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Biomedical subjects

J Y Pan

Publications and source records attributed to J Y Pan.

At least 19 recordsLinked to original sources
PubMed1992

[Different changes in renal sympathetic nerve activity and adrenal sympathetic nerve activity produced by hemorrhage].

The present study was undertaken to investigate the changes in renal sympathetic nerve activity (RSNA) and adrenal sympathetic nerve activity (AdSNA) due to acute hemorrhage in anesthetized rabbits. The animals were bled to a mean arterial pressure (MAP) of 5.3 kPa within 10 minutes from the femoral artery. Acute hemorrhage elicited a biphasic responses of RSNA with an initial excitation and a late inhibition during hemorrhage. But hemorrhage only induced a lasting excitation in AdSNA which could be abolished by sino-aortic denervation (SAD). Bilateral vagotomy either before or after hemorrhage could reverse the late inhibition in RSNA, but did not abolish the excitation in AdSNA. Intravenous injection of naloxone or microinjection of naloxone into rostral ventrolateral medulla (RVLM) could reverse the late inhibition in RSNA, but had no significant effect on the initial excitation in RSNA and AdSNA during hemorrhage. Hemorrhage-induced heart (HR) change was similar that in RSNA, but could not be reversed by naloxone. These results indicate that the late inhibition in RSNA is mediated by inputs from vagus nerves and opiate peptide, particularly that in RVLM, and the excitation in AdSNA during hemorrhage is related to arterial baroreceptor reflex.

Adrenal Glands↗
PubMed1992

[Effects of stimulation of renal afferent nerve on renal excretion of water, sodium and potassium].

The present study was designed to investigate the effect of stimulation of the renal afferent nerve (RAN) on renal excretory function and its mechanism. In pentobarbital-anesthetized, sino-aortic denervated and vagotomized (SAD+VD) cats, stimulation of the RAN caused a significant rise in arterial pressure. In the denervated kidney urine volume (Vu) and sodium excretion (UNa V) were greatly increased, no changes in potassium excretion (UK V) and glomerular filtration rate (GFR) were observed. In the innervated kidney, UNa V was greatly increased, but Vu, UK V and GFR were not different from those observed during the control period. When arterial pressure was held constant at the control level, stimulation of the RNA reduced the Vu, UK V of both the innervated and denervated kidneys and GFR in the innervated but not in the denervated kidney. Transection of spinal cord at C7 level did not abolish the changes in Vu, UNa V, and UK V in the innervated kidney, but completely eliminated the changes in the excretory function in the denervated kidney. These data suggest that when arterial pressure is controlled, stimulation of the RAN causes a decrease in Vu, UNa V, UK V in SAD+VD cats and that these responses in the innervated kidney can be performed at the spinal level.

Afferent Pathways↗
PubMed1991

[Role of paraventricular nucleus of hypothalamus in pressor response to stimulation of renal afferent nerve in cats].

The purpose of this study is to investigate the role of paraventricular nucleus of the hypothalamus (PVN) and alpha 1 adrenergic receptor of PVN in the pressor responses to stimulation of renal afferent nerve in alpha 1-chloralose-anesthetized cats with carotid sinoaortic denervation and vagotomy. The pressor response to stimulation of renal afferent nerve consisted of a primary and a second components. The primary component response was completely blocked while the second component was not blocked by autonomic blocking agents (hexomethonium and atropine). Bilateral lesions of PVN greatly attenuated the pressor response before and after autonomic blockade. Intracerebroventricular and PVN injection alpha 1, adrenergic antagonist (prazosin) significantly decreased in the pressor response to stimulation of renal afferent nerve. These results indicate that paraventricular nucleus of the hypothalamus and alpha 1 adrenergic receptors in central nervous system, especially in PVN, play an important role in the pressor responses to stimulation of renal afferent nerve.

Afferent Pathways↗
PubMed1991

[Effect of hypertonic NaCl solution on arterial pressure compensation after hemorrhage in rats].

Rats were bled within 5 min in lowering mean arterial pressure (MAP) to 25 mmHg and were subsequently infused intravenously with hypertonic (7.5% NaCl) or normal saline in a volume equal to 10% of the amount of the lost blood. Intravenous infusion of hypertonic saline significantly facilitated posthemorrhagic recovery of MAP, which was markedly attenuated by 6-hydroxydopamine or Captopril. When these two drugs were used together, the attenuation effect was complete. While hypertonic saline significantly increased plasma Na+ concentration, normal saline only gave rise to a decrease. Intracerebroventricular injection of hypertonic NaCl solution also facilitated the recovery of MAP significantly. These results suggest that after hemorrhage increased plasma Na+ concentration following i.v. of a small amount of hypertonic saline may act on the central nervous system and activate sympathetic nervous system and renin angiotensin system to facilitate a rapid recovery of MAP.

Animals↗
PubMed1991

[Observation on the contraction process of ovarioles of Anopheles sinensis and Anopheles anthropophagus after oviposition].

In order to know the process of ovariole contraction after oviposition in Anopheles sinensis and An. Anthropophagus, and to determine the relationship between the ovariole contraction and the physiological age, the observation was conducted in 1988. The laboratory-reared female mosquitoes after 3-5 days of eclosion were fed with mouse blood and were kept in separate finger tubes for oviposition. After oviposition, the mosquitoes were dissected at different time. 30 ovarioles for each mosquito were examined and recorded by Detinova's method. A total number of 75 An. sinensis with 2,262 ovarioles and 87 An. anthropophagus with 2,591 ovarioles were examined after first oviposition. The duration for ovariole contraction in the phase of A,B,C,D,E was 1, 3-6, 9-14, 15-18 and 21h respectively. A total number of 40 An. sinensis with 1,337 ovarioles and 34 An. anthropophagus with 1,099 ovarioles were examined after third oviposition. The duration for ovariole contraction in the phase of A,B,C,D,E was 1, 3-9, 12-15, 18 and 21h respectively. E phase can be found in 21-24h after oviposition. There were 29.3% and 38.0% ovarioles in C and D phase for first oviposition while 48.4% and 46.0% ovarioles in C and D phase for third oviposition. It was found that the contraction occurred first in breadth and then in length.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Effects of morphine of different concentrations on myocardial action potential].

The effects of morphine at different concentrations on myocardial action potential were studied in isolated right ventricular papillary muscles of the guinea pig. It was observed that morphine at low concentrations (0.2-1.6 mumol/L) shortened the action potential duration (ADP) and effective refractory period (ERP) in a concentration dependent manner. These effects could be abolished by naloxone (1 mumol/L), phentolamine, tetraethylammonium (TEA) and cesium chloride (Cs+), but not by verapamil. On the other hand, morphine at high concentrations (15-120 mumol/L) prolonged ADP and ERP in a concentration dependent manner. The effects were unaffected by low dose of naloxone (1.2 mumol/L) but were abolished by high dose of naloxone (10 mumol/L), phentolamine, TEA, Cs+ and verapamil. These results suggest that morphine at low and high concentrations might stimulate different subtypes of opioid receptors. The effects of morphine in low concentrations are associated with the activation of potassium channel, whereas the effects of morphine at high concentrations are associated with the activation of potassium channel, calcium channel or calcium activated potassium channel. The action of opioid receptor was closely related to alpha adrenoreceptors.

Action Potentials↗
PubMed1989

[Effects of intracisternal injection of naloxone on the depressor response to stimulation of renal afferent nerve in rabbits].

The purpose of this study was to observe the effects of opioid receptor and alpha-adrenergic receptors in the lower brain stem on the depressor response to electrical stimulation of renal afferent nerve, using intracisternal injection of blockers of these receptors. Experiments were conducted in sodium pentobarbital-anesthetized rabbits. The intracisternal injection (ict) of artificial cerebrospinal fluid (CSF) did not greatly affect the depressor response to stimulation of renal afferent nerve (RAS) and of aortic nerve (ANS). Ict of 550 nmol naloxone significantly inhibited the depressor response to RAS (P less than 0.05) but enhanced the depressor response to ANS (P less than 0.05). Ict of 335 nmol phentolamine significantly inhibited the depressor response to both RAS and ANS. Ict of naloxone reversed the phentolamine inhibition of the depressor response to ANS but did not affect the phentolamine inhibition of the depressor response to RAS. Ict of both naloxone and phentolamine did not affect the inhibitory interaction between the RAS-induced depressor and aortic baroreflex. Ict of phentolamine significantly decreased MAP, and ict of naloxone did not decrease MAP but reversed the decrease in MAP by ict of phentolamine. These data suggest that the activation of opioid receptors in the lower brain stem enhances the depressor response to RAS and attenuates the depressor response to ANS. Moreover, activation of alpha-adrenergic receptors in the lower brain stem facilitates the depressor response to RAS and ANS.

Animals↗
PubMed1985

Molecular cloning and sequencing of H-2Kk cDNA: comparison with other H-2 genes and evidence for alternative splicing.

A cDNA library was constructed from mouse L cells that were transfected with a human HLA-B7 gene fragment lacking the 5'-segment of exon 2 and all upstream sequences. A cDNA clone (pESP-C103) which is of mouse origin was detected by hybridization with the HLA-B7 gene. Comparison of the amino acid (aa) sequence predicted from the nucleotide sequence of the cDNA and the partial aa sequence of the H-2Kk antigen suggests that this cDNA (pESP-C103) codes for the H-2Kk antigen. This cDNA clone extends to the middle of the leader sequence. Comparison of the nucleotide and deduced aa sequences with those of other H-2 genes revealed an alternative splicing in exon 8 in the case of the H-2Kk gene.

Amino Acid Sequence↗
PubMed1985

Baroreflex control of sympathetic nerve activity after elevations of pressure in conscious rabbits.

The purpose of this study was to assess the effect of rapid baroreceptor resetting on the baroreflex control of renal sympathetic nerve activity in conscious rabbits. Renal sympathetic nerve activity was recorded and used as an index of the efferent limb of the baroreflex. Heart rate and arterial pressure were also recorded. Arterial pressure was raised with either phenylephrine or angiotensin II to a level that eliminated renal sympathetic nerve activity and was maintained at this level for periods of time ranging from 1 to 60 min. On returning pressure to control levels, renal sympathetic nerve activity remained suppressed for up to 90 min, with the duration of the suppression dependent on the magnitude and duration of the pressure stimulus. During this period of suppressed nerve activity, baroreflex curves were generated. The curves produced at this time were also suppressed as compared with control baroreflex curves. With time, the suppressed baroreflex curves returned to control. Further studies were performed to show that the suppression of renal sympathetic nerve activity was mediated via the prolonged increase in baroreceptor afferent activity during the pressure stimulus and was not due to a central effect of phenylephrine. This study indicates that although baroreceptor afferent activity may reset rapidly, there does not appear to be an augmentation of renal sympathetic nerve activity as would be expected.

Animals↗