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R R He

Publications and source records attributed to R R He.

At least 73 records · Page 4Linked to original sources
PubMed1996

[Effects of microinjection of L-NNA and SNP into ventrolateral medulla on blood pressure, heart rate and renal sympathetic nerve activity in rats].

The effects of microinjection of a NO synthase inhibitor--N-nitro-L-arginine (L-NNA) and NO donor-sodium nitroprusside (SNP) into ventrolateral medulla on blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were examined in anesthetized rats to define the role of L-arginine: NO pathway in the central regulation of BP and to explore the underlying mechanism. The results obtained were as follows: (1) Following microinjection of L-NNA into rostral ventrolateral medulla (RVLM), both of MAP and RSNA were increased. The effects lasted for more than 30 min and could be reversed by prior intravenous injection of L-arginine. (2) In response to microinjection of SNP into RVLM, MAP and RSNA were decreased, while HR showed no significant change. (3) During microinjection of L-NNA into caudal ventrolateral medulla (CVLM), MAP, HR and RSNA were decreased. (4) Upon injection of SNP into CVLM, MAP and RSNA were increased, but HR showed no significant change. The above-mentioned results indicate that the L-arginine: NO pathway may exhibit a modulatory action on the activity of ventrolateral medulla neurons.

Animals↗
PubMed1995

Effects of N6-cyclopentyladenosine on afterdepolarizations and triggered activity induced by isoproterenol in guinea pig papillary muscle.

AIM: To investigate the effects of N6-cyclopentyladenosine (CPA, selective adenosine A1 receptor agonist) on afterdepolarizations and triggered activity induced by isoproterenol (Iso) in guinea pig papillary muscle. METHODS: The stable and reproducible early afterdepolarization (EAD) and delayed afterdepolarization (DAD) of guinea pig papillary muscle were induced by Iso 50 nmol.L-1. The parameters of EAD and DAD were recorded using intracellular microelectrodes. RESULTS: CPA markedly attenuated the development of EAD, DAD, and triggered activity (TA) induced by Iso in guinea pig papillary muscle. The inhibitory effects of CPA on Iso-induced EAD and DAD were antagonized by 8-phenyltheophylline (8-PT) and glibenclamide (Gli). CONCLUSION: ATP-sensitive K+ channels were involved in Iso-induced EAD and DAD, and in the inhibitory effects of CPA on EAD and DAD.

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PubMed1995

Endogenous adenosine and ATP-sensitive potassium channel modulate anoxia-induced electrophysiological changes of pacemaker cells in sinoatrial node of guinea pigs.

AIM: To investigate the electrophysiological effects of adenosine deaminase (ADase, an enzyme converting adenosine to inosine and ammonia), 8-phenyltheophylline (8-PT, a nonselective antagonist of adenosine receptors) and glibenclamide (Gli, a potent blocker of ATP-sensitive K+ channels) on anoxic pacemaker cells of SA node. METHODS: Anoxia of pacemaker cells in SA node of guinea-pig was induced by perfused for 20 min with a modified K-H solution gassed with 100% N2 deprived of glucose. Parameters of action potentials including maximal diastolic potential (MDP), amplitude of action potential (APA), duration of 90% repolarization (APD90), maximal rate of depolarization (Vmax), rate of pacemaker firing (RPF), and velocity of diastolic (phase 4) depolarization (VDD) were recorded using intracellular microelectrodes. RESULTS: Anoxia increased MDP, APA, and Vmax and decreased VDD, RPF in a time-dependent manner. ADase 10 U.L-1, 8-PT 0.1 mumol.L-1 and Gli 10 mumol.L-1 significantly attenuated the electrophysiological changes of pacemaker cells in sincatrial node induced by anoxia. CONCLUSION: Endogenous adenosine and ATP-sensitive K+ channels may play an important role in the generation of anoxic bradycardia in guinea pigs.

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PubMed1995

Protective effect of preconditioning on ischemic heart and characterization of adenosine receptors in ischemic rabbit hearts.

AIM: To assess the role of adenosine receptors in the cardioprotective effect of preconditioning and the characterization of adenosine receptors in heart. METHODS: In 18 anesthetized rabbits, myocardial ischemia was induced by occlusion of left descending coronary artery. ST segment elevation in epicardial electrogram was used as a criterion of acute ischemic injury. Myocardial adenosine receptors were measured using [3H] adenosine ligand. RESULTS: After 60-min ischemia, epicardial ST segment elevation was higher in ischemia group (13.9 +/- 0.6 mV) than in the ischemic preconditioning group (3.1 +/- 0.5 mV). In membranes of the ventricular myocytes prepared from ischemic-preconditioning group, the density of adenosine receptors was higher than that of ischemia and sham ischemia groups (Bmax being 602 +/- 40, 348 +/- 28, and 335 +/- 30 pmol/g protein, respectively). Affinity of the receptors for the [3H] adenosine was not different in the 3 groups (Kd being 181 +/- 18, 169 +/- 21, and 196 +/- 24 nmol . L-1, respectively). CONCLUSION: Activation of adenosine receptors along with an increase in adenosine receptor density during ischemic-preconditioning provides the basis for adenosine to exert its protective effect on the ischemic heart.

Animals↗
PubMed1994

Effect of dipfluzine on platelet aggregation and thrombus formation.

Dipfluzine (Dip) is a novel diphenylpiperazine calcium channel blocker first synthesized in China. Effects of Dip on experimental thrombosis and platelet aggregation were studied in vitro and in vivo compared with cinnarizine (Cin). Dip 1 and 2 mg.kg-1 i.v. and incubated in 1-100 mumol.L-1 in vitro inhibited dose- or concentration-dependent rabbit platelet aggregation induced by ADP and by arachidonic acid (AA), respectively. Dip 2.5-10 mg.kg-1 i.v. and 50-100 mg.kg-1 ip inhibited the thrombosis in rats. Dip 10 mg.kg-1 i.v. and 200 mumol.L-1 depressed the in vitro thrombosis. These results suggest that attenuation of disturbed platelet-vessel wall reaction associated with platelet activation and vasoconstriction may be a main factor involved in the antithrombotic action of Dip, and that the effects of Dip were more potent than those of Cin.

Animals↗
PubMed1994

Protective effect of dipfluzine on experimental brain edema in rats.

The effects of dipfluzine (1-diphenylmethyl-4-(3-(4-fluorobenzoyl))-piperazine, Dip), a new calcium antagonist developed in China, on experimental brain edema in female Wistar rats with bilateral carotid artery ligation were compared with those of cinnarizine (Cin). Dip 25-100 mg.kg-1 i.p. protected the rats against the characteristic signs of global cerebral ischemia that correlate well with the development of brain edema. Its effects were more potent than those of Cin; and the effects of both drugs were more potent by both pretreatment and posttreatment than those by posttreatment alone. Dip 50 mg.kg-1 i.p. attenuated the reduction in cerebral blood flow (CBF) and the infarct size after occlusion, but did not alter CBF before ischemia. These findings suggested that Dip may be potentially useful to treat ischemic brain edema in part by preserving CBF in the ischemic zone.

Animals↗
PubMed1993

Electrophysiological effects of N6-cyclopentyl-adenosine and [-]-N6-[phenylisopropyl]-adenosine on pacemaker cells in sinoatrial node of guinea pigs.

The electrophysiological effects of N6-cyclopentyladenosine (CPA) and [-]-N6-[phenylisopropyl]adenosine (R-PIA) (both are selective adenosine A1 receptor agonists) on pacemaker cells in sinoatrial (SA) node of guinea pigs were investigated using intracellular microelectrodes. CPA and R-PIA increased the amplitude of action potential, amplitude of the maximal diastolic potential and maximal rate of depolarization (phase 0), but decreased the velocity of diastolic (phase 4) depolarization, the rate of pacemaker firing, and the duration of 90% repolarization in pacemaker cells of guinea pigs. 8-Phenyltheophylline (a nonselective antagonist of adenosine receptors) and glibenclamide (a potent blocker of ATP-sensitive K+ channels) inhibited the electrophysiological responses of pacemaker cells to CPA. These results suggest that the electrophysiological changes induced by CPA are adenosine receptor-dependent and mainly mediated by activation of ATP-sensitive K+ channels coupled to adenosine receptors.

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PubMed1993

Selective vasodilatory effect of dipfluzine on vertebral artery in anesthetized dogs.

Dipfluzine (Dip) is a novel calcium antagonist first developed by Department of Chemistry, Beijing University. The effects of Dip on hemodynamics and vascular resistance in vertebral (VVR), coronary (CVR), and femoral (FVR) arteries were compared with those of cinnarizine (Cin) in anesthetized dogs. Dip iv decreased dose-dependently VVR at 0.1, 0.3, 1, and 3 mg.kg-1, CVR at 3 mg.kg-1, and FVR at 1 and 3 mg.kg-1. The fall of VVR by Dip iv was more remarkable than that by Cin at the matching doses. The systolic, diastolic, and mean blood pressure and total peripheral resistance were temporarily reduced equally by both of them at 1 mg.kg-1 iv, while Dip and Cin produced no obvious changes in heart rate, cardiac index, stroke index, LVP, and dP/dtmax at all doses. These results suggested that Dip possessed a high selectivity at different sites of the vasculature and was a more potent selective cerebral vasodilator than Cin.

Animals↗
PubMed1992

[Cardiovascular responses to microinjection of atrial natriuretic peptide into ventrolateral medulla of rat].

Application of atrial natriuretic peptides (alpha-ANP and AP III) to glutamate sensitive area of ventrolateral medulla produced a dose-dependent decrease in MAP and HR in anesthetized rats. Lower dosage of AP III induced hypotension without bradycardia, whereas the higher dosage of AP III decreased both blood pressure and heart rate. The results suggested that ANP may inhibit the medullary sympathetic center.

Animals↗
PubMed1992

Effects of m-nisoldipine on transmembrane currents of guinea pig papillary muscles.

Effects of m-Nis on the transmembrane currents were studied using single sucrose gap voltage clamp technique. The amplitude of slow inward current (I(si)) was 10.6 +/- 4.1 microA. Maximal inward current was induced at a membrane potential range between -20 to -25 mV. The amplitude of I(si) were significantly decreased by m-Nis (0.2 mumol.L-1) with a reduction of 47.3%. The transient inward current (I(ti)) induced by ouabain was also greatly depressed or prevented by m-Nis, resulting in the inhibition of DAD.

Animals↗
PubMed1992

Rate- and voltage-dependent effects of m-nisoldipine on action potential of partially depolarized guinea pig papillary muscle.

The rate- and voltage-dependent effects of m-Nis were studied using standard microelectrode technique and real-time microcomputer analyzing system. The onset rate for rate-dependent inhibition (RDI) on action potentials of partially depolarized papillary muscle of guinea pig was accelerated as the concentration of m-Nis was increased from 0.5 to 2 mumol.L-1 or the driving frequency decreased from 0.8 to 0.2 Hz. The steady-state values of Vmax and APA were markedly decreased by elevating the concentration of m-Nis or increasing the driving frequency. The recovery time constants of Vmax, APA, and latency period from RDI were all increased by m-Nis (1 mumol.L-1). The inhibitory effects of m-Nis on Vmax and APA were more pronounced as the resting membrane potential was decreased by elevating K+ concentration in the perfusate.

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PubMed1992

Effects of m-nisoldipine and nisoldipine on electric activity of human atrial tissue.

Using intracellular microelectrode technique and microcomputer analyzing system, the effects of m-nisoldipine (m-Nis) and nisoldipine (Nis) on spontaneous electric activity of human atrial tissue were studied. APA and Vmax were remarkably decreased by m-Nis (0.25 and 1.25 mumol.L-1) and Nis (0.25 mumol.L-1). RPF was also greatly decreased as a result of inhibition in VDD. The inhibitory effects of m-Nis on transmembrane potentials were less than those of Nis at equal concentration (0.25 mumol.L-1). Neither MDP nor APD90 was affected by m-Nis and Nis.

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PubMed1992

Effects of m-nisoldipine on delayed afterdepolarization of canine Purkinje fibers.

Effects of m-nisoldipine (m-Nis) on delayed after depolarization (DAD) and triggered activity (TA) were studied using standard microelectrode technique. The development of DAD and TA were markedly inhibited by pre-treatment with m-Nis (1-4 mumol.L-1) as well as m-Nis treatment after DAD and TA had been elicited. The amplitude of DAD was reduced from 15.3 +/- 2.7 to 2.3 +/- 2.0 mV, and the duration from 980 +/- 45 to 130 +/- 27 ms. The occurrence of TA was also reduced or prevented by m-Nis. These effects of m-Nis might be attributed to its blocking effects on voltage-dependent calcium channel and the resultant alleviation of intracellular calcium overload.

Animals↗
PubMed1991

Electrophysiological effects of m-nisoldipine and nisoldipine on pacemaker cells in sinoatrial node of rabbits.

UNLABELLED: The effects of m-nisoldipine (m-Nis) and nisoldipine (Nis) on the electrical activity of pacemaker cells in sinoatrial node (SAN) of rabbit were studied using intracellular microelectrodes. THE RESULTS: APA and Vmax in SAN pacemaker cells were markedly reduced by m-Nis and Nis. The inhibitory effects of Nis on APA and Vmax were greater than those of the m-Nis. Elevation of Ca2+ concentration in the perfusate partially antagonized the inhibitory actions of m-Nis and Nis. VDD of SAN pacemaker cells were reduced by m-Nis. The change of RPF was not consistent with that of VDD. CSRT was prolonged by m-Nis and Nis in a dose-dependent manner. The inhibitory effects of Nis on SAN pacemaker cells were greater than that of the m-Nis. Both MDP and APD50 were not affected by m-Nis and Nis.

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