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C Y Chai

Publications and source records attributed to C Y Chai.

At least 145 records · Page 8Linked to original sources

Afferent and efferent connections of the mesencephalic cardioinhibitory area (CIM) in the cat.

The afferent and efferent connections between the cardioinhibitory area in the midbrain tegmental field (CIM) and brain stem structures related to cardiovascular integration in cats were investigated by horseradish peroxidase (HRP) for both cell origins and axonal terminations and by chemical (kainic acid) lesion for topographic pathways. Retrogradely labeled neurons were observed in the gigantocellular reticular nucleus (GRN), the pontine reticular nucleus of the pons (PON), the ambiguus nucleus (AN) and the paramedian reticular nucleus (PRN). A few neurons were also labeled in the following structures i.e., ventrolateral medulla (VLM), dorsomedial medulla (DMM), dorsomotor nucleus of the vagus nerve (DMV) and nucleus of solitary tract (NTS). Anterograde HRP labeled terminals were found surrounding the cell bodies of the aforementioned structures. They were most abundant in VLM, DMM, DMV, NTS, moderate in GRN, PRN and AN, but only scanty in hypothalamus. The fiber pathway of CIM neurons was also traced by degenerating fibers consequent to kainic acid lesion and by means of silver stain. Degenerating fiber bundle was found primarily projecting through the medial portion of the mesencephalic pontine structures. As the bundle reached the medulla oblongata, it bifurcated into a dorsal and a ventral tracts on its course. The dorsal tract was primarily coursing through the dorsomedial area, including DMM, NTS and DMV, and the ventral tract was mainly passing VLM, AN and inferior olivary nucleus (ION) areas. The present findings suggest that neurons in the CIM may receive inputs from various cardiovascular-related structures and make output bilaterally to some of pontine and medullary structures to modulate cardiovascular functions. Based on the anatomical findings, the profound bradycardia produced by CIM stimulation may be mediated through the following mechanisms: A. Direct activation of vagal preganglionic neurons in DMV, AN and ION. B. Indirect activation of neurons in GRN for vagal activation and of neurons in PRN for sympathetic inhibition.

Afferent Pathways↗

Paramedian reticular nucleus: a thermolytic area in the rat medulla oblongata.

The effects of stimulation or ablation of the paramedian reticular nucleus (PRN) of the rat medulla oblongata on the thermal responses induced by ambient temperature changes, a pyrogen, or a hypothermic substance were assessed. Electrical stimulation of the PRN elicited thermolytic reactions (including decreased metabolism, cutaneous vasodilation and hypothermia) which could be mimicked by micro-injection of kainic acid (an excitotoxic amino acid) into the same region. Bilateral electrolytic lesions in the PRN prevented the animals from responding to heat stress (35 degrees C for 30 min) to some extent, but did not prevent responses to cold stress (4 degrees C for 60 min). In addition, the thermogenic reactions induced by intrahypothalamic injection of polyriboinosinic acid: polyribocytidylic acid (a pyrogenic substance), or the thermolytic reactions induced by intraperitoneal administration of chlorpromazine (a tranquilizer), were antagonized respectively by activation or ablation of the PRN. This suggests that the PRN of the caudal medulla may function as a thermolytic area.

Animals↗

Inhibition of spinal reflexes by paramedian reticular nucleus.

The inhibitory actions of the paramedian reticular nucleus (PRN), and its neighbouring structures, i.e., midline raphe nuclei (MRN) and dorsal medullary depressor area (DMD) on the knee jerk (KnJ) and crossed extension movement (CEM) induced by central sciatic stimulation and on the L5 ventral root response (EVRR) evoked by central tibial stimulation, were studied in cats under urethane (400 mg/kg) and alpha-chloralose (40 mg/kg) anesthesia alone, IP or further paralyzed with atracurium besylate (0.5 mg/kg/30 min), IV. Electrical stimulation of the above areas with rectangular pulses (80 Hz, 1.0 msec, 100-200 microA) decreased systemic arterial blood pressure (SAP) in an average value of: 36 +/- 3 mmHg for PRN; 19 +/- 2 mmHg for MRN; and 23 +/- 3 mmHg for DMD. The KnJ and CEM were almost completely suppressed by simultaneous PRN stimulation. The EVRR, including mono- and polysynaptic spinal reflexes with transmission velocity from 10 to 60 m/sec or above, were also suppressed. MRN stimulation only inhibited the KnJ, CEM and polysynaptic spinal reflexes with transmission velocities between 25 and 60 m/sec, but facilitated spinal reflexes with conduction velocities below 10 m/sec. On the other hand, DMD stimulation resulted in small suppression of KnJ, CEM and inhibition of polysynaptic spinal reflexes with conduction velocities between 25 and 60 m/sec. Even though MRN and DMD partially inhibited polysynaptic spinal reflexes, the magnitude of such inhibition was much smaller than that produced by PRN (-20% and -22% vs. -48%). The above-mentioned PRN effects on SAP and EVRR persisted in chronic animals decerebellated 9-12 days before.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Castration may not affect the penile erection ability in terms of peripheral neurocavernous mechanism in dogs.

The penile erection ability (PEA) was assessed in 27 dogs with intact orchids (Group I), seven dogs with bilateral orchidectomy for one month (Group II) and four dogs with bilateral orchidectomy for three months (Group III). PEA was indicated by the increase of the intracorporeal pressure (ICP) upon electrical stimulation of the cavernous nerves. PEA was significantly decreased in both orchidectomized groups. However, when reduction in the blood pressure was considered, the difference in PEA between Group I and the orchidectomized group was no longer significant. Before the orchidectomy, plasma testosterone level of 22 adult male dogs varied widely from 105 to 6302 pg./ml. At one or three months after the orchidectomy in 11 dogs, it decreased to a level below 100 pg./ml. There was no significant change in the body weight in the post orchidectomy period. These findings indicate that the castration and/or the resulting low plasma testosterone level does not directly affect PEA through the peripheral neural and cavernosal mechanism.

Animals↗

Persistence of renal nerve and spinal reflex activities and visceral motility after asphyxial anoxia.

Phrenic and renal nerves activities, spinal reflex (knee jerk and the evoked monosynaptic reflex response from the 5th lumbar ventral root), motility of the stomach, duodenum, jejunum and colon, and motility of urinary bladder during and after the lethal asphyxia were studied in cats under intraperitoneal urethane (400 mg/kg) and chloralose (40 mg/kg) anesthesia. Asphyxial anoxia produced one or two peaks of elevation of systemic arterial pressure (SAP) followed by a progressive decrease of SAP and narrowing of pulse pressure and eventual complete cardiovascular arrest. The phrenic nerve activity increased markedly during the final asphyxial SAP elevation; it then decreased along with the decline of SAP and ceased permanently when the SAP reached about 50 mmHg. The renal nerve activity increased along with each phase of pressure elevation. During the terminal stage of progressive SAP fall, the renal nerve activity fluctuated up and down 2-3 times before the SAP dropped to zero, and the activity persisted for an average of 202 sec thereafter. Data suggest that the motoneurons of the phrenic nerve in the cervical spinal cord and medulla oblongata are more vulnerable to asphyxia than the motoneurons responsible for the spinal reflex in the pathway from medulla, the intermediolateral column of the spinal cord and the celiac ganglion. During anoxia, the lumbar spinal reflex showed an initial inhibition then potentiation afterward. Even after the SAP had reached zero, the spinal reflex could still be elicited for one to a few minutes. This suggests that the spinal cord can function sometime after complete cardiac arrest subsequent to asphyxia. The motility of the stomach, duodenum, jejunum, colon and urinary bladder usually decreased during the period of pressure elevation. However, the activity was enhanced during the terminal stage of pressure decline. The enhancement of the colon and bladder motility, spasmodic in nature, was particularly prominent, more so than the others. After complete cardiovascular arrest, the motility of the above viscera became temporary quiescent but about 10 minutes later, it resumed activity again with an enhancement of action in some of the animals. The motility, persisted from few minutes to over six hours. These phenomena indicate that despite a complete deprivation of circulatory and respiratory supports, or death of the animal, the viscera can still contract for a certain period of time.

Animals↗

Multiple inhibitory actions of the paramedian reticular nucleus--effects on blood pressure and motor activities in rats.

The paramedian reticular nucleus (PRN) is a triangle midline structure located in the caudal medulla. Electrophysiological and biochemical evidence has suggested that PRN is an important depressor area, and it regulates various cardiovascular functions. The present results have demonstrated that PRN also plays an inhibitory role in a variety of behavioral functions. Lesions of this nucleus produced augmentations of many behavioral measures including: locomotor activity, clockwise and anti-clockwise turnings, as well as stereotyped behavior in rats. It also produced an increased and a more randomized pattern of locomotion. Destructions of the area of nucleus of solitary tract, which affects bradycardia and sometimes hypotension; as well as the midbrain reticular formation, which does not show any cardiovascular responses, yielded much less significant effects. These results confirm previous physiological findings from our laboratory and further suggest that PRN is a unique and independent area which exerts multiple inhibitory actions upon various physiological and behavioral functions in animals.

Animals↗

Homocysteic acid elicits pressor responses from ventrolateral medulla and dorsomedial medulla.

In rats and cats anesthetized with alpha-chloralose and urethane, the pressor response and its relative reactivity were studied following microinjection of dl-homocysteic acid (DLH, 2 nmol in 40 nl of saline) into the dorsomedial medulla (DM) or the ventrolateral medulla (VLM). DLH, which excites only cell bodies of neurons but not fibers of passage, consistently produced pressor responses in DM and VLM in both cats and rats. The pressor effects elicited from VLM were more pronounced than those from DM. In cats, the most active areas for DLH were found in the rostral and midmedulla; the pons and caudal medulla were less active. The pressor responses from DM and VLM were augmented following bilateral vagotomy, persisted after sectioning of the carotid sinus and aortic depressor nerves, and after cauterization of the carotid bodies with phenol. The response induced by DLH was more apparent from VLM than that from DM. These pressor effects were evoked directly by activation of neurons in these two regions, and were not necessarily related to any homocysteate blockade of baroreceptor and/or chemoreceptor reflexes. These results suggest that in the medulla there reside at least two discrete pressor areas, DM and VLM containing neuronal perikarya.

Animals↗

Contribution between dorsal and ventrolateral regions of medulla oblongata in vasomotor function of cats.

In cats anesthetized with alpha-chloralose and urethane, the medulla oblongata was explored with electrical and/or chemical stimulation for vasopressor actions. Chemical stimulation included semimicroinjection of sodium glutamate or microinjection of dl-homocysteic acid (DLH). The dorsal (DM), particularly its dorsomedial (DMM) portion, and the ventrolateral (VLM) regions were found to be most sensitive to both electrical and chemical stimulation. In between these two regions there was an area in the ventral portion of the gigantocellular and the parvocellular reticular nuclei that was sensitive to electrical and somewhat sensitive also to chemical stimulation. The responses to chemical stimulation indicate the existence of perikarya in these three areas for vasopressor actions. The most active response of VLM followed microinjection of DLH into the region of nu. paragigantocellularis lateralis (PGL) and subretrofacial nu. These responses were about 30% greater than those from DM where the most active area was found in the DMM region including the nu. and tractus solitarius. When an extensive area of VLM was lesioned bilaterally with kainic acid (KA, 1 micrograms/100 nl), the resting systemic arterial blood pressure (SAP) fell 42% and the pressor response on DM stimulation fell by more than 80%. In contrast, after similar KA bilateral destruction of DM the resting SAP fell 38% and the pressor responses from 67%. When only a limited area in the PGL/subretrofacial nu. of the rostral VLM (3-4 pressor sites, 1 mm apart) on one side was lesioned, the resting SAP remained unaltered while the pressor response on the ipsilateral DMM decreased 76%. On the other hand, when a similar smaller KA lesion (3-4 sites) was made in the DMM, although the resting SAP did not change, the pressor response on stimulation of the ipsilateral rostral VLM decreased 28%. Further lesioning of the contralateral DMM then decreased the rostral VLM pressor response 62% without much alternation in the resting SAP. Results of the present experiments are in accordance with our previous results that neuronal perikarya for vasopressor action exist not only in VLM but also in DM (18,34) with the function of VLM slightly predominant over DM. It seems highly possible that reciprocal innervation exists between DM and VLM, at least between DMM and the PGL/subretrofacial nu. region.

Animals↗

Existence of a powerful inhibitory mechanism in the medial region of caudal medulla--with special reference to the paramedian reticular nucleus.

Inhibitory actions of the medial trigon of the caudal medulla (ITM) with special reference to the paramedian reticular nucleus (PRN) were explored in cats under chloralose (40 mg/kg) and urethane (400 mg/kg) anesthesia. Stimulation with square wave pulses (80 Hz, 1 msec, 100-200 microA) produced a reduction of mean systemic arterial blood pressure (MSAP) of 15-90 mmHg, and change in heart rate (HR) that varied from mild increase of 15 to reduction of 85 beats/min. These responses were not affected by mid-collicular decerebration nor by bilateral vagotomy. Destruction of PRN did not change the resting MSAP, HR or baroreceptor reflex responses. Stimulation of PRN suppressed the sympathetic pressor and cardioacceleratory and the vagal bradycardia responses resulting from activating cardiovascular (CV) regulatory mechanisms in the hypothalamus, midbrain and medulla, or from activating the somatic or the baroreceptive afferents. Activation of the PRN suppressed the MSAP-increase produced by direct stimulation of the stellate or celiac ganglion. PRN stimulation could eliminate the pronounced CV reactions consequent either to asphyxial anoxia during occlusion of the trachea or to cerebral ischemia following occlusion of vertebral and carotid arteries. Furthermore, PRN activation could stop the general convulsion of the animal induced by picrotoxin, 4 mg/kg, IV. Our findings suggest that in the trigon area especially in the PRN, there resides an independent mechanism which exerts very powerful and broad inhibitory actions on the autonomic as well as somatic nervous system.

Afferent Pathways↗

Paramedian reticular nucleus--sympathetic inhibition in spontaneously hypertensive rats.

The cardiovascular reactivity of various areas in the medulla related to sympathetic or parasympathetic activation, or to sympathetic inhibition, was compared in spontaneously hypertensive rats (SHR) and in normotensive rats Wistar-Kyoto (WKY) or Sprague-Dawley (SD). In SHR, which has an elevated resting systemic arterial blood pressure (SAP), the sympathetic pressor responses elicited from electrical stimulation of the dorsomedial medulla (DMM), parvocellular lateral nucleus (PVC) or ventrolateral medulla (VLM) were more profound than those in WKY and SD. The depressor and bradycardia responses elicited from electrical stimulation of the paramedian reticular nucleus (PRN) (which exerts both sympathetic and parasympathetic inhibitions) or from the area of the solitary nucleus/dorsomotor nucleus of vagus (NTS/DMV) (where stimulation leads to both parasympathetic activation and sympathetic inhibition) were also more intensive in SHR than in WKY and SD. The elicited pressor and depressor responses, however, were not significantly different between WKY and SD. Our results are consistent with previous findings (15) that in SHR an increased sympathetic activity of the pressor areas of medulla contributes to the pathogenesis of hypertension. Sympathetic inhibition (PRN and NTS/DMV areas) and parasympathetic activation (NTS/DMV area) from these areas, however, may not be critically involved.

Animals↗

Pressor responses from electrical or glutamate stimulations of the dorsal or ventrolateral medulla.

In rats, rabbits, and cats anesthetized with alpha-chloralose and urethan, responses of the pressor areas of the dorsal portion (DM) and ventrolateral portion (VLM) of medulla and pons were compared. Electrical stimulation (monopolar square-wave pulses) on monosodium glutamate solution (Glu, 100-200 nl, 1 M) was delivered through an electrode-needle tubing connected to a Hamilton syringe for semimicroinjection. In all three of these species, pressor responses were elicited from both DM and VLM by either Glu or electrical stimulation. The most active parts of DM were found in the dorsomedial reticular formation of the rostral medulla to mid-medulla. In the pons and caudal medulla, the Glu-induced response was mild, although the electrically induced response was marked. Application of kainic acid (KA) to either DM or VLM produced an initial pressor response but was followed by a reduction of the pressure rise on subsequent electrical stimulation. Glu, unlike electrical stimulation, excites neural perikarya, not fibers of passage. KA initially excites the neural perikarya before causing damage that spares axons. These results thus suggest that both DM and VLM contain neural perikarya that mediate pressor effects.

Animals↗

Predominance of vagal bradycardia mechanism in the brain stem of turtles.

Cardiovascular parameters of spontaneously breathing pond turtles (Cyclemys flavomarginata) anaesthetized with chloralose (4 mg 100 g-1) and urethane (40 mg 100 g-1), were examined during exploratory electrical stimulation of the brain stem. Turtles exhibited a low mean systemic arterial blood pressure (MSAP, average 25 mmHg) and slow heart rate (average 24 beats min-1). Upon stimulation, pressor (sympathetic), depressor (sympathetic inhibition), bradycardia and hypotensive (vagal) responses were elicited from regions of the brain stem extending from the hypothalamus to the medulla, principally in the medial region. The pressor response appeared after a longer latency than did the bradycardia and hypotensive responses. It developed rather slowly, and rarely attained a magnitude double its resting value. In contrast, stimulation of many points in the brain stem produced marked slowing or even cessation of the heart beat, and thus resulted in an immediate fall of the blood pressure even to zero. This cardio-inhibitory response depended on the integrity of the vagus nerves and was particularly marked upon stimulation in the caudal medulla, the areas of the ambiguus, solitary and dorsomotor nuclei of the vagus and the midline structures. When such an area was stimulated continuously the heart stopped beating throughout the stimulation. The longest period of cardiac arrest before the appearance of escape was 35 min. With continuous stimulation of the peripheral end of the cut vagus, the earliest escape beat occurred even later (65 min). Epinephrine given intravenously produced an increase of MSAP and force of cardiac contraction, although the slope of pressor rise was shallow. Reflex bradycardia, however, was not observed. These experiments show that a very prominent vagal bradycardia can be evoked from the turtle brain stem, which may contribute to its well-known capacity for tolerating anoxia.

Animals↗

Effects of calcium-channel blockers on picrotoxin-induced centrogenic arrhythmias in cats.

Intravenous picrotoxin injection has been established as a model of producing arrhythmias, mainly through enhanced central sympathetic outflow. The effects of calcium-channel blockers, and a beta-blocker on these arrhythmias were tested in chloralose-anesthetized cats. Picrotoxin (10 mg/kg, i.v.) produced mostly ventricular, sometimes supraventricular tachycardias and ectopic beats, as well as a marked elevation of arterial blood pressure. Nifedipine at the doses of 2 micrograms/kg (i.v. or i.c.) and 5 micrograms/kg (i.v.) transiently suppressed the arrhythmias in some of the cats tested. With the dose of 10 micrograms/kg (i.v.), it promptly and consistently abolished the arrhythmias without recurrence and significantly reduced the blood pressure (-62 +/- 8/-59 +/- 8 mmHg, delta systolic pressure/delta diastolic pressure, p less than 0.001, n = 9). A similar degree of blood pressure reduction (-69 +/- 8/-67 +/- 7 mmHg, n = 6) after sodium nitroprusside (4-5 mg/kg, i.v.) injection abolished the arrhythmias in 4 of 6 cats; however, there was marked ECG evidence of myocardial ischemia in 3 cats. Verapamil (50 micrograms/kg, i.v.) transiently abolished the arrhythmias and significantly decreased the blood pressure (7/7 cats), whereas a larger dose (150 micrograms/kg) had a persistent effect (2/4 cats). Propranolol at a dose of 240 micrograms/kg also consistently abolished the arrhythmias without recurrence in all 4 cats. We conclude that nifedipine, verapamil and propranolol are effective in the treatment of picrotoxin-induced arrhythmias. This result indicates that calcium-channel blockers or beta-blockers may be clinically effective in the treatment or prevention of arrhythmias caused by intracranial lesions with enhanced sympathetic outflow.

Animals↗

Influence of rostral neural structures on the vasomotor functions of the medulla oblongata.

Chinese J. Physiol 31(2): 79-93, 1988. In cats, the resting systemic arterial blood pressure (SAP) which rises on electrical stimulation of the dorsal medulla (DM), ventrolateral medulla (VLM) and paramedian reticular nucleus (PRN) under anesthesia with 2% halothane in oxygen were compared with those 30 min after termination of the inhalation (with application of lidocaine on the surgical wound and i.v. gallamine 2 mg/kg). The resting SAP under halothane were significantly lowered and functions of the DM and VLM much depressed. The depressor response of PRN stimulation was converted to the pressor one after deprivation of halothane anesthesia. In animals under little anesthetic influence, midcollicular decerebration significantly lowered the resting SAP, but both DM and VLM pressor responses were not significantly changed. In addition, the decerebration significantly diminished the peak pressor effects on PRN stimulation. Findings suggest that rostral neuro-structures do exert tonic influence (both excitatory and inhibitory) on medulla vasomotor functions. This is quite different from the classical concept, first proposed by Dittmar and Owsjannikown (1870s) and still considered nowadays as truthful, that the neural structures rostral to the caudal one third of pons was not critical in maintaining the resting SAP.

Animals↗

Reduction of common carotid resistance upon stimulation of an area dorsal to the facial nucleus of cats.

In chloralose-urethane-anesthetized cats, electrical stimulation and glutamate injection on a small reticular area just dorsal to the facial nucleus (DFA) elicited an ipsilateral reduction in the common carotid resistance (CCR-reduction) with no or minimal change in other cardiovascular parameters. CCR-reduction was mediated via facial and glossopharyngeal nerves, involving partially muscarinic and partially non-muscarinic mechanisms.

Animals↗

Association between the behavioral and neurochemical effects of amphetamine: hemispheric asymmetry study.

Effects of amphetamine on concentrations of dopamine, norepinephrine and serotonin in several monoamine-containing cell body and terminal regions were examined left and right separately in rats. Results suggest that amphetamine reduced the L-R asymmetry of most of these measures, and this effect is more significant in the cell body than in the terminal regions. Behaviorally, amphetamine also decreased L-R asymmetry of the spontaneous turning behavior in rats and this latter effect is most closely associated with the reductions of dopamine and norepinephrine asymmetries in the substantia nigra and reduction of norepinephrine asymmetry in the locus coeruleus.

Animals↗

Stress and corticotropin-releasing factor potentiate center region activity of mice in an open field.

The effects of corticotropin-releasing factor (CRF) and previously published effect of stress on the locomotor activity of mice in different regions of an open field were compared. Intracerebroventricular (ICV) administration of 0.2 microgram CRF, like stress, significantly increased center region activity; this effect was reversed by the benzodiazepine diazepam (DZP) at a dose of DZP having no significant effect alone. A dose of DZP that antagonized CRF-potentiated center region activity did not block amphetamine-stimulated center area activity. These results suggest that CRF may normally be responsible for many behavioral changes during conditions of stress.

Amphetamine↗