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Biomedical subjects

J M Juliard

Publications and source records attributed to J M Juliard.

96 records · Page 6Linked to original sources
PubMed1983

[Ventricular pre-excitation revealed by idioventricular rhythm and large QRS tachycardias. Apropos of an operated case].

A 15 year old boy presented with palpitations of sudden onset and termination over a two month period. The heart was clinically and radiologically normal. The electrocardiogramme showed sinus rhythm with a short PR interval (0,11 sec) and narrow QRS complexes (0,08 sec) associated with an intermittent escape accelerated idioventricular rhythm (AIVR). During an attack of palpitations a regular tachycardia (250/min) with wide QRS complexes of the same configuration as those of the AIVR (left side delay). The diagnosis of ventricular tachycardia was retained. Endocavitary electrophysiological recording demonstrated preexcitation of the right ventricle associated with accelerated nodal conduction explaining the narrow QRS complexes in sinus rhythm. The wide complex tachycardias initiated and terminated by paired ventricular stimulation were identical to the spontaneous attacks and were attributed to an antidromic reciprocating rhythm. The hypothesis of a rhythm arising from the accessory pathway is suggested. This would explain the identical configuration of the QRS complexes of the AIVR and of the antidromic reciprocating-rhythm and the disappearance of the AIVR after surgical section of the accessory pathway.

Adolescent↗
PubMed1983

[Hemodynamic and coronary effects of molsidomine in patients with stable coronary insufficiency in the basal state, during an atrial stimulation test and a cold test].

The heart rate (HR), the cardiac output (Qc) and the coronary sinus flow rate (Qcs), the left ventricular systolic and end-diastolic pressures (LVSP, LVEDP), the femoral artery pressure (FAP) and the difference between the coronary arterial and coronary venous oxygen tension (DAVcO2) were measured in patients with stable coronary insufficiency without cardiac failure, before and 40 to 60 minutes after 2 or 3 mg of molsidomine (M). In 20 patients, these measurements were made in the basal state, in spontaneous rhythm (SP). In 8 of these patient, (including 3 receiving beta-blockers) the measurements were made during an atrial stimulation test (ST) and in 8 other patients, all receiving long-term beta-blocker therapy, the measurements were made during a cold test (CT). At the basal state in SR, a gradual reduction in the LVSP to 70% or less of its initial value was observed in the patients receiving 3 mg of M (2 of whom received beta-blocker treatment). The LVSP was immediately restored by vascular filling. In 16 patients, M decreased the LVSP, the LVEDP, the FAP, the Qc and the double product (DP = LVSP X HR). The DAVcO2 was unchanged. Qcs and MVO2 (MVO2 = Qcs X DAVcO2) were decreased. In the course of ST, the haemodynamic and coronary changes are similar to those seen in the basal state. During the Ct, the increase in the LVSP, FAP and DP was significantly reduced by M. The variations in Qcs and coronary resistance (FAP/Qcs) were also significantly different after M., with better metabolic regulation of the coronary circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Hemodynamic effects of medroxalol in the anesthetized dog. Relation between adrenolytic properties and plasma concentration].

Hemodynamic properties of medroxalol (MDL), a new alpha-and-beta adrenoceptor antagonistic drug, were studied in eight pentobarbital-anesthetized (open chest) dogs. MDL was injected in three doses (1.5, 3.0 and 9.0 mg/kg i.v.) at one hour intervals. A control group (n = 5) received three successive vehicle injections at the same time intervals. Heart rate, systolic and diastolic arterial pressure, cardiac output and stroke volume (using an intrathoracic flowmeter), and peripheral resistance were recorded 45 min before the first injection and 15 min after each administration. Isoproterenol (ISP) and neosynephrine (NSP) dose-response curves were recorded before the first dose and after each injection in both group. Log-linear regression analyses were used to estimate the ISP chronotropic dose 25 (DC 25) and the ISP barotropic dose 30 (DB 30). The results show that medroxalol possesses beta-adrenoreceptor antagonistic properties which are 35 times greater than its alpha-antagonistic properties. Beta-blockade was evidenced by bradycardia and increase in DC 25, beginning at the first dose used. Alpha-blockade was not significant at that first dose and therefore cannot alone explain the strong hypotension observed. All these effects were related to the plasma-concentration of MDL.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

[Quinidine plasma concentration-cardiac electrophysiologic effects relationships in anesthetized dogs (author's transl)].

1. The electrophysiologic effects of quinidine (Q)were studied in 15 pentobarbital-anesthetized dogs using intracardiac electrography and programmed stimulation. With four successive bolus i.v. injections of Q gluconate (1, 3, 9, 18 mg/kg cumulative doses) at 30 min intervals, Q plasma concentration (Cp) ranged from 1.02 +/- 0.1 micrograms/ml to 5.7 +/- 0.6 micrograms at the time of electrophysiologic measurements 20 min after each injection. 2. In six control dogs, heart rate (HR), sinus node recovery time (TRS), conduction times (StH, HV, QRS), ventricular repolarization time (QTc) Wenckebach cycle length (L.W), and atrial refractory periods (RP) did not change significantly while the functional nodal (PRFN) and the effective ventricular (PREV) RPs significantly increased with time. 3. Quinidine produced a significant log- Cp related decrease in HR and increase in TRS corresponding to a decreased sinus automaticity. 4. StH and HV conduction times increased proportionally to log CpQ while the increase in QRS was not Cp-dependent. QTc did not increase significantly. 5. Quinidine resulted in significant log Cp-related increases in atrial RP PRFN and LW while the Q-induced changes in PREV were not Cp-dependent.

Anesthesia↗