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Biomedical subjects

M Akhtar

Publications and source records attributed to M Akhtar.

At least 469 records · Page 26Linked to original sources

Characteristics and coexistence of two forms of ventricular echo phenomena.

During the scanning of paced basic ventricular cycle lengths (V1V1) with extrastimulus method (V2) two forms of ventricular echo phenomena (Ve) were recognized. The Ve resulting from A-V nodal re-entry (VeAVN) occurred in 12 of 45 patients, from re-entry in the His-Purkinje system (Ve-HPS) in 20 of 45 patients, and simultaneous dual re-entry (Ve-AVN and Ve-HPS) occurred in five of 45 patients. The Ve-AVN (1) appeared at longer V1V2 intervals, (2) was dependent on retrograde A-V nodal conduction delay, (3) had normal QRS complexes and H-V intervals, and (4) did not occur when V2 blocked in the A-V node. (5) Ve-AVN had aberrant QRS complexes when preceded by Ve-HPS. The Ve-HPS (1) appeared at shorter V1V2 intervals, (2) was dependent upon retrograde conduction delay in the HPS, (3) its QRS morphology and axis orientation resembled V2, i.e., left bundle branch block pattern, when right ventricular apex was the site of stimulation, (4) persisted when V2 blocked in the A-V node and was abolished when V2 blocked below the bundle of His, and (5) rarely occurred in patients with pre-existing right bundle branch block. It is concluded that (1) at least two forms of Ve can result from induced premature ventricular beats, (2) Ve-HPS is more common than Ve-AVN in the presence of normal QRS complexes, and (3) coexistence of Ve-AVN and Ve-HPS can give rise to complex ECG pattern mimicking multiple multifocal premature ventricular beats.

Arrhythmias, Cardiac↗

The mechanism of the bond forming events in pyridine nucleotide linked oxidoreductases. Studies with epoxide inhibitors of lactic dehydrogenase and beta-hydroxybutyrate dehydrogenase.

2,3-Epoxybutyrate and 2,3-epoxypropionate act as effective competitive inhibitors of pig heart lactic dehydrogenase. KIapp for both inhibitors was pH dependent and varied according to the general equation KIapp = KI(1 +Ka/H+) which may be predicted if the binding of the epoxide to the E-NADH complex involves a compulsory protonation step. Values of KI(epoxybutyrate), KI(epoxypropionate) and pKa were estimated as 150 muM, 860 muM, and 6.8, respectively. The formation of an E-NADH epoxide inhibitor complex was followed directly by fluorescence measurements. Both epoxybutyrate and epoxypropionate enhanced fluorescence of the E-NADH complex and caused a 20-nm blue shift in the maximum emission wavelenght. The dissociation constants measured by fluorescence titration for both epoxides increased as the pH was raised reflecting a decreased affinity for the E-NADH complex. 2,3-Epoxybutyrate was also shown to inhibit beta-hydroxybutyrate dehydrogenase by a mechanism which is consistent with compulsory protonation prior to addition of the epoxide. These results are discussed in terms of a general mechanism for the bond forming events in pyridine nucleotide linked oxidore-ductases.

Animals↗

Ultrastructure of endometrial stromal sarcoma.

An endometrial stromal sarcoma from a 48-year-old woman was studied by light and electron microscopy. Ultrastructurally most of the tumor cells resembled the stromal cells of midproliferative endometrium. There was no evidence of a pericytic differentiation of the tumor cells. These findings lend further support to the concept of an endometrial histogenesis of stromal sarcoma.

Cell Nucleus↗

Electrophysiologic effects of isoproterenol on cardiac conduction system in man.

The effects of isoproternol (ISOP) on the functional properties of the A-V conduction system were studied in 16 patients using His-bundle recordings and the atrial extrastimulus technique. In all patients, ISOP at an infusion rate of 1 mcg. per minute resulted in sinus acceleration and enhancement of A-V nodal conduction, but had no effect on His-Purkinje conduction time. ISOP significantly decreased both functional and effective refractory periods of the A-V node. The relative refractory period of the His-Purkinje system decreased by a small amount in five patients in whom the parameter could be compared before and after the drug.

Adult↗

Sinus node re-entrant tachycardia in man.

Sinus node re-entry (SNR) usually appears as a single beat. Tachycardias (SNRT) consistent with sustained SNR were seen in six patients and were initiated by premature stimulation of the high right atrium (six patients) and coronary sinus (four patients), and after continuous pacing from the high right atrium (four patients) or right ventricle (one patient) at rates of 130 to 200 per minute. During SNRT: (1) atrial beats exhibited a high-to-low atrial activation sequence, (2) the P-waves were similar in morphology to P-waves during sinus rhythm, and (3) re-entry in the A-V node or at the site of stimulation could be excluded. The cycle length of SNRT ranged from 625 to 320 msec. and SNRT either terminated spontaneously (six patients) or after premature atrial capture and/or vagal maneuvers (two patients). The electrophysiologic characteristics of SNRT and differentiation of SNRT from A-V nodal re-entry are discussed.

Aged↗

Electrophysiologic effects of tolamolol on atrioventricular conduction in man.

The electrophysiologic effects of tolamolol (UK-6558-01), a beta-adrenergic blocking agent, were studied in 13 patients by means of intracardiac electrograms and the extrastimulus method. Tolamolol (4 to 30 mg. intravenously) resulted in : (1) prolongation of sinus cycle length (SCL) in all patients (p less than 0.01); (2) prolongation of sinus escape time (SET) in 11 of 13 patients (p less than 0.001); (3) prolongation of A-V nodal conduction time during sinus rhythm in 1i of 13 patients (p less than 0.001); (4) onset of A-V nodal Wenckebach block at longer paced cycle lengths in 10 of 11 patients (p less than 0.001); (5) prolongation of the functional refractory period (FRP) of the A-V node in 11 of 11 patients (p less than 0.001); and (6) prolongation of the effective refractory period (ERP) of the A-V node in 10 of 10 patients (P less than 0.001). Tolamolol had no effect on His-Purkinje system (HPS) conduction time in any patient, including 3 patients with abnormal H-V intervals. Because of the marked increase in A-V nodal conduction time encountered by premature atrial depolarizations, the relative and effective refractory periods of the HPS could not be determined in any patient after tolamolol. Atropine (0.5 or 1.0 mg. intravenously) significantly reversed the effects of tolamolol on: sinus cycle length (4 of 5 patients); sinus escape time (3 of 3 patients); A-V nodal conduction time (4 of 5 patients); and A-V nodal refractioriness (5 of 5 patients).

Adult↗

Induction of atrioventricular nodal reentrant tachycardia after atropine. Report of five cases.

After intravenous administration of 0.5 mg of atropine sustained atrioventricular (A-V) nodal reentrant tachycardia could be produced in five patients who had no prior historical or electrocardiographic evidence of supraventricular tachycardia. During the control period single atrial echo beats could be demonstrated in four of the five patients, but no instance of sustained tachycardia occurred. Atropine, known to enhance A-V nodal conduction, allowed achievement of longer A-H intervals (Case 1) and provided the necessary balance of conduction and refractoriness within the A-V nodal reentrant pathways (Cases 1 to 5) to sustain A-V nodal reentry in these patients.

Adolescent↗

Mechanistic, inhibitory and stereochemical studies on cytoplasmic and mitochondrial serine transhydorxymethylases.

By using cytoplasmic and mitochondrial serine transhydroxymethylase isoenzymes from rabbit liver, it was shown that both enzymes exhibited similar ratios of serine transhydroxymethylase/threonine aldolase activities. Both enzymes catalysed the removal of the pro-S hydrogen atom of glycine, which was greatly enhanced by the presence of tetrahydrofolate. The cytoplasmic as well as the mitochondrial enzyme catalysed the synthesis of serine from glycine and [3H2]formaldehyde in the absence of tetrahydrofolate. The results are consistent with our previous suggestion that a role of tetrahydrofolate in the serine transhydroxymethylase reaction is to transport formaldehyde in and out of the active site (Jordan & Akhtar, 1970). The isoenzymes, however, showed remarkable differences in their inactivation by inhibitors. The serine transhydroxymethylase as well as the threonine aldolase activities of the cytoplasmic enzyme were inactivated in a similar fashion by chloroacetaldehyde, iodoacetamide, bromopyruvate and glycidaldehyde (2,3-epoxypropionaldehyde). These inhibitors had no effect on the two activities of the mitochondrial enzyme. The rate of inactivation of the cytoplasmic enzyme by glycidaldehyde was enhanced by the presence of glycine but decreased by the presence of serine. The implications of these results to the mechanism of catalysis and the nature of the active site of the enzymes are discussed.

Acetaldehyde↗

The role of a 5alpha-hydroxylated intermediate in the formation of the 5, 6-double bond in cholesterol biosynthesis.

If the biological conversion of cholest-7-en-3beta-ol (I) into cholesterol (IV) occurred thorugh the intermediacy of cholest-7-ene-3beta,5alpha-diol (II) then the factor(s) adversely affecting the convwesion of the 5alpha-hydroxy sterol (II) into cholesterol must at least equally adversely affect the formation of cholesterol from cholest-7-en-3beta-ol. By using partial denaturation techniquws and dual-labelled precursors it was shown that the enzyme system responsible for the conversion of the 5alpha-hydroxy sterol (II) into cholesterol denatured faster than that for the corresponding conversion from cholest-7-en-3beta-ol (I).

Animals↗

The mechanism of C-4 demethylation during cholesterol biosynthesis.

The conversion of 4,4-dimethylcholest-7-enol into 4alpha-methylcholest-7-enol by rat liver microsomal preparations involves the decarboxylation of a sterol 3-oxo-4alpha-carboxylic acid. By using an (18)O-labelled substrate it was shown that this decarboxylation does not involve a Schiff-base intermediate.

Animals↗

Anterior pituitary component in benign cystic ovarian teratomas. Report of three cases.

This paper documents three cases of benign cystic ovarian teratoma in which elements of adenohypophysis was recognized as one of the tissue components. Such findings have been recorded but not unequivocally documented in any of the previous reports of benign cystic teratomas. One of the tumors in this series also contained neuroglial tissue closely associated with the adenohypophyseal elements. The possibility that these neural elements might represent neurohypophysis is briefly discussed.

Adult↗

A comparative analysis of antegrade and retrograde conduction patterns in man.

Patterns of antegrade and retrograde conduction and refractory periods were studied using His bundle electrogram recordings, incremental atrial and ventricular pacing and the extrastimulus technique. In 36/50 patients antegrade conduction was "better" than retrograde conduction (group I), as evidenced by a) onset of retrograde atrioventricular (A-V) nodal Wenckebach phenomenon at a slower rate compared to the antegrade counterpart (25 patients: group IA) or b) no ventriculo-atrial conduction at all ventricular paced rates (11 pts: group IB). The site of retrograde block in group IB patients was the A-V node. In eight patients (group II), antegrade and retrograde conduction appeared to be equal up to maximum paced rates of 160 beats/min. In six patients (group III) retrograde conduction was "better" than antegrade conduction, as indicated by onset of antegrade A-V nodal Wenckebach periods at slower rates than retrograde Wenckebach periods. During antegrade refractory period studies the area of maximum refractoriness was the A-V node in 19/40 patients, the His-Purkinje system (HPS) 6/40, and the atrial muscle in 15/40. During retrograde refractory period studies the A-V node was the area of maximum refractoriness in 12/36 pts (4/40 patients had A-V dissociation during ventricular pacing), the HPS in 12/36, and the ventricular muscle in 10/36. In 2/36 patients the site of maximum refractoriness retrogradely could not be determined: The area of maximum refractoriness during both antegrade and retrograde refractory period studies was the same in 11 patients (A-V node in seve and HPS in four), was different (i.e., A-V node or HPS) in 18 patients, and was the artrial or ventricular muscle in six patients. In five patients, including four patients in whom V-A conduction failed to occur, the above comparisons were not made. It is concluded that 1) antegrade conduction is better than retrograde conduction in most patients; 2) it is not always possible to predict area of maximum refractoriness during premature stimulation (both atrium and ventricle) from observations made during incremental pacing; 3) it is equally difficult to extrapolate patterns of retrograde conduction and refractory periods from results of antegrade conduction and refractory period studies.

Adult↗