemical system was preferentially influenced by either drug alone. The most significant findings were that caffeine stimulated the release of catecholamines and nicotine decreased the concentrations of tyrosine and tryptophan in brain. The combined effects of caffeine and nicotine on these brain amines were not different from those of each drug alone. Together with the report that caffeine and nicotine had differential actions on different activity measures, the present results support the hypothesis that caffeine and nicotine affect locomotor activity via different neurochemical mechanisms.

Animals↗
PubMed1987

A cardioinhibitory area in the midbrain central tegmental field of cats.

A cardioinhibitory area in the central tegmental field of the midbrain (CIM) was studied in cats under chloralose-urethane anesthesia. Electrical and chemical (glutamate and DL-homocysteic acid) stimulations in this area produced marked bradycardia accompanied by mostly hypotension or minimal change in arterial pressure and by occasional hypertension particularly in the dorsal portion. CIM excitation potentiated the reflex bradycardia induced by IV phenylephrine, while bilateral electrolytic lesion of CIM neither changed the resting cardiovascular parameters nor the reflex bradycardia. The CIM bradycardia was not affected by supracollicular decerebration, but substantially reduced by unilateral vagotomy and completely eliminated by bilateral vagotomy. Destruction of the ambiguus nucleus (NA) and solitary and dorsal motor nuclei (NTS/DMV) abolished the bradycardia. Midline bisection at the midbrain-pontine level only slightly reduced the bradycardia while at the medullary level it was moderately attenuated. Electrolytic lesion of the cardioinhibitory area in gigantocellular reticular nucleus (GRN) abolished the bradycardia. These findings suggest that CIM is an independent mechanism which may send axons to GRN from which the axons may in turn synapse with the NTS/DMV complex and NA. Its final output may utilize both vagus nerves to modulate baroreceptor reflex in promoting bradycardia.

Animals↗
PubMed1987

The Cushing responses in the systemic and pulmonary circulation: the role of adrenal glands, bronchial circulation and pulmonary innervation.

Systemic hypertension and increased total peripheral vascular resistance are the most consistent observations in the Cushing responses to an increase in intracranial pressure (ICP). In the present study, we evaluated the participation of adrenal glands, bronchial circulation and pulmonary innervation in the systemic and pulmonary hemodynamics following an intracranial hypertension (ICH). In a total of 18 anesthetized, vagotomized and open-chest dogs, total heart bypass was performed to perfuse the systemic and pulmonary circulation with constant flow. The venous outflows were diverted into reservoirs. The preparation allowed us to observe the simultaneous changes in the systemic vascular resistance (SVR) and capacity (SVC) as well as the pulmonary vascular resistance (PVR) and capacity (PVC). ICH was produced by inflation of an epidural balloon to elevate the ICP to a level of 165-175 mmHg for 1.5 min. Our data showed that ICH induced drastic increases in SVR and PVR accompanying decreases in SVC and PVC. Vascular occlusion of the adrenal glands (n = 6) did not affect the hemodynamic changes. Arrest of bronchial circulation (n = 6) or pulmonary denervation (n = 6) also did not affect the changes in systemic circulation (SVR and SVC), but greatly diminished the pulmonary hemodynamic changes (PVR and PVC). The results suggest that the adrenal glands are not involved in the systemic and pulmonary hemodynamic responses to this degree of ICH. The changes in the pulmonary vascular resistance and capacity require the integrity of bronchial blood supply and sympathetic innervation.

Adrenal Glands↗
PubMed1986

Vagal cardioinhibitory area in and around the caudal inferior olivary nucleus of cats. I. Localization and connection.

Bradycardia was produced by electrical stimulation and injection of glutamate (200 nl, 1 M) to the regions in and around the extremely caudal parts of the inferior olivary nucleus (ION) in chloralose-urethane anesthetized cats. Either medullary transection at 4 mm rostral to the obex, spinal transection at C2-3 or both transections together did not abolish the ION-induced bradycardia. Bradycardia induced by stimulating one ION was slightly reduced and completely abolished by unilateral and bilateral vagotomies, respectively. The ION-evoked bradycardia was also slightly reduced by a raphe lesion. This lesion together with unilateral vagotomy abolished only the bradycardia induced from the ION on the vagotomized side. In 28 left vagotomized cats, the left ION-induced bradycardia was subjected to the effects of destroying the right ION, dorsal motor/solitary nucleus (DM/SN) and ambiguous nucleus (AN). The bradycardia was completely abolished by ION lesion (7/7), greatly reduced (7/13) or completely abolished (6/13) by DM/SN lesion, and slightly increased (5/8) or decreased (3/8) by AN lesion. We concluded that cells and/or fibers in and around the ION may project fibers to the ipsilateral DM/SN and through the raphe nucleus to the contralateral ION which may send fibers to the other DM/SN.

Animals↗
PubMed1986

Vagal cardioinhibitory area in and around the caudal inferior olivary nucleus of cats. II. Modulatory actions.

In chloralose-urethane anesthetized cats, bilateral destruction of the caudal part of the inferior olivary nucleus (ION) produced neither apparent alteration of the basal arterial blood pressure and heart rate, nor discernible influence on the degree of the induced reflex bradycardia by phenylephrine and reflex tachycardia by nitroglycerin. Apart from directly producing cardioinhibition, stimulation of the ION was capable of interacting synergistically with the reflex bradycardia and antagonistically with the reflex tachycardia. Stimulation of the ION was also capable of potentiating the bradycardias induced from stimulating other cardioinhibitory areas, including the ION of the other side and the gigantocellular reticular nuclei of both sides of the medulla. These interactions were still feasible when one vagus nerve remained intact, but not after both nerves were cut. The results suggest that the ION may not be a primary component of the neural loops subserving the baroreceptor reflex arch, but instead, assumes modulatory actions to this reflex mechanism via both vagus nerves.

Animals↗
PubMed1986

Stress selectively influences center region activity of mice in an open field.

Effects of immobilization and footshock stress on locomotor activity in different areas of an open field were examined in mice. Center region activity, peripheral region activity and total activity were used as measurement indices. These results indicate that both immobilization and footshock stress significantly increased total activity across 24 min of behavioral testing. Further analyses revealed that the difference in total activity between the experimental and control groups were mainly attributal to an increase in center region activity. Both stress manipulations markedly augmented peripheral region activity for only the first 6 min. More important, when the proportion of center to peripheral activity was used as an index, both experimental groups manifested an inverted U shape relationship with the maximum effect occurring between 13-18 min of behavioral testing. Similarities of these activity measures in response to different stressors suggests that common neurochemical and/or neurohormonal mechanisms may mediate these behavioral changes.

Animals↗
PubMed1979

Cardio-inhibitory mechanism in the gigantocellular reticular nucleus of the medulla oblongata.

A cardio-inhibitory mechanism was localized in the ventral part of the medullary gigantocellular reticular nucleus (GRN) in chloralose--urethane anesthetized cats. Stimulation of this mechanism produced an average 58.9% reduction of the heart rate (calculated from 55 responsive points having more than 40% reduction) associated mostly with hypotension, or no change or occasionally a slight increase of the arterial blood pressure. Midcollicular decerebration did not affect this bradycardia. The bradycardia following GRN stimulation of either side by a pair of symmetrically placed electrodes was reduced slightly but equally by: (1) sectioning either side of the vagus nerve; (2) hemisection at a level 4 mm rostral of the obex on either side; or (3) partial destruction of the dorsal motor (DM) and solitary (SN) nuclei on either side. Additional section of the vagus nerve on the opposite side completely abolished the bradycardiac response. Besides, the GRN bradycardia was also slightly but equally attenuated by making a midline bisection in a length extending from 10 to 4 mm rostral of the obex. Additional section of the vagus nerve on either side abolished completely only the bradycardia following electrical stimulation of the GRN on the same side, while that following electrical stimulation of the GRN on the opposite side remained unaffected. On the other hand, the GRN bradycardia was not affected by simply making a caudal midline bisection in a length extending from 3 or 4 mm rostral to 2 mm caudal of the obex. The results suggest: (1) the ventral part of the GRN is a cardio-inhibitory mechanism independent of the higher center; (2) the efferent pathway descends both ipsilaterally and contralaterally and makes synaptic relay in the areas of DM and/or SN and finally exits via the vagus nerves; (3) the fibers decussate rostral to the level 4 mm rostral of the obex; and (4) both ipsilateral and contralateral descending fibers appeared to exert the same degree of suppressive influence in the heart rate.

Animals↗
PubMed1979

Naloxone antagonism of electrical stimulation induced tail erection in mice.

Tail erection was induced by focal electrical stimulation of the mesencephalic central gray through chronically implanted electrodes in mice. The response was current intensity dependent. Pretreatment with naloxone (5 mg/kg IP), a specific narcotic antagonist, abolished tail erection produced by low electrical current. In contrast, the tail response elicited by higher current was only partially blocked by naloxone. The results suggest that electrical stimulation induces tail erection by releasing an endogenous opioid peptide from the mesencephalic central gray.

Animals↗
PubMed1978

Morphine-induced tail erection: site of action.

Acute ablation techniques were used to localize morphine-induced tail erection (MITE) within the central nervous system of mice. Morphine produced no elevation of tails in mice whose spinal cord had been transected at the lower thoracic or lumbar levels. Decortication and high-level precollicular decerebration did not prevent MITE while morphine caused no tail response at all in low-level inferior collicular decerebrate mice. Lesions in various portions of the mesencephalon revealed that the degree of MITE was closely related to the size of the lesions of the central gray matter. The larger the lesion, the smaller the degree of tail elevation. MITE could not be elicited in mice when the mesencephalic central gray matter had been completely destroyed. Results indicate that morphine acts on the mesencephalic central gray matter producing tail erection and the pathway responsible for the reaction descends from the midbrain downward to the spinal cord.

Animals↗
PubMed1977

Myocardial lesions produced by external heat or cold exposure in rats.

Three groups of Sprague-Dawley rats were kept at the ambient temperatures of 8, 24 and 32 degrees C respectively for 3 to 7 days. These animals maintained their rectal temperatures within normal limits. However, the animals of either the heat-stressed or the cold-stressed group yielded not only the functional but also the organic effects to their hearts when compared to those of the control group (24 degrees C exposure). Heat exposure produced a lower heart rate and higher cutaneous temperature, while cold exposure produced a higher heart rate and a lower cutaneous temperature. In addition, the ECG recordings showed a predominant S wave and probably a depressed S-T segment in response to either heat or cold exposure. At the end of either 3-day or the 7-day thermal exposure, the animals were subjected to decapitation. Their hearts were sampled for both light and electron microscopic examinations. It was found that the heat-stressed animals shared with the cold-stressed animals a common picture of the myocardial changes. The subcellular changes in the myocardium in response to external heat or cold were characterized by the mitochondrial hypertrophy, the intracellular edema, the destruction of myofibrils, the dilatation of the intercalated discs, and some abnormalities in their capillaries. The data demonstrate that a short term (3 to 7 days) of moderate heat (32 degrees C) or cold (8 degrees C) exposure produces myocardial lesions in rats, although they maintain their body temperatures within normal limits.

Animals↗
PubMed1977

Effects of neuroleptics on morphine-induced tail erection in mice.

Morphine elicits dose-dependent tail erection in mice. Pretreatment of mice with atropine, phenoxybenzamine, propranolol, diphenhydramine, cyproheptadine or parachlorophenylalanine did not interfere with tail erection induced by morphone. Several neuroleptic drugs which are dopamine receptor blocking agents showed a clear antagonistic effect on morphine-induced tail erection (MITE). Haloperidol and penfluridol blocked MITE at doses which only produced a slight behavioral depression. Pimozide and chlorpromazine were less antagonistic than haloperidol and penfluridol and inhibited MITE only at doses which produced a marked behavioral depression. Results indicated that dopamine might be involved in tail erection induced by morphine. MITE in mice might be a useful model for the evaluation of neuroleptic drugs.

Animals↗
PubMed1977

Mechanisms of amitriptyline induced hypothermia in the rat.

Effects of amitriptyline on rectal temperature of male rats were studied at the ambient temperature of 25 degrees C. Drugs were administered intraperitoneally. Amitryptyline elicited a dose related hypothermia. The hypothermia was attenuated by phenoxybenzamine 10 mg/kg, haloperidol 2 mg/kg, diphenhydramine 5 mg/kg, atropine 20 mg/kg, and cyproheptadine 5 mg/kg. Propranolol, at a dose of 5 mg/kg, had no effect on the hypothermia. Theophylline 50 mg/kg and dibutyryl cyclic AMP 20 mg/kg inhibited the hypothermia produced by anitriptyline. Pretreatment with parachloroamphetamine (PCA), 2 or 5 mg/kg daily for 3 days, strongly antagonized the hypothermia. In addition, pretreatment with parachlorophenylalanine (PCPA), 100 mg/kg daily for three days, reduced the brain 5-hydroxytryptamine (5-HT) concentration to 20% of the control level and completely blocked the hypothermia response. When brain 5-HT concentration recovered to 50% of the control level in PCPA treated rats following the administration of 10 mg/kg 5-hydroxytryptophan (5-HTP) the hypothermia induced by amitriptyline was restored. However, the administration of 5-HT, 5 mg/kg, to PCPA treated rats did not increase brain 5-HT concentration or restore the amitriptyline induced hypothermia (AIH). Results suggest that amitriptyline interacts with several transmitter substances to produce hypothermia. Since the ability of amitriptyline to produce hypothermia was correlated with brain 5-HT content, 5-HT might play an important role in the mediation of AIH.

Amitriptyline↗
PubMed1977

The enhancement of chlorpromazine-induced hypothermia by lesions in the anterior hypothalamus.

1 Administration of chlorpromazine (Cpz), either systemically or centrally, to unanaesthetized rats at an environmental temperature of 23 degrees C caused dose-dependent hypothermia. 2 In order to achieve equivalent hypothermia, intraventricular administration required a total dose of 20 microgram Cpz and and intraperitoneal administration a dose of 9.7 mg/kg body weight. Accordingly, the dose-ratio between intraventricular and intraperitoneal administration was 1 to 110. Cpz apparently exerts its hypothermic effect by acting directly on central nervous structures rather than through peripheral sites. 3 Cpz-induced hypothermia was potentiated by preoptic anterior hypothalamic (POAH) lesions but not by lesions of the ventromedial nucleus (VMN) of the hypothalamus. It was found that Cpz induced hypothermia most readily in rats with large POAH lesions (-10.4 degrees C), less so in rats with spinal lesions (-5.5 degrees C) at least with control rats (-2.9 degrees C).

Animals↗