Biomedical subjects

D G Chen

Publications and source records attributed to D G Chen.

At least 37 records · Page 2Linked to original sources

PubMed1990

[Modulation of norepinephrine release in sympathetic nerve endings in renal hypertensive dogs].

Experimental renal hypertensive and normal dogs with femoral arteries constantly perfused were studied. Cocaine was used to block the presynaptic norepinephrine (NE) reuptake and tyramine to initiate the release of NE in sympathetic nerve endings. NE spillover and infusion pressure were measured under basic conditions and during intraarterial infusion of cocaine, tyramine and in combination with alpha 1 and alpha 2 adrenoceptor antagonists. The extent of NE spillover increase induced by infusion of tyramine, the increased infusion pressure by cocaine and tyramine, and the reduced infusion pressure by prazosin were all greater in hypertensive dogs than those in normal dogs, but adrenoceptor antagonist idazoxan further increased tyramine-induced NE spillover in normal dogs only. It was suggested that reduced-regulation of presynaptic alpha 2 adrenoceptors to NE release and increased responsiveness of postsynaptic alpha 1 adrenoceptors to NE were present in hypertensive dogs.

Adrenergic alpha-Antagonists↗

PubMed1990

Nifedipine pharmacodynamics and pharmacokinetics in treatment of congestive heart failure.

In 22 of 27 cases of congestive heart failure (CHF) treated with nifedipine (NIF), significant improvements in resting hemodynamics were noticed. The higher the basal systemic vascular resistance (SVR) and pulmonary artery end diastolic pressure (PAEDP), the greater the magnitude of reduction was achieved (r = 0.84 and 0.77, P less than 0.01, respectively). Exercise hemodynamic investigation showed that NIF lowered SVR, PAEDP and pulmonary vascular resistance (PVR), with an increase in stroke volume (SV) at the serum concentration of 5-10 ng/ml. Maximum effect was observed at the concentration of 20 ng/ml. No further vasodilation was attainable with serum concentrations above 20 ng/ml. No remarkable deviation of NIF pharmacokinetic parameters from the normal ranges was found in CHF patients. The plasma norepinephrine level decreased markedly 2 and 7 hours after the use of NIF. It is concluded that oral NIF is beneficial to severe CHF patients with low cardiac output and high SVR.

Adolescent↗

PubMed1989

Alpha-adrenergic effects of dopamine and dobutamine on the coronary circulation.

After beta-adrenergic blockade, dopamine causes coronary vasoconstriction that is blocked by non-selective alpha-adrenergic antagonists. This study was carried out to determine the relative importance of alpha 1- and alpha 2-adrenoceptors in mediating coronary vasoconstriction in response to dopamine. Because dobutamine has been reported to cause alpha-adrenergic stimulation, the response to dobutamine was also examined. The circumflex coronary artery was cannulated and perfused at a constant blood flow rate in 14 dogs; coronary vasomotor responses were assessed from changes in perfusion pressure. Central effects were eliminated by vagotomy and stellate ganglionectomy; propranolol (1 mg/kg i.v.) was administered to block beta-adrenergic effects. The coronary responses to intracoronary bolus doses of dopamine and dobutamine were determined; the effects of selective alpha 1-blockade with prazosin (600 micrograms/kg i.v.) and selective alpha 2-blockade with idazoxan or rauwolscine (1-5 micrograms/kg per min intracoronary for 10 min) were examined. Dopamine produced dose-related coronary vasoconstriction; this response was not significantly altered by alpha 1-blockade with prazosin, but was abolished by the addition of alpha 2-adrenergic blockade with idazoxan or rauwolscine. Dobutamine did not produce coronary vasoconstriction at any dose tested. These data demonstrate that coronary vasoconstriction produced by dopamine is mediated through postjunctional alpha 2-adrenergic receptors.

Animals↗

PubMed1989

[Clonidine stimulates central nervous alpha 2 adrenoceptors not mediating Ca2+ channels].

Seven renal hypertensive (2 kidneys--2 clipped) and 8 normotensive conscious dogs were given icv clonidine. After the medication the mean arterial blood pressure (MAP) were lowered and the heart rate (HR) and plasma norepinephrine (NE) were decreased. The magnitude of the decrease of MAP was greater than normotensive dogs; while no differences of decrease of NE was found. Nicardipine (10 micrograms/kg) icv caused significant increases of MAP and HR in both hypertensive and normotensive groups. The decrease of MAP induced by clonidine was not changed by the pretreatment of nicardipine icv in both groups. It is thus concluded that clonidine stimulates central nervous alpha adrenoceptors not mediating Ca2+ channels.

Animals↗

PubMed1989

[Pharmacodynamics and pharmacokinetics of nifedipine in patients with congestive heart failure].

Twenty-seven cases of congestive heart failure (CHF) were treated with nifedipine (Nif) 20 mg po. Significant improvements in resting hemodynamics were found in 22 cases. The higher the basal systemic vascular resistance (SVR) and pulmonary artery end diastolic pressure (PAEDP) were, the greater the magnitudes of reduction found (r = 0.84 and 0.77, P less than 0.01, respectively). Exercise hemodynamic investigation showed that Nif led to a lowering of SVR, PAEDP and pulmonary vascular resistance (PVR), with increases in SV and concentration of 5-10 ng/ml, with a maximum being observed at the concentration of 20 ng/ml. No further vasodilation was found when the plasma concentration exceeded 20 ng/ml. No remarkable deviations from the normal ranges of Nif pharmacokinetics were found in CHF patients. The plasma norepinephrine level decreased markedly 2 and 7 h after Nif. Thus, it is concluded that oral Nif is beneficial in severe CHF patients having low cardiac output and high SVR.

Adolescent↗

PubMed1988

Postsynaptic alpha 1- and alpha 2-adrenergic mechanisms in coronary vasoconstriction.

This study examined the relative importance of postsynaptic alpha 1- and alpha 2-adrenoceptors in mediating coronary vasoconstriction in open chest dogs in which the left circumflex coronary artery was cannulated and perfused at a constant rate. The cervical vagus nerves and central connections of the stellate ganglia were transected, and beta-adrenergic blockade was produced with propranolol. Coronary vasoconstriction occurred in response to intraarterial administration of both the alpha 1-agonist phenylephrine and the alpha 2-agonist BHT 933. The response to phenylephrine was partially blocked with prazosin and nearly completely eliminated by yohimbine. The response to BHT 933 was resistant to prazosin, but almost completely blocked by yohimbine. Coronary vasoconstriction produced by norepinephrine was resistant to prazosin, but was blunted by alpha 2-adrenergic blockade with yohimbine or idazoxan. Prazosin produced some blunting of coronary vasoconstriction in response to small doses of epinephrine, while yohimbine markedly attenuated epinephrine-induced vasoconstriction at all doses used. Measurements of regional myocardial blood flow with radioactive microspheres demonstrated no transmural redistribution of perfusion during vasoconstriction produced by either alpha 1- or alpha 2 stimulation. Thus, although stimulation of both alpha 1- and alpha 2-adrenoceptors is capable of causing coronary vasoconstriction, vasoconstriction in response to norepinephrine and epinephrine is mediated principally by postsynaptic alpha 2-adrenoceptors.

Animals↗

PubMed1988

Postsynaptic adrenoceptor-mediated vasoconstriction in coronary and femoral vascular beds.

This study examined the response to intra-arterial norepinephrine and sympathetic nerve stimulation on perfusion pressure of cannulated dog femoral and left circumflex coronary arteries perfused at constant flow rates. Sympathetic nerve stimulation was delivered through the decentralized inferior cardiac nerve and the lumbar sympathetic chain; beta-adrenergic blockade was maintained with propranolol. In the coronary artery, the vasoconstrictor response to norepinephrine was blunted by alpha 1-adrenergic blockade with prazosin but was abolished by alpha 2-adrenergic blockade with rauwolscine, indicating postsynaptic alpha 2-adrenoceptor-mediated vasoconstriction. In the femoral artery, prazosin decreased norepinephrine-induced vasoconstriction by 20-40%; the subsequent addition of rauwolscine completely abolished vasoconstriction, indicating that both alpha 1- and alpha 2-adrenoceptors contributed to vasoconstriction. Sympathetic nerve stimulation produced frequency-dependent increases of perfusion pressure in both coronary and femoral vascular beds. Prazosin caused approximately 50% reduction in the vasoconstrictor response of the coronary vascular bed and approximately 30% reduction in the femoral bed. The addition of rauwolscine completely blocked the response to sympathetic nerve stimulation in coronary and femoral vascular beds. These studies demonstrate that postsynaptic alpha 2-adrenoceptor-mediated mechanisms participate in vasoconstriction in response to both exogenous norepinephrine and sympathetic nerve stimulation in the canine coronary and femoral vascular beds.

Adrenergic beta-Antagonists↗

PubMed1988

Effects of atrial natriuretic peptide in the canine coronary circulation.

Atriopeptin II has been reported to cause profound coronary vasoconstriction in the isolated perfused guinea pig heart and in the blood perfused canine heart. Consequently, this study was carried out to examine possible mechanisms by which vasomotor effects of human atrial natriuretic peptide (ANP) occur in the canine coronary circulation. Bolus dosages of ANP were administered into the left circumflex coronary artery of in situ dog hearts perfused at constant flow rate. ANP produced dose-related coronary vasodilation with a threshold dosage of 2 ng/kg; a dosage of 2 micrograms/kg caused a 27 +/- 4% decrease in coronary vascular resistance. Coronary vasodilation produced by ANP was not altered by beta-adrenergic blockade with propranolol (1 mg/kg i.v.). In addition, neither adenosine receptor blockade with 8-phenyltheophylline (5 mg/kg i.v.) nor cyclooxygenase inhibition with indomethacin (5 mg/kg i.v.) significantly altered the response to intra-arterial ANP. These data demonstrate that in the in vitro blood perfused canine heart, ANP administered intra-arterially results in coronary vasodilation that does not utilize adenosine-dependent or prostaglandin-dependent mechanisms.

Animals↗

PubMed1988