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R Parent

Publications and source records attributed to R Parent.

At least 37 records · Page 2Linked to original sources

Nitric oxide formation contributes to beta-adrenergic dilation of resistance coronary vessels in conscious dogs.

The contribution of the L-arginine/nitric oxide pathway to beta-adrenergic dilation of resistance coronary vessels was examined in conscious dogs instrumented for measuring coronary blood flow (CBF), left ventricular (LV) wall thickening, and LV and aortic pressures and for intracoronary injections of acetylcholine (0.003 micrograms/kg), nitroglycerin (0.175 micrograms/kg), and graded doses of isoproterenol (0.0005 to 0.004 micrograms/kg). Peak increases in CBF with intracoronary isoproterenol (0.001 micrograms/kg) averaged 105 +/- 10% from baseline. With acetylcholine, CBF increased by 158 +/- 11%, and with nitroglycerin, CBF increased by 139 +/- 10%. After the administration of intracoronary N omega-nitro-L-arginine methyl ester (L-NAME, 10 micrograms/kg per minute for 12 minutes) to block nitric oxide synthesis from L-arginine, baseline CBF was not altered, and CBF increased by 49 +/- 7% with isoproterenol and by 94 +/- 6% with acetylcholine; both values were smaller (P < .01) than those before the arginine analogue. With nitroglycerin, CBF was increased by 145 +/- 11%, not significantly different from the value before L-NAME. Intracoronary L-arginine (1.0 mg/kg per minute for 12 minutes), the precursor of nitric oxide synthesis, partially reversed the inhibition of L-NAME on CBF responses to acetylcholine and isoproterenol. After beta 1-adrenergic blockade, CBF responses to isoproterenol and acetylcholine were also reduced (P < .05) by the arginine analogue. When increases in CBF were prevented, peak changes in coronary vascular conductance with intracoronary bolus doses of acetylcholine and isoproterenol were attenuated (P < .01) by L-NAME. Thus, nitric oxide formation is an important intermediate in beta-adrenergic dilation of resistance coronary vessels in conscious dogs.

Acetylcholine↗

The chloramphenicol acetyltransferase gene of Tn2424: a new breed of cat.

We have sequenced the gene coding for the chloramphenicol acetyltransferase of Tn2424 of plasmid NR79. This gene codes for a protein of 23,500 Da, and the derived protein sequence is similar to those of the chromosomal chloramphenicol acetyltransferases of Agrobacterium tumefaciens and Pseudomonas aeruginosa and of unidentified open reading frames, which may encode chloramphenicol acetyltransferases, adjacent to the ermG macrolide-lincosamide-streptogramin resistance gene of Bacillus sphaericus and the vgb virginiamycin resistance gene of Staphylococcus aureus. Weaker similarity to the LacA (thiogalactoside acetyltransferase) and CysE (serine acetyltransferase) proteins of Escherichia coli and the NodL protein of Rhizobium leguminosarum is also observed. There is no significant similarity to any other chloramphenicol acetyltransferase genes, such as that of Tn9. The Tn2424 cat gene is part of a 4.5-kb region which also contains the aacA1a aminoglycoside-6'-N-acetyltransferase gene; Tn2424 is similar to Tn21 except for the presence of this region. Sequences flanking the cat gene are typical of those flanking other genes inserted into pVS1-derived "integrons" by a site-specific recombinational mechanism.

Agrobacterium tumefaciens↗

Contribution of nitric oxide to dilation of resistance coronary vessels in conscious dogs.

Endothelium-dependent relaxation of conductance coronary vessels involves nitric oxide formation from L-arginine. The present study examines whether a similar mechanism intervenes in the vasomotor control of resistance coronary vessels. In conscious dogs, the excess of coronary blood flow (CBF) created by intracoronary acetylcholine (3.0 ng/kg) averaged 7.2 +/- 1.1 ml. Intracoronary adenosine (100 ng/kg) increased CBF by 12.4 +/- 1.4 ml. Intracoronary nitroglycerin (175 ng/kg) increased CBF by 7.4 +/- 1.2 ml. CBF repayment-to-debt ratio after a 15-s coronary arterial occlusion averaged 2.8 +/- 0.2. After an intracoronary N omega-nitro-L-arginine dose (10 micrograms.kg-1.min-1 x 12 min) was given to inhibit nitric oxide formation, baseline CBF was not altered. CBF increases with acetylcholine averaged 2.4 +/- 0.5 and 6.4 +/- 0.7 ml with adenosine, both less (P less than 0.01) than responses before the arginine analogue. CBF increases with nitroglycerin averaged 7.2 +/- 1.1 ml, similar to control responses. CBF repayment-to-debt ratio during reactive hyperemic responses fell (P less than 0.01) to 1.7 +/- 0.1. L-Arginine (1.0 mg.kg-1.min-1 x 12 min) partially reversed the inhibitory effect of the arginine analogue on CBF responses to acetylcholine. Thus nitric oxide formed in resistance coronary vessels is a major mediator of coronary vasodilation to acetylcholine, adenosine and transient ischemia.

Acetylcholine↗

Time course of left ventricular function after cardiac denervation in conscious dogs.

The time course of left ventricular (LV) function was compared in normal (N) and cardiac-denervated (CD) dogs over an 8-week period after instrumentation with solid-state LV pressure gauges and three pairs of ultrasonic crystals to measure LV long and short axes and wall thickness. Baseline LV systolic, end-systolic, and end-diastolic pressures did not differ in N and CD dogs. Heart rate was higher (p less than 0.01) and LV dP/dt was lower (p less than 0.05) in CD dogs. LV short-axis shortening, shortening fraction, velocity of circumferential fiber shortening, and ejection fraction were consistently lower (p less than 0.01) in CD dogs. With angiotensin II to increase LV afterload, relations of LV short-axis shortening, shortening fraction, velocity of circumferential fiber shortening, and ejection fraction to average LV systolic wall stress were shifted downward (p less than 0.01) in CD dogs at 2, 4, and 8 weeks. Relations of LV short-axis shortening to LV end-diastolic wall stress also differed (p less than 0.01) in N and CD dogs. Ganglionic blockade abolished differences in LV function between N and CD dogs during elevated LV systolic wall stress with angiotensin II. Thus, in conscious dogs, cardiac denervation results in a sustained reduction of LV function over a wide range of ventricular loading conditions.

Animals↗

Disparate effects of substance P on systemic and coronary beds in conscious dogs.

BACKGROUND: Previous studies in anesthetized animals indicated that substance P is a coronary and peripheral vasodilator. However, coronary vasodilation was only transient perhaps because of tachyphylaxis. In the present study, the steady-state effects of intravenous substance P on systemic and coronary beds were investigated in conscious, instrumented dogs. METHODS AND RESULTS: With intact autonomic reflexes, 5 ng/kg/min i.v. substance P resulted in increases (p less than 0.01) in cardiac output by 22 +/- 5%, in decreases (p less than 0.01) in mean arterial pressure by 9 +/- 2%, and in total peripheral resistance by 23 +/- 4% 7-9 minutes after the beginning of substance P infusion. Heart rate increased (p less than 0.01) by 35 +/- 7% and left ventricular dP/dt (p less than 0.05) by 13 +/- 4%. In this situation, coronary blood flow decreased (p less than 0.01) by 19 +/- 4% and coronary vascular resistance increased (p less than 0.05) by 13 +/- 5%. Myocardial oxygen delivery was reduced (p less than 0.05) by 13 +/- 5% and the arteriovenous oxygen difference widened (p less than 0.01). After ganglionic blockade, increases in cardiac output, heart rate, and left ventricular dP/dt with substance P administration were abolished, but total peripheral resistance and mean arterial pressure decreased (p less than 0.01) by 12 +/- 3% respectively. Under these conditions, coronary blood flow decreased (p less than 0.01) by 37 +/- 5% and coronary vascular resistance increased (p less than 0.01) by 47 +/- 8%, which were more (p less than 0.01) than control responses. In this situation, myocardial oxygen delivery was reduced (p less than 0.01) by 37 +/- 4% and the arteriovenous oxygen difference widened (p less than 0.01). Intracoronary infusion of substance P (0.4 ng/kg/min) resulted in significant and sustained decreases in coronary blood flow, which were similar before and after ganglionic blockade. CONCLUSIONS: Thus, in conscious dogs, systemic vasodilation is the prevailing effect of substance P, but paradoxically, this peptide simultaneously elicits coronary vasoconstriction.

Animals↗

Opposite effects of substance P on conductance and resistance coronary vessels in conscious dogs.

The effects of substance P (SP) on epicardial coronary diameter (CD) and coronary blood flow (CBF) were examined in conscious dogs. SP (5.0 ng/kg) induced transient increases (P less than 0.01) in CBF by 139 +/- 19% from 26.5 +/- 1.5 ml/min followed by sustained decreases (P less than 0.01) averaging 22 +/- 2% when mean arterial pressure had returned to preinjection base line. CD increased (P less than 0.01) by 6.7 +/- 1.4% from 3.47 +/- 0.35 mm. After ganglionic blockade with hexamethonium (35 mg/kg), the transient increases (P less than 0.01) in CBF (95 +/- 10% from 28.6 +/- 1.9 ml/min) were smaller (P less than 0.05), but the late decreases (P less than 0.01) in CBF averaged 23 +/- 3%, similar to responses before ganglionic blockade. Increases (P less than 0.01) in CD (4.1 +/- 0.7% from 3.49 +/- 0.35 mm) were smaller (P less than 0.05) than before ganglionic blockade. During steady-state effects of SP (5.0 ng.kg-1.min-1) under ganglionic blockade, CBF fell (P less than 0.01) by 39 +/- 3% from 26.4 +/- 2.3 ml/min, but CD increased (P less than 0.01) by 6.6 +/- 1.6% from 3.45 +/- 0.40 mm. Additional experiments indicated that coronary sinus blood oxygen content fell and myocardial arteriovenous O2 difference increased during steady-state effects of SP under ganglionic blockade. Cyclooxygenase inhibition did not alter coronary responses to SP. Endothelial denudation abolished increases in CD after SP. Therefore, under steady-state conditions and in the absence of autonomic reflexes, SP is a potent endothelium-dependent dilator of conductance coronary vessels but paradoxically a constrictor of resistance coronary vessels.

Animals↗

Hemodynamic and endocrine effects of acute and chronic administration of nifedipine.

Although it is well known that calcium channel blockers can influence contraction of vascular smooth muscle, there is less knowledge on its effect on excitation contraction coupling in the endocrine glands and more specifically on insulin and glucagon release. In this study, nifedipine was administered in doses of 40 to 80 mg/day to 14 patients with essential hypertension, and its hemodynamic effects were evaluated by non-invasive methods, and its effect on glucose metabolism by an arginine infusion test. Nifedipine produced a significant reduction in systolic and diastolic blood pressure, both after the first dose (30/12 mm Hg) and after 8 weeks of administration (19/12 mm Hg). There were no significant changes in cardiac output (5.1 to 4.9 L/min), muscle (2.4 to 3.2 mL/sec/min) or cutaneous basal flow (9.8 to 8.6 mL/100 mL) as measured non-invasively by echocardiogram and by plethysmography. Insulin and glucagon release were evaluated by the arginine infusion test. Nifedipine produced a tendency toward an increase in glucagon release and a reduction in insulin release although these changes did not reach statistical significance. In this group of patients, nifedipine produced a significant reduction in systolic and diastolic pressure, but no significant changes in insulin or glucagon plasma levels.

Adult↗

Hemodynamic and endocrine effects of acute and chronic administration of nifedipine.

Although it is well known that calcium channel blockers can influence contraction of vascular smooth muscle, there is less knowledge on its effect on excitation contraction coupling in the endocrine glands and more specifically on insulin and glucagon release. In this study, nifedipine was administered in doses of 40 to 80 mg/day to 14 patients with essential hypertension, and its hemodynamic effects were evaluated by non-invasive methods, and its effect on glucose metabolism by an arginine infusion test. Nifedipine produced a significant reduction in systolic and diastolic blood pressure, both after the first dose (30/12 mm Hg) and after 8 weeks of administration (19/12 mm Hg). There were no significant changes in cardiac output (5.1 to 4.9 L/min), muscle (2.4 to 3.2 mL/sec/min) or cutaneous basal flow (9.8 to 8.6 mL/100 mL) as measured non-invasively by echocardiogram and by plethysmography. Insulin and glucagon release were evaluated by the arginine infusion test. Nifedipine produced a tendency towards an increase in glucagon release and a reduction in insulin release although these changes did not reach statistical significance. In this group of patients, nifedipine produced a significant reduction in systolic and diastolic pressure, but no significant changes in insulin or glucagon plasma levels.

Aldosterone↗

Opposite effects of lidocaine and diltiazem on electrophysiologic alterations in acutely ischemic porcine myocardium.

To investigate the actions of lidocaine and diltiazem on the ischemic alterations associated with the onset of acute ischemic arrhythmias, the left anterior descending coronary artery was occluded for 6-min periods separated by 30 min of reperfusion, under control conditions and after injection of lidocaine (2.4-3.8 micrograms/mL of plasma) or diltiazem (390-510 ng/mL) in open-chest anesthetized pigs. Sixty-one unipolar electrograms were continuously recorded in the ischemic zone. Isochronal maps and isopotential maps were determined by computer analysis. The magnitude of beat-to-beat alternation of unipolar waveforms was described by the difference between the time integrals subtended by electrograms of consecutive beats. Activation times were prolonged by ischemia and the ST segment became elevated. Delay and ST elevation developed at a faster rate in the presence of lidocaine than under control conditions, but were reduced by diltiazem. ST-T alternation was not significantly different between control and lidocaine occlusions, but the incidence of negative T waves and that of ventricular tachycardia degenerating to fibrillation were higher in lidocaine occlusions than in control occlusions. In contrast, unipolar waveform alternation and negative T waves were virtually abolished by diltiazem, even at fast pacing rates (180-210 beats/min) at which diltiazem did not reduce ST elevation. Ventricular arrhythmias also were abolished by diltiazem. Thus, lidocaine and diltiazem produce opposite effects on the ischemic alterations most closely associated with the initiating mechanism of tachycardia. This could be related to differences between these drugs with regard to their actions on transmembrane currents during repolarization.

Animals↗

Long-term daily study of blood volume in cardiac autotransplanted dogs.

Cardiac transplantation is followed by the interruption of afferent nerves to the heart. Knowing that some of the afferent nerves are responsible for the homeostasis of the blood volume, we undertook a serial and long-term study of the blood volume in 25 dogs with denervated hearts. The animals were autotransplanted in order to eliminate repercussions linked to rejection and to its treatment. To discern the effects of surgery and of extracorporeal circulation from those of denervation, a group of 11 control dogs was operated upon and subjected to a period of extracorporeal circulation. In both groups, serial and long-term studies of blood volume were carried out daily with 131I-labeled albumin. Analysis of the results demonstrated that in the hours following surgery, blood volume is significantly decreased by 11% in the control group and by 22% in group 2. By the 5th postoperative day, the blood volume had increased gradually to attain normal values in both groups. At the 2nd postoperative week, the total blood volume remained normal in the control group, whereas blood volume had increased by 5.7% in the autotransplanted dogs, this being due to a 38% increase of the plasmatic phase. This increment persisted from the 14th to the 42nd postoperative day and attained 7.4%. Our conclusion is that the variations in blood volume during the 1st postoperative week in the autotransplanted heart are inherent in surgery and in extracorporeal circulation. Afterwards, the hypervolemia shown in the transplanted dogs is secondary to cardiac denervation.

Afferent Pathways↗

[Effect of cardiac rejection on blood volume].

The variations of blood volume after autotransplantation have been documented recently by our group. Since, in the homotransplanted heart, acute rejection affects cardiac function we felt that the blood volume variations might be different than that of the autotransplants. In thirty-one immunosuppressed dogs with an orthotopic homotransplanted heart, daily assessments of blood volume with iodine 131 tagged albumin was carried out from preoperative period (control) until death from acute rejection. In the immediate postoperative period there was a significant fall of 21% of the blood volume caused by a 20% fall of plasmatic volume and of a 23% fall in erythrocyte volume. From the second to the fifth postoperative day in spite of persistence of a low erythrocyte volume the blood volume progressed to normal due to a compensatory increase of the plasmatic volume. In the terminal phase of rejection there was a 32% increase of the plasmatic volume leading to an 8% increase of the total blood volume.

Animals↗

Human and animal serotypes of Bacteroides gingivalis defined by crossed immunoelectrophoresis.

The antigenic complexity of three strains of Bacteroides gingivalis and four strains resembling B. gingivalis isolated from animals was analyzed and compared by crossed immunoelectrophoresis. Thirteen antigens of the human biotype were present in all human strains and six antigens of the animal biotype were present in all animal strains, indicating a marked serological homogeneity within each biotype. Four antigens cross-reacting between the human B. gingivalis and the animal strains were identified. This antigenic relatedness defined the serological homogeneity of the two biotypes within the species and allowed recognition of four species-specific antigens. Two antigens specific to the human strains and two antigens specific to the animal strains were identified, indicating that serotype-specific antigens can distinguish each biotype. It is thus proposed that the oral, black-pigmented asaccharolytic Bacteroides strains of animal origin be classified as catalase-positive variants of B. gingivalis. It is also proposed that two serotypes be recognized within the species B. gingivalis. Serotype 1 includes the catalase-negative human biotype, and serotype 2 includes the catalase-positive animal biotype.

Animals↗

Effects of propranolol and exercise on cardiac dynamics and organ blood flow distribution in dogs.

The additive effects of propranolol and exercise on peripheral blood flow distribution were studied in conscious dogs. During treadmill exercise (8-10 km/h and 0% grade for 15 min.) cardiac performance increased significantly in parallel with myocardial and muscular blood flow (greater than 100%). Blood perfusion to liver and spleen decreased significantly (30% and 34%) while blood flow to other organs was unaltered. Under resting conditions propranolol only modified blood flow to liver and spleen (-50% and -38%). During exercise after propranolol a limited augmentation in cardiac performance and in myocardial and muscular blood flow was observed; splanchnic blood flow which was most affected by propranolol at rest did not further decrease during exercise after propranolol. The present observations demonstrate that propranolol, despite minor haemodynamic modifications, induces significant alterations in blood flow to splanchnic organs. The influence of beta-adrenoreceptor blockade was even more evident under conditions of augmented sympathetic activity as reflected by a significant limitation of increase in cardiac performance, myocardial and muscular blood flow and by a sustained redistribution of splanchnic blood flow during exercise after propranolol.

Animals↗

Administration and service delivery in the SSI program: the first 10 years.

This article provides an overview of the administrative structures and processes through which the Social Security Administration delivers its services to Supplemental Security Income (SSI) claimants and recipients. It documents the improvements and adjustments that have been made in the administration of SSI from 1974, when the program began, through 1983, the 10th year of its operation. The first decade of SSI was marked by significant changes that have led to improvements in fiscal responsibility and administrative efficiency for the program. Among the subjects covered are the legislative history of the program, the claims process, posteligibility procedures, underpayments and overpayments, the administrative complexities that have had to be surmounted, and administrative efforts aimed at quality assurance.

Aged↗