Biomedical subjects

J Z Guo

Publications and source records attributed to J Z Guo.

At least 19 recordsLinked to original sources

PubMed2001

Allitridum mimics effect of ischemic preconditioning by activation of protein kinase C.

AIM: To investigate whether allitridum has the effect of pharmacological preconditioning and whether protein kinase C (PKC) plays a role in myocardial protection. METHODS: Thirty-four isolated rabbit hearts which subjected to 30 min of regional myocardial ischemia and 2 h reperfusion, were randomly divided into 5 groups: control group, ischemic preconditioning (PC) group, allitridum (A) group, polymyxin B (Poly B) group, allitridum + polymyxin B (A + Poly B) group. Infarct size was determined by triphenyltetrazolium staining. RESULTS: Pharmacological preconditioning in hearts with a 5 -min allitridum infusion 10 min before the prolonged regional ischemia resulted in significantly smaller infarcts (7 % +\- 6 % of risk area) than in control hearts (25 % +\- 7 %, P < 0.05). There is no significant difference in infarct size between (A+Poly B) group and control hearts (23 % +\- 5 % vs 25 % +\- 7 %, P > 0.05). CONCLUSION: These data indicate that allitridum can precondition rabbit ischemic myocardium and this protection can be effectively blocked by administration of Poly B, an inhibitor of PKC, implying that PKC has an important role in preconditioning.

Allyl Compounds↗

PubMed2000

Muscarinic receptors mediate enhancement of spontaneous GABA release in the chick brain.

The functional role of muscarinic acetylcholine receptors in the lateral spiriform nucleus was studied in chick brain slices. Whole-cell patch-clamp recordings of neurons in the lateral spiriform nucleus revealed that carbachol enhanced GABAergic spontaneous inhibitory postsynaptic currents. The duration of the response to carbachol was significantly reduced after blockade of muscarinic receptors with atropine. In the presence of the nicotinic receptor antagonist dihydro-beta-erythroidine, carbachol produced a delayed but prolonged enhancement of spontaneous GABAergic inhibitory postsynaptic currents that was completely blocked by atropine. Muscarine also enhanced the frequency of spontaneous GABAergic inhibitory postsynaptic currents in a dose-dependent manner, but had no effect on inhibitory postsynaptic current amplitude. While 4-diphenylacetoxy-N-(2-chloroethyl)-piperidine hydrochloride, a M3 antagonist, completely blocked muscarine's effect, telenzepine, a M1 antagonist, and tropicamide, a M4 antagonist, only partially decreased the response to muscarine. Pirenzepine, a M1 antagonist, and methoctramine, a M2 antagonist, potentiated muscarine's enhancement of spontaneous GABAergic inhibitory postsynaptic currents. Muscarine's action was blocked by tetrodotoxin, cadmium chloride and omega-conotoxin GVIA, but was not affected by dihydro-beta-erythroidine, 6-cyano-7-nitroquinoxaline-2,3-dione, D(-)-2-amino-5-phosphonopentanoic acid, naloxone or fluphenazine. These results demonstrate that activation of both muscarinic and nicotinic acetylcholine receptors can enhance GABAergic inhibitory postsynaptic currents in the lateral spiriform nucleus. The muscarinic response has a slower onset but lasts longer than the nicotinic effect. The M3 receptor subtype is predominantly involved in enhancing spontaneous GABAergic inhibitory postsynaptic currents. These M3 receptors must be located some distance from GABA release sites, since activation of voltage-dependent sodium channels, and consequent activation of N-type voltage-dependent calcium channels, is required to trigger enhanced GABA release following activation of muscarinic receptors.

Animals↗

PubMed2000

Speech evaluation of partially implantable piezoelectric middle ear implants in vivo.

OBJECTIVE: Cochlear microphonic responses (CMs) were measured in a rabbit model in the intact ear (CM1) and in ears with a partially implantable piezoelectric middle ear implant (P-MEI) (CM2) to investigate the characteristics of speech transmission of the P-MEI in vivo. DESIGN: The spectra of pure tones, voices, and elicited CM1 and CM2 obtained from the round window before and after the implantation of a P-MEI device were calculated by using fast Fourier transform. Frequency response functions of CM1 and CM2 were used to demonstrate the functional similarity between the implanted P-MEI and the normal ossicular chain. The coherence functions between the voices and CM1 and between CM1 and CM2 were evaluated to characterize speech transmission of the P-MEI in vivo. Ten rabbit ears were used in this study. Pure tones, six Chinese vowels, and six Chinese characters were the acoustic stimuli. The CMs elicited by a list of bisyllabic words were tape-recorded and then recognized by subjects with normal hearing. RESULTS: Using pure tones at the same intensity of 90 dB SPL, frequency response functions of the CMs between the two states (the intact ear with normal hearing and ears with a P-MEI device at the medium volume) were calculated showing great resemblance in shape. Compared with that at 1 kHz, gain factors were 10 and 20 dB, respectively, at higher frequencies. The correlation and spectral analyses of the vocalizations, CM1 and CM2, demonstrated that the harmonics of CM1 were approximately identical as those of the voices between 0.5 and 5.0 kHz with coherence functions of about 0.7 to approximately 1 at the formants' frequencies, whereas the harmonics of CM2 between 0.5 and 2.5 kHz were enhanced with the coherences near to unity at the formants' frequencies, and others <0.5 kHz and >2.5 kHz were attenuated. The recognition score of the CMs elicited by a list of bisyllabic words was >90% using subjects with normal hearing. CONCLUSIONS: Data from this study suggest that cochlear microphonic potentials can be used as an important tool to evaluate objectively whether the implantation of a P-MEI device is successful and whether the quality in speech transmission of the P-MEI is satisfactory. Thus, the method would be of significance to clinically ascertain the performance of the device in vivo.

Animals↗

PubMed2000

[Hemangioma of external ear: an analysis of 8 cases].

OBJECTIVE: To investigate approaches of diagnosis and therapy to hemangioma of external ear and improve the effects of diagnosis and therapy. METHOD: Eight cases of hemangioma of external ear were analyzed retrospectively. All patients were unilateral hemangioma. 5 were performed digital subtraction angiography (DSA) before operation, of which 3 were performed embolization simultaneously. 7 were operated, 1 was not done. Racemose hemangioma was 5 and cavernous hemangioma was 2 according to pathologic diagnosis. RESULT: All patients have followed up 1 to 5 years, 5 were healed, 2 were controlled, and 1 was not treated. CONCLUSION: Surgery was effective approach to hemangioma of adults. It suggested that it was the key of controlling bleeding during operation that DSA and embolization before operation or ligating artery of blood supply during operation.

Adult↗

PubMed1999

N-type voltage-dependent calcium channels mediate the nicotinic enhancement of GABA release in chick brain.

The role of voltage-dependent calcium channels (VDCCs) in the nicotinic acetylcholine receptor (nAChR)-mediated enhancement of spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) was investigated in chick brain slices. Whole cell recordings of neurons in the lateral spiriform (SpL) and ventral lateral geniculate (LGNv) nuclei showed that cadmium chloride (CdCl2) blocked the carbachol-induced increase of spontaneous GABAergic IPSCs, indicating that VDCCs might be involved. To conclusively show a role for VDCCs, the presynaptic effect of carbachol on SpL and LGNv neurons was examined in the presence of selective blockers of VDCC subtypes. omega-Conotoxin GVIA, a selective antagonist of N-type channels, significantly reduced the nAChR-mediated enhancement of gamma-aminobutyric acid (GABA) release in the SpL by 78% compared with control responses. Nifedipine, an L-type channel blocker, and omega-Agatoxin-TK, a P/Q-type channel blocker, did not inhibit the enhancement of GABAergic IPSCs. In the LGNv, omega-Conotoxin GVIA also significantly reduced the nAChR-mediated enhancement of GABA release by 71% from control values. Although omega-Agatoxin-TK did not block the nicotinic enhancement, L-type channel blockers showed complex effects on the nAChR-mediated enhancement. These results indicate that the nAChR-mediated enhancement of spontaneous GABAergic IPSCs requires activation of N-type channels in both the SpL and LGNv.

Agatoxins↗

PubMed1998

Glutamate and GABA release are enhanced by different subtypes of presynaptic nicotinic receptors in the lateral geniculate nucleus.

The functional role of nicotinic acetylcholine receptors (nAChRs) in the ventral lateral geniculate nucleus (LGNv) was examined in chick brain slices. Whole-cell patch-clamp recordings of neurons in the LGNv revealed the presence of bicuculline-resistant spontaneous postsynaptic currents (PSCs), which were subsequently blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an AMPA receptor antagonist. Carbachol and other nicotinic agonists produced marked increases in the frequency of the glutamatergic spontaneous PSCs in the presence of tetrodotoxin, whereas they had little or no effect on current amplitude. The nicotinic receptor antagonist dihydro-beta-erythroidine (DHbetaE) blocked the carbachol-induced enhancement of spontaneous glutamatergic PSCs. alpha-bungarotoxin (alpha-BgTx) selectively blocked the nAChR-mediated enhancement of spontaneous glutamatergic PSCs but did not prevent nAChR-mediated enhancement of spontaneous GABAergic PSCs in the LGNv. Methyllycaconitine and strychnine, other blockers of nAChRs containing the alpha7 subunit, failed to inhibit carbachol's increase of spontaneous glutamatergic and GABAergic PSCs. These results demonstrate that the LGNv neurons receive both glutamatergic and GABAergic inputs and that the release of these transmitters can be modulated by different presynaptic nAChRs. Thus, the regulation of synaptic efficacy in the brain by presynaptic nAChRs can be complex, involving multiple neurotransmitters acting on the same neuron.

Animals↗

PubMed1998

Effects of a tachykinin NK3 receptor antagonist, SR 142801, studied in isolated neonatal rat spinal cord.

Effects of a nonpeptide tachykinin NK3 receptor antagonist, SR 142801, were studied in the isolated spinal cord preparation of the neonatal rat. Potential changes were recorded extracellularly from a lumbar ventral root. Bath-application of neurokinin B induced a dose-dependent depolarization of the ventral root. SR 142801 caused rightward shifts of the concentration-response curve for neurokinin B with pA2 of 6.57, but did not affect the depolarizing responses to other agonists. Stimulation of a dorsal root evoked in the ipsilateral ventral root of the same segment monosynaptic and polysynaptic reflexes of fast time course which were followed by a slow depolarization (ipsilateral slow ventral root potential). SR 142801 depressed the ipsilateral slow ventral root potential. The present results indicate that SR 142801 is a specific antagonist for tachykinin NK3 receptors in the spinal cord and suggest that NK3 receptors are involved in primary afferent-evoked nociceptive responses of spinal neurones.

Animals↗

PubMed1998

Differential effects of wortmannin on the release of substance P and amino acids from the isolated spinal cord of the neonatal rat.

1. Effects of wortmannin, an inhibitor of myosin light chain kinase, on the release of substance P and amino acids, GABA and glutamate, were investigated in the isolated spinal cord preparation of the neonatal rat. 2. Wortmannin at 0.5 - 10 microM depressed the release of substance P evoked by high-K+ (90 mM) medium from the spinal cord (IC50 = 1.1 microM). Wortmannin also depressed the high-K+ (70 mM)-evoked release of substance P from cultured dorsal root ganglion neurons of neonatal rats. In contrast, the high-K+ (90 mM)-evoked release of GABA and glutamate from the spinal cord was not affected by wortmannin (0.1 - 10 microM). 3. Upon stimulation of a dorsal root, a monosynaptic reflex and a subsequent slow ventral root depolarization were evoked in the ipsilateral ventral root of the same segment in the isolated spinal cord preparation. The magnitude of the slow ventral root depolarization was depressed gradually to about 70% of the control during the course of 30 min under wortmannin (1 microM). In contrast, the monosynaptic reflex was unaffected by wortmannin. 4. Immunofluorescent staining revealed that immunoreactivities of substance P and myosin II were colocalized at presynaptic terminals in the dorsal horn of the neonatal rat spinal cord. 5. The present results suggest that myosin phosphorylation by myosin light chain kinase may play a crucial role in the release of substance P, but not in the release of GABA and glutamate in the neonatal rat spinal cord. This may reflect a difference in the exocytic mechanisms of substance P-containing large dense core vesicles and amino acid-containing small clear vesicles.

Amino Acids↗

PubMed1997

Tachykinin receptors on motoneurons in the spinal cords of neonatal rats, gerbils and hamsters.

As a step to clarify the profiles of tachykinin receptors in the mammalian central nervous system, we examined the effects of various tachykinin receptor agonists and antagonists on motoneurons in isolated spinal cord preparations from rats, gerbils and hamsters. After treatment with tetrodotoxin, potential changes were recorded extracellularly from lumbar ventral roots at 27 degrees C. Bath-application of tachykinin NK1, NK3 receptor agonists produced depolarizing responses of ventral roots. In contrast, selective NK2 agonists exerted no or only marginal depolarizing action. Neurokinin A (NKA), however, exerted a distinct depolarizing action on motoneurons. Tachykinin NK1 receptor antagonists antagonized the actions of SPOMe and NKA in a competitive manner. The present results suggest that tachykinin NK1 and NK3 receptors are present on spinal motoneurons of newborn rats, gerbils and hamsters, and that NKA acts on the NK1 receptors.

Animals↗

PubMed1996

The effect of specific hormones on fibrinolysis in pregnancy.

OBJECTIVE: Plasminogen activator inhibitor-1, the major serum protease inhibitor of fibrinolysis, increases steadily during pregnancy. The study objective was to examine four hormones, namely, estradiol-17 beta, progesterone, prolactin, and hydrocortisone to determine their individual contributions in the production of tissue plasminogen activator antigen, plasminogen activator inhibitor-1 antigen, and plasminogen activator inhibitor-1 activity. STUDY DESIGN: Human umbilical vein endothelial cells were grown with physiologic third-trimester concentrations of the above hormones, and fibrinolytic parameters were measured. RESULTS: Of the four hormones evaluated, only hydrocortisone significantly increased plasminogen activator inhibitor-1 antigen and activity at both concentrations tested (p < 0.001). Estradiol-17 beta significantly increased tissue plasminogen activator antigen and progesterone significantly decreased tissue plasminogen activator antigen, but neither affected the overall fibrinolytic balance. CONCLUSION: Hydrocortisone demonstrated antifibrinolytic properties at physiologic concentrations in pregnancy, suggesting that there may be a role for hydrocortisone in the prothrombotic tendency associated with pregnancy. The overall process of fibrinolysis was unaffected by estradiol-17 beta, progesterone, or prolactin.

Cells, Cultured↗

PubMed1996

Tachykininergic synaptic transmission in the coeliac ganglion of the guinea-pig.

1. The responses of coeliac ganglion neurones of the guinea-pig to electrical stimulation of the mesenteric nerves and applications of tachykinin receptor agonists were investigated by use of intracellular recording techniques. 2. Ganglion neurones were classified into three groups based on firing patterns in response to a depolarizing current pulse: phasic (38% of the population), tonic (39%) and atypical (23%). In the majority of phasic neurones (91%) a long after-hyperpolarization (LAH) lasting 5-8 s followed action potentials induced by a train of depolarizing current pulses. In contrast, LAH was rarely observed in tonic neurones (5%). 3. In most of tonic neurones (90%) slow excitatory post-synaptic potentials (e.p.s.ps) lasting 3-10 min were evoked by repetitive electrical stimulation of the mesenteric nerves. Prolonged depolarizations were also evoked in most tonic neurones by applications of substance P (SP), neurokinin A (NKA) or senktide, a tachykinin NK3 receptor agonist. 4. In most of phasic neurones (73%), mesenteric nerve stimulation did not induce an obvious depolarization but induced a prolonged inhibition of LAH lasting 3-10 min. Bath-applied tachykinin receptor agonists similarly induced an inhibition of LAH without causing depolarization in most of the phasic neurones. 5. GR 71251 (5 microM), a tachykinin NK1 receptor antagonist, partially depressed the nerve-evoked slow e.p.s.ps in tonic neurones and the nerve-evoked LAH inhibition in phasic neurones. 6. Capsaicin (0.1-5 microM) induced a prolonged depolarization in tonic neurones and an inhibition of LAH in phasic neurones. 7. A mixture of peptidase inhibitors potentiated the depolarization and the LAH inhibition evoked by nerve stimulation, SP and NKA, but not those evoked by senktide. 8. It is concluded that tonic neurones respond to repetitive mesenteric nerve stimulation preferentially with slow e.p.s.ps and that phasic neurones respond preferentially with LAH inhibition. The present study further suggests that SP and NKA, released from axon collaterals of primary afferent neurones, produce slow e.p.s.ps in tonic neurones and the LAH inhibition in phasic neurones via NK1 receptors.

Animals↗

PubMed1995

Pharmacological characterization of GR82334, a tachykinin NK1 receptor antagonist, in the isolated spinal cord of the neonatal rat.

Pharmacological characteristics of [D-Pro9,[spiro-gamma-lactam]Leu10,Trp11]physalaemin-(1-11) (GR82334), a tachykinin NK1 receptor antagonist, and its effects on slow depolarizing responses of lumbar ventral roots evoked by primary afferent stimulation were examined in isolated spinal cord preparations of neonatal rats. GR82334 (1-3 microM) caused dose-dependent rightward shifts of the concentration-response curves for substance P, substance P methyl ester, delta-aminovaleryl [Pro9,N-Me-Leu10]substance P-(7-11) (GR73632) and neurokinin A in normal artificial cerebrospinal fluid and those for substance P methyl ester, GR73632 and neurokinin A in the presence of tetrodotoxin. GR82334 (10 microM) did not evoke gamma-aminobutyric acid (GABA) release from spinal cords of neonatal rats, whereas [D-Pro9,[spiro-gamma-lactam] Leu10,Trp11]substance P (GR71251), another tachykinin NK1 receptor antagonist, induced a significant increase in GABA release. GR82334 (1-3 microM) markedly depressed the slow depolarizing response of ventral roots, referred to as slow ventral root potential, evoked by the stimulation of the contralateral dorsal root or the ipsilateral saphenous nerve. In contrast, cyclo[Gln,Trp,Phe,Gly,Leu,Met] (L-659,877, 1 microM), a selective tachykinin NK2 receptor antagonist, did not depress the saphenous nerve-evoked slow ventral root potential and did not antagonize the action of neurokinin A to induce ventral root depolarization. The present results provide further evidence for the involvement of substance P, neurokinin A and tachykinin NK1 receptors in the primary afferent-evoked slow ventral root potentials.

Amino Acid Sequence↗

PubMed1995

Subtypes of tachykinin receptors on tonic and phasic neurones in coeliac ganglion of the guinea-pig.

1. Intracellular recording techniques were used to investigate the characteristics of tachykinin receptors and their subtypes in tonic and phasic neurones, which constituted two major neuronal populations in the coeliac ganglion of the guinea-pig. 2. In 95% of phasic neurones a long-lasting after-hyperpolarization (LAH), 5-8 s in duration and 10-20 mV in amplitude, was observed following action potentials evoked by passing a train of depolarizing current pulses into the neurones. In contrast, LAH was observed in only 4% of tonic neurones. 3. In most tonic neurones, substance P (SP), neurokinin A (NKA) and senktide induced depolarizations, whereas in phasic neurones they usually inhibited LAH but rarely induced depolarization. 4. Tonic and phasic neurones were further classified into three groups based on their responses (depolarization for tonic neurones and LAH inhibition for phasic neurones) to these tachykinin receptor agonists: (1) neurones responsive to SP, NKA and senktide (71-78%); (2) those responsive to senktide but not to SP and NKA (12-23%) and (3) those not responsive to any of the three agonists (7-11%). 5. GR71251 (5 microM), an NK1-selective tachykinin receptor antagonist, depressed the depolarization in tonic neurones and the LAH inhibition in phasic neurones induced by SP and NKA, but not those induced by senktide. 6. Selective NK2 receptor agonists, [Nle10]NKA4-10, [beta-Ala8]NKA4-10 and GR64349, were without effect in both tonic and phasic neurones. Furthermore, an NK2 receptor antagonist, L659,877, did not inhibit the depolarization induced by NKA, SP or senktide in tonic neurones. 7. It is suggested that NK1 and NK3 receptors are present on a large proportion of coeliac ganglion neurones. In tonic neurones both subtypes of tachykinin receptors are coupled to membrane depolarization,whereas in phasic neurones activation of these receptors leads to inhibition of LAH. The present study also suggests that NKA evokes the depolarization in tonic neurones and the LAH inhibition in phasic neurones via NK1, but not NK2 receptors.

Animals↗

PubMed1995

Use of NK1 receptor antagonists in the exploration of physiological functions of substance P and neurokinin A.

Tachykinin NK1 receptor antagonists were used to explore the physiological functions of substance P (SP) and neurokinin A (NKA). Pharmacological profiles of three NK1 receptor antagonists, GR71251, GR82334, and RP 67580, were examined in the isolated spinal cord preparation of the neonatal rat. These tachykinin receptor antagonists exhibited considerable specificities and antagonized the actions of both SP and NKA to induce the depolarization of ventral roots. Electrical stimulation of the saphenous nerve with C-fiber strength evoked a depolarization lasting about 30 s of the ipsilateral L3 ventral root. This response, which is referred to as saphenous-nerve-evoked slow ventral root potential (VRP), was depressed by these NK1 receptor antagonists. In contrast, the saphenous-nerve-evoked slow VRP was potentiated by application of a mixture of peptidase inhibitors, including thiorphan, actinonin, and captopril in the presence of naloxone, but not after further addition of GR71251. Likewise, in the isolated coeliac ganglion of the guinea pig, electrical stimulation of the mesenteric nerves evoked in some ganglionic cells slow excitatory postsynaptic potentials (EPSPs), which were depressed by GR71251 and potentiated by peptidase inhibitors. These results further support the notion that SP and NKA serve as neurotransmitters producing slow EPSPs in the neonatal rat spinal cord and guinea pig prevertebral ganglia.

Animals↗

PubMed1994

Review of pneumatic reduction of intussusception: evolution not revolution.

Pneumatic insufflation of the colon for reduction of pediatric intussusception has recently been recognized in the United States as an alternative method for the more traditional hydrostatic reduction with contrast material. The experience with pneumatic reduction in China is extensive; more than 14,000 cases have been reported in the English language literature. In this review, the general technique used in China is summarized, and the international experience with air insufflation is included in a comparison of hydrostatic and pneumatic reduction techniques.

Humans↗

PubMed1994

Effects of RP 67580, a tachykinin NK1 receptor antagonist, on a primary afferent-evoked response of ventral roots in the neonatal rat spinal cord.

1. The pharmacological characteristics of RP 67580, a non-peptide tachykinin NK1 receptor antagonist, and its effects on a reflex response evoked by stimulation of primary afferent fibres, were examined in isolated neonatal spinal cord preparations of the rat. Potentials were recorded extracellularly from a lumbar ventral root and drugs were bath-applied in normal artificial cerebrospinal fluid (CSF) or in the presence of tetrodotoxin (TTX). 2. In normal artificial CSF, RP 67580 (0.1-0.3 microM) caused rightward shifts of the concentration-response curves for substance P (SP), neurokinin A (NKA) and substance P methyl ester (SPOMe), an NK1-selective agonist, with pA2 values of 7.25, 7.47 and 7.49, respectively. 3. In the presence of TTX (0.3 microM), RP 67580 also caused rightward shifts of the concentration-response curves for SPOMe and NKA. The pA2 value of RP 67580 against SPOMe (6.75) was significantly lower than that against NKA (7.22). RP 67580 (0.3-1 microM) did not cause a clear parallel shift of the concentration-response curves for SP, and it depressed the depolarizations induced by low concentrations of SP, but slightly potentiated those induced by high concentrations of SP. 4. RP 67580 (1 microM) did not depress the depolarizing responses to bombesin, L--glutamate, gamma-aminobutyric acid (GABA), thyrotropin-releasing hormone and muscarine. RP 67580 (1 microM), however, depressed the response to acetylcholine in the presence of atropine and the response to nicotine. RP 68651 (1 microM), the enantiomer of RP 67580 devoid of activity at tachykinin NK1 receptors, also depressed the response to acetylcholine in the presence of atropine. 5. RP 67580 (1 gAM) did not induce GABA release from the rat spinal cord.6. In the neonatal gerbil spinal cord, the antagonist effects of RP 67580 (0.3-1 JAM) against SPOMe were much less potent than in the neonatal rat spinal cord.7. In the rat spinal cord-saphenous nerve preparation, electrical stimulation of the saphenous nerve atC-fibre strength evoked a prolonged depolarization of the ipsilateral L3 ventral root (slow VRP).RP 67580 (0.1-1 JM) depressed the saphenous nerve-evoked slow VRP. In contrast, RP 68651 (0.3 JAM)had no effect on the slow VRP.8. The results of the present study indicate that RP67580 acts as a high affinity NK, receptor antagonist in the neonatal rat spinal cord, although it also possesses an antinicotinic action. This study further suggests the existence of a subpopulation of tachykinin NK, receptors that are activated by NKA and SPOMe, as well as by low concentrations of SP, and are sensitive to the antagonist action of RP 67580 in the neonatal rat spinal cord. This study also provides further evidence for the involvement of SP and NKA in the slow VRP evoked by C-fibre stimulation in the neonatal rat spinal cord.

Animals↗

PubMed1994

[Pharmacokinetics and pharmacodynamics of slow release tablet of diltiazem in hypertensive patients with various renal functions].

Twenty hypertensive patients were equally divided into 2 groups: A) with normal renal function (NRF) and B) with impaired renal function (IRF) according to creatinine clearance, blood urea nitrogen and creatinine levels. The pharmacokinetic and pharmacodynamic effects of diltiazem (Dil, 90 mg, bid x 7 d, p.o.) were studied. The pharmacokinetic parameters in IRF patients (Ka 0.7 +/- 0.2 h-1, T 1/2e 3.7 +/- 0.7 h, Cmax1 45 +/- 4 ng.ml-1, Tmax1 3.1 +/- 0.4 h) did not differ from those in NRF patients (0.7 +/- 0.5 h-1, 4.1 +/- 1.3 h, 41 +/- 5 ng.ml-1 and 3.4 +/- 0.4 h, P > 0.05). Antihypertensive efficacy of Dil in patients with IRF was similar to that in those with NRF, and the hypotensive effect lasted over 24 h. The plasma Dil concentrations were strongly correlated with a decrease in BP in both groups. It was concluded that IRF did not affect the disposition of slow release Dil tablet under a steady state. No dosage adjustment of Dil is necessary in hypertensive patients with IRF.

Adult↗

PubMed1993

Electrophysiological identification of horizontal synaptic connections in rat visual cortex in vitro.

The presence of intrinsic horizontal synaptic connections in rat visual cortex was explored electrophysiologically using in vitro slice preparations. Intracellular recordings were made from pyramidal neurons located in the superficial and deep layers. Electrical stimulation at the gray matter in the same or different layers but 0.8-2.7 mm apart from the recording site evoked compound synaptic potentials composed of excitatory and inhibitory postsynaptic potentials of fast and slow time courses. Glutamate blockers, DNQX (5 microM) and kynurenate (2 mM) reduced the excitatory postsynaptic potential (EPSP), and GABAB receptor antagonist, phaclofen (0.5 mM), abolished the inhibitory postsynaptic potential of the slow time course. EPSP of the fast time course followed 20 Hz repetitive stimulation in the medium of high Ca2+ (6.0 mM) and Mg2+ (4.0 mM) concentration, suggesting that this fast EPSP was monosynaptic. Conduction velocity of the fibers mediating the monosynaptic EPSP was estimated to be 0.15-0.55 m/s. These results provide physiological evidence for the horizontal synaptic connections in the rat visual cortex, which had been previously suggested by morphology.

Animals↗