Mean Cycle Length Research Articles

Urine production and bladder function in fetuses with open spina bifida.

Hourly fetal urine production rate (HFUPR) and bladder filling and voiding were determined by real-time ultrasonography in 13 fetuses with open spina bifida (OSB) and compared with those of 101 normal fetuses from uncomplicated pregnancies at 16-40 weeks gestation. In normal pregnancy, the fetal bladder volume increases linearly with time and then decreases rapidly with micturition. The mean cycle length does not change significantly with gestation but both the mean bladder volume and HFUPR increase. In fetuses with OSB, ultrasonographic examination has demonstrated deviations from normal in both bladder filling and bladder emptying.

Evaluation of Rodent Sperm, Vaginal Cytology, and Reproductive Organ Weight Data from National Toxicology Program 13-Week Studies

Evaluation of Rodent Sperm, Vaginal Cytology, and Reproductive Organ Weight Data from National Toxicology Program 13-Week Studies. Morrissey, R. E., Schwetz, B. A., Lamb, J. C, IV, Ross, M. D., Teague, J. L., and Morris, R. W. (1988). Fundam. Appl Toxicol. 11, 343-358. Sperm morphology and vaginal cytology examinations (SMVCEs), which include evaluations of motility, concentration and head morphology of sperm from the cauda epididymis, and male reproductive organ weight data, were developed by the National Toxicology Program as a screening system for reproductive toxicants. An analysis was conducted of SMVCE studies carried out at the end of fifty 13-week studies (25 for rats, 25 for mice) over a 3-year period. Statistically significant changes in these studies were summarized, as were control data for each male endpoint (mean, SD, 95% confidence limits around the mean, median, and statistical power). Reproductive organ weights (testis, epididymis, cauda epididymis) and sperm motility were the most statistically powerful endpoints evaluated; sperm head morphology may also be a sensitive endpoint for detecting reproductive toxicants. For 24 chemicals tested in both rats and mice, the concordance of results [i.e., no adverse effect in either species, or at least one SMVCE endpoint (not necessarily the same one) adversely affected in both species] was 58%. These data suggest that detection of potential reproductive toxicants might be best when both species are used. Types of sperm head abnormalities and their relative proportion of the total did not differ among control and treatment groups. Estrous cycle data were obtained in the final week of forty-six 13-week studies (23 for mice, 23 for rats). Only 3 chemicals caused an increase in mean cycle length compared with the control group. More data from breeding studies in which female estrous cycle length is measured are needed to assess fully the association of cycle length with reproductive outcome; stages of the estrous cycle are so variable that they may not be useful in assessing potential toxicity. Interiaboratory variability in SMVCE values for many endpoints was documented. Very few of the chemicals that form the basis of this report have been evaluated in definitive reproductive toxicology protocols; a companion paper compares changes in SMVCE endpoints with the outcome of continuous breeding reproduction studies.

Dissociation of electrophysiologic and pharmacologic stability during an abbreviated oral loading regimen of amiodarone

Thirty-three patients treated with an abbreviated oral amiodarone loading regimen for ventricular tachycardia underwent electrophysiologic testing in the control state, after 1 week of high-dose (1170 ± 88 mg/day) inpatient therapy; and after an 8-week intermediate (669 ± 129 mg/day) dosing phase. Serum levels of amiodarone and desethylamiodarone were measured by high-pressure liquid chromatography during follow-up electrophysiologic studies. Although the corrected sinus node recovery time, sinoatrial conduction time, and AH and HV intervals remained unchanged throughout the loading period, the sinus cycle length, Wenckebach cycle length, atrial and ventricular refractory periods, and ventricular tachycardia mean and return cycle lengths lengthened significantly by 1 week. They then remained stable for the remainder of the treatment period (control < 1 and 8 weeks, p < 0.05). In contrast, amiodarone and especially desethylamiodarone levels rose from 1 to 8 weeks: 1.29 ± 0.56 to 1.97 ± 0.90 μg/ml ( p = 0.001) and 0.63 ± 0.29 to 1.29 ± 0.61 μg/ml ( p < 0.0001), respectively. Because this regimen produces relatively prompt electrophysiologic changes, which then stabilize, early outpatient management becomes feasible before pharmacologic steady state is attained.

Influence of the cycle length of basic drive on induction of sustained ventricular tachycardia associated with coronary artery disease

The relation between the cycle length of basic drive during programmed ventricular stimulation and the coupling intervals at which sustained monomorphic ventricular tachycardia (VT) was initiated was analyzed in patients with coronary artery disease and documented sustained VT. The study included 28 patients in whom hemodynamically tolerable, monomorphic sustained VT was inducible at different cycle lengths of basic drive during the same electrophysiologic study. The stimulation protocol included single or double premature stimuli during paced ventricular rhythms at different cycle lengths of basic drive. The coupling intervals of premature stimuli for induction of VT (considered the outer margin of the echo zone) during step 1 of the stimulation protocol (basic drive at cycle lengths of 500 or 430 ms) were compared with those during step 2 (basic drive at cycle lengths of 370 or 330 ms). The mean cycle length of induced sustained VT was 370 ± 79 ms. The mode of induction of VT remained the same in 23 patients (single or double premature stimuli); in 5 patients, fewer premature stimuli were required during step 2 than step 1. By moving from step 1 to step 2, VT could be induced at longer coupling intervals of the premature stimuli in 23 patients (82.1%). The mean increase in the sum of the coupling intervals was 52 ± 37 ms. In 5 patients, the coupling intervals either did not change from step 1 to step 2 (n = 1) or decreased by an average of −40 ± 14.1 ms. The results suggest that inducibility of VT is favored by a decrease in the cycle length of basic drive. Shortening the cycle length of basic drive may lead to a more pronounced slowing of conduction and a greater heterogeneity in refractory periods in the reentrant circuit. This may enable induction of VT by premature stimuli at longer coupling intervals than during longer cycle lengths of basic drive.

The effect of Trypanosoma congolense infection on the oestrous cycle of the goat

The oestrous cycle of four goats was monitored during the course of an infection with T. congolense maintained with sub-curative doses of diminazene aceturate. Four uninfected control goats also given diminazene aceturate acted as controls. Cyclical ovarian function was monitored by daily determination of plasma progesterone concentrations. According to plasma progesterone profiles, control goats continued to cycle throughout the experiment, completing 24 cycles in total. Mean (± SEM) cycle length in the control of goats was 21·1 ± 0·8 days, with mean plateau progesterone concentrations during the luteal phase averaging 8·95 ± 0·28 ng/ml. Three goats developed persistent corpora lutea following T. congolense infection. In two of these goats the luteal phase was extended for 48 and 94 days respectively, and the presence of corpora lutea on the ovaries confirmed at autopsy. In the third goat, the persistent corpus luteum regressed spontaneously after an extended cycle of 53 days. After a short 6 day cycle this goat completed 2 oestrous cycles of normal length. Progresterone concentrations were reduced by approximately half during the period of extended luteal function in the 3 infected goats with persistent corpora lutea. The fourth infected goat continued to cycle throughout the experiment, but also exhibited reduced progesterone concentrations in the cycle following infection.

MECHANISM OF 2:1 ATRIOVENTRICULAR BLOCK IN INFANTS WITH CONGENITAL LONG QT SYNDROME

The mechanism of 2:1 atrioventricular block in infants with the congenital long QT syndrome has been postulated to result from a long ventricular effective refractory period interrupting conduction of successive sinus impulses. Three infants age 1-2 days exhibited bradycardia demonstrated to be 2:1 atrioventricular block by the surface electrocardiogram. Mean sinus cycle length (SCL) was 0.56 sec where as mean QT interval was 0.65 sec (QTc 0.63); this .07 sec difference between the SCL and mean QTc was sufficient to block successful capture of the ventricles by successive sinus impulses. Programmed ventricular extrastimulation in one patient demonstrated a markedly prolonged ventricular effective period (480 sec) at ventricular basic cycle length (BCL) 1000 msec shortening to 280 msec with a ventricular BCL of 400 msec. Permanent ventricular pacing shortened the ventricular effective refractory period in each infant and effectively suppressed polymorphic ventricular arrhythmias in the affected two. We conclude that the mechanism of 2:1 atrioventricular block in infants with the congenital long QT syndrome is a function of the age related SCL relative to the QT interval as well as the markedly prolonged but rate dependent ventricular effective refractory period. Ventricular pacemaker implant is effective in increasing ventricular rate, shortening ventricular effective refractory period, and suppressing complex ventricular arrhythmias.

Effect of autonomic nervous system modulation on retrograde atrioventricular nodal conduction in the human heart.

Although the influence of the autonomic nervous system on anterograde atrioventricular nodal conduction is well established, its effect on retrograde atrioventricular nodal conduction has not been examined systematically. Since retrograde atrioventricular nodal conduction in subjects with normal anterograde conduction may vary from intact retrograde conduction to complete retrograde block when assessed during ventricular pacing, in this study patients with (a) intact retrograde atrioventricular nodal conduction (group 1) were studied during parasympathetic (vagal) stimulation by carotid sinus pressure and during sympathetic inhibition (propranolol 0.2 mg.kg-1 intravenously) and (b) retrograde atrioventricular nodal block (group 2) were studied during vagal blockade (atropine 0.04 mg.kg-1 intravenously) and during sympathetic stimulation (isoproterenol 1-4 micrograms.min-1 infusion). In both groups changes in sinus cycle length and anterograde atrioventricular nodal conduction were measured. In group 1 vagal stimulation by carotid sinus pressure in 20 patients caused the cycle length at which retrograde atrioventricular nodal block was induced to be significantly lengthened from a mean(SD) of 375(59) to 451(51) ms in six patients; caused complete retrograde block in 10 patients; and had no effect in four patients. Sympathetic inhibition by propranolol in another 15 patients delayed the onset of pacing induced retrograde atrioventricular nodal block from a mean(SD) of 340(60) to 418(80) ms in 11 patients; caused complete retrograde atrioventricular nodal block in three patients; and had no effect in one patient. In group 2 vagal blockade by atropine caused a 1:1 retrograde response during ventricular pacing up to a mean(SD) cycle length of 470(135) ms in six out of eight patients. The infusion of isoproterenol caused the retrograde atrioventricular nodal block to be abolished and 1:1 conduction to be resumed up to a ventricular pacing mean(SD) cycle length of 364(57) ms in six out of eight patients. It is concluded that (a) the autonomic nervous system modulates retrograde atrioventricular nodal conduction in a similar manner to its anterograde counterpart and (b) that since retrograde atrioventricular nodal conduction was reversible after the administration of either atropine or isoproterenol retrograde atrioventricular nodal block may be dynamic (physiological) rather than fixed (anatomical) in nature.

Behavioural and ovarian changes during the oestrous cycle in the boran ( Bos indicus)

Ten Boran ( Bos indicus) cows were studied over 64 oestrous cycles. Alterations in sexual behaviour and of the ovaries palpated per rectum were related to the plasma progesterone profiles detemined using an extracted double antibody radioimmunoassay. The mean cycle length in the cows was 23 ± 0 · 4 days. Oestrus detection efficiency using standing to be mounted, was 27 percent. Restlessness, where observed, reliably indicated that a cow was in the period of basal progesterone concentration. Mounting, sniffing, head-butting, being sniffed, being mounted with avoidance behaviour, although shown by 50 percent of cows during the basal progesterone period were not confined solely to this part of the cycle. Use of Kamar heat-mount detectors in conjunction with standing to be mounted identified 44 percent of oestrous animals. However, the occurrence of false positives during the rest of the cycle precluded their use as sole indicators of oestrus. Accuracy of palpation of corpora lutea was 61 percent during periods of elevated and 98 percent in periods of basal progesterone concentrations.

The cycle length of the U Geminorum star HT Cassiopeiae

AbstractThe mean cycle length of the catalysmic binary HT Cas, which is remarkable because of the shortness of its orbital period, has been determined as 400d±50d. The hitherto assuixed value of 30d proved unfounded. Some aspects arising when classifying long‐cycle objects and SU Ursae Majoris variables are pointed out, a s well as the relation between large cycle length and small accretion rate.

Effects of adenosine and adenosine 5′-triphosphate on ventricular escape rhythm in the canine heart

The effects of adenosine and adenosine 5'-triphosphate (ATP) on ventricular escape rhythms were studied in 16 closed chest dogs after electroablation of the His bundle region. All dogs exhibited complete atrioventricular (AV) block and stable ventricular escape rhythm with a mean cycle length of 1,210 +/- 80 ms and a QRS width of 91 +/- 5 ms. Physiologic AV sequential pacing was operative during experiments and was interrupted for rapid (less than or equal to 1 second) administration of either adenosine or ATP (3 mumol/kg) into the right atrium. Adenosine and ATP effectively depressed ventricular escape rhythms in a similar manner both qualitatively and quantitatively (cycle length from 1,210 +/- 80 to 1,764 +/- 132 ms and from 1,274 +/- 84 to 2,000 +/- 150 ms, respectively; each p less than 0.01). These effects were not significantly altered by either physostigmine (an acetylcholinesterase inhibitor) or atropine (a muscarinic cholinergic blocker), but were slightly attenuated by propranolol (a beta-adrenoceptor blocker). In the presence of autonomic blockade, the adenosine transport blocker dipyridamole markedly enhanced the depressant effects of adenosine and ATP. The adenosine competitive antagonist aminophylline reversed the action of dipyridamole. Thus, both adenosine and ATP depress ventricular escape rhythms in vivo, independent of the autonomic nervous system. Moreover, the effects of ATP can be accounted for in large part by its rapid breakdown to adenosine.

Resetting response patterns during sustained ventricular tachycardia: relationship to the excitable gap.

We analyzed the resetting response (a noncompensatory pause after electrical stimulation) during 37 hemodynamically tolerated ventricular tachycardias (VTs) induced by programmed electrical stimulation in 32 patients with chronic coronary artery disease. The mean cycle length of VT was 369 +/- 59 msec. Single extrastimuli were delivered at the right ventricular apex during all 37 VTs, and double extrastimuli were delivered at the same site during 23 VTs. The resetting response pattern was considered increasing, decreasing, or flat if the return cycle increased, decreased, or remained constant in response to progressively shorter coupling intervals of the extrastimuli. Ten VTs had an increasing pattern and nine a flat pattern. In 11 VTs the pattern was mixed (flat at longer coupling intervals and increasing at shorter ones), and in the remaining seven the pattern could not be defined. No VT had a decreasing pattern. The mean duration of the resetting interval (range of coupling intervals resulting in resetting) was 66 +/- 45 msec, or 17% of the cycle length of VT. VT with a mixed pattern had longer resetting intervals than VT with an increasing pattern (102 +/- 34 vs 64 +/- 40 msec; p less than .035); however, cycle lengths of VT were similar (370 +/- 58 vs 386 +/- 86, p = NS). An excellent correlation was observed between the shortest return cycles in response to single and double extrastimuli (r = .99), with a mean difference of 5 msec. The cycle length of VT exceeded the return cycle (measured to the QRS onset) during 15 VTs (41%).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of the resetting phenomenon in sustained uniform ventricular tachycardia: Incidence and relation to termination

Although the phenomenon of resetting has been studied in several experimental and clinical rhythms, it has not been systematically analyzed in ventricular tachycardia. To define the incidence and determinants of resetting as well as its relation to ventricular tachycardia termination, the response to programmed stimulation was prospectively studied during 78 electrically induced episodes of sustained, uniform ventricular tachycardia (mean cycle length 365 +/- 59 ms) in 53 patients. Single and double ventricular extrastimuli were introduced during 78 and 39 episodes of ventricular tachycardia, respectively. Rapid ventricular pacing was performed during 27 episodes. Resetting occurred in response to single ventricular extrastimuli in 43 (55%) of 78 ventricular tachycardias, to double extrastimuli in 31 (79%) of 39 ventricular tachycardias and to rapid pacing in 23 (85%) of 27 ventricular tachycardias. No ventricular tachycardia characteristic distinguished those tachycardias that were reset from those not reset. Termination of ventricular tachycardia occurred in 7 (9%) of 78 episodes with single ventricular extrastimuli, 14 (36%) of 39 episodes with double ventricular extrastimuli and 13 (48%) of 27 episodes with rapid pacing. Termination was less frequent than resetting with both single (9 versus 55%) and double (36 versus 79%) extrastimuli, as well as rapid pacing (48 versus 85%). Resetting preceded termination in 7 of 7 ventricular tachycardias terminated with single ventricular extrastimuli, 12 of 14 terminated with double ventricular extrastimuli and 9 of 13 terminated by rapid pacing. Ventricular tachycardias that were terminated could not be differentiated from those that were reset without termination. Resetting with programmed extrastimuli is common in hemodynamically stable sustained ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Pacing-induced angina pectoris and induction of ventricular arrhythmias in coronary artery disease

Ischemia caused by rapid pacing during electrophysiologic study could facilitate induction of ventricular arrhythmias. The results of extrastimulation were retrospectively analyzed in 32 patients with coronary artery disease (CAD) without a history of symptomatic arrhythmia. These patients were studied at cardiac catheterization for angina pectoris refractory to medical therapy. Eleven patients (group I) had typical angina during trains of rapid right ventricular pacing (repeated trains of 8 stimuli [mean cycle length (CL) 473 ± 47 ms]) but were asymptomatic during slower trains (CL 800 ± 100 ms). Twenty-one patients (group II) had no symptoms with either rapid (CL 448 ± 51 ms) or slow (CL 688 ± 105 ms) trains, despite comparable left ventricular function, CAD severity and medication. Effective refractory periods (S 1S 2) after rapid drive were shorter in group I than in group II patients (225 ± 9 vs 240 ± 14 ms, p < 0.002), but refractory periods during slow pacing were similar (251 ± 12 vs 253 ± 17 ms, difference not significant). No patient in either group had sustained arrhythmia (more than 15 beats) induced by single and double ventricular extrastimuli, decrementally applied at the right ventricular apex. The number of extra beats provoked in group I when rapid trains caused angina (4.3 ± 3.6) was similar to that induced by extra stimulation after slower pacing without angina (4.4 ± 3.5) and to that obtained with rapid or slow pacing in group II (3.1 ± 3.3 and 2.8 ± 2.2). Intraventricular reentry was just as frequent in group I during rapid drive (55%) as with slow drive (73%), and with rapid and slow drive in group II (43 and 67%, respectively). Therefore, pacing-induced angina did not facilitate the induction of unheralded ventricular arrhythmias during electrophysiologic study of patients with CAD.

LUTEOLYTIC ACTION OF PROSTAGLANDINS IN SWINE AND THE EFFECTS OF CLOPROSTENOL ON LUTEINIZING HORMONE RECEPTORS AND MEMBRANE STRUCTURE OF PORCINE CORPORA LUTEA

The luteolytic action of prostaglandin F2α (PGF2α), 15-keto-PGF2α, 15-methyl-PGF2α, and cloprostenol was evaluated in cycling gilts and sows after intramuscular injection on day 13 of the estrous cycle. Only cloprostenol significantly shortened the mean cycle length (18.5 vs. 20.3 d, P &lt; 0.05). Cloprostenol also caused a more rapid decline in serum progesterone concentrations than did the other prostaglandins. Serum concentrations of the prostaglandin metabolite 13,14-dihydro-15-keto-PGF2α (PGFM), showed rapid transitory peaks after PGF2α or 15-keto-PGF2α and a lower, later rise after cloprostenol. A second experiment examined luteal luteinizing hormone (LH) receptors and luteal membrane ultrastructure during the estrous cycle and pregnancy and the effect of cloprostenol on these parameters during the estrous cycle. The number of unoccupied luteal LH receptors, as measured by specific 125I-hCG binding, dropped significantly from mid to late pregnancy and from mid to late cycle. Cloprostenol lowered serum progesterone concentrations but did not affect hCG binding. X-ray diffraction showed no correlation of gel or liquid-crystalline phase lipids in luteal microsomes with the stage of the estrous cycle or pregnancy or cloprostenol treatment. Key words: Swine, luteolysis, estrous cycle, prostaglandins, luteal LH receptors

Electrophysiologic characteristics of ventricular tachycardia or fibrillation in relation to age of myocardial infarction

Evaluation of ventricular myocardium after the onset of acute myocardial infarction (AMI) suggests that the substrate for ventricular arrhythmias changes as the AMI heals. To determine if the ability of programmed stimulation to initiate ventricular tachycardia (VT) varies according to the interval between AMI and electrophysiologic testing, the clinical and electrophysiologic data of 42 patients with spontaneous sustained VT and 12 patients with ventricular fibrillation (VF) more than 3 days after a single AMI were analyzed. For patients with VT, there were no significant differences in the incidence of initiation of sustained monomorphic VT among those evaluated 1 to 3 weeks (100%), 3 to 8 weeks (75%), 2 to 6 months (100%), 6 to 18 months (80%) or more than 18 months (81%) after AMI, and the mean number of extrastimuli required for initiation did not differ among the groups. Patients evaluated more than 4 weeks after the initial episode of VT had a lower incidence of inducible VT than those studied earlier (14 of 21 [71%] vs 21 of 21 [100%], p < 0.05), although this appeared to be a result of earlier termination of the stimulation protocol owing to initiation of polymorphic arrhythmias in those studied later. The 14 patients evaluated within 8 weeks of AMI had significantly faster VT rates (mean cycle length 269 ± 45 ms) than the 28 patients studied later (320 ± 75 ms, p < 0.01), possibly because of more out-of-hospital presentations of VT in patients studied later. More patients studied within 3 weeks of AMI had anterior infarcts (100%), but otherwise there were no differences in age, AMI location or ejection fraction. Among patients with VF, 5 of 7 (71%) studied less than 8 weeks and 3 of 5 patients (60%) studied more than 8 weeks after AMI had inducible VT (difference not significant). Thus, the ability to induce sustained VT in patients with spontaneous episodes of sustained VT or VF after AMI appears to be independent of the interval between AMI and programmed stimulation.

Chenodeoxycholic and ursodeoxycholic acids alter motility and fluid transit in the canine ileum.

We examined the effects of chenodeoxycholic acid (CDCA) and ursodeoxycholic acid (UDCA) on fasting motility patterns and transit in ileocolonic loops of 5 dogs. Animals were prepared with isolated loops (40 cm ileum and 5 cm colon) which maintained neuromuscular continuity with the intact bowel through a bridge of tunica muscularis. Myoelectrical activity was recorded from multiple serosal, monopolar electrodes and muscle contractions recorded from serosal strain gauges; fluid transit was assessed by continuous perfusion (1.4 ml min-1) of solutions containing polyethylene glycol 4000 marker, with or without bile acids. Saline perfusion did not disturb the fasting cycle of motility and mean cycle length in unperfused (106 +/- 7 min) loop was the same as during perfusion of saline (108 +/- 9 min). Bile acids abolished interdigestive cycles in 11 of 12 experiments, fasting patterns returned 64-106 min after bile acid perfusion was stopped. The fasting pattern continued to cycle normally in the proximal small bowel during bile acid perfusion. CDCA (15 mM) stimulated the occurrence of propulsive contractions of long duration. Bile acids shortened transit time through the loops and altered the pattern of flow towards a more continuous, steady stream. These effects of bile acids on ileal motility, like those described previously in the colon, could play a role in bile acid diarrhea.

Pattern of endocardial activation during sustained ventricular tachycardia

Fifty-five patients with sustained ventricular tachycardia due to prior myocardial infarction underwent intraoperative endocardial activation mapping during ventricular tachycardia to guide subendocardial resection. The mapping data were analyzed to determine the pattern of endocardial activation during tachycardia. Of a total of 122 tachycardias, 101 had a pattern of activation assigned: in 90 (90%), endocardial activation spread centrifugally from a tachycardia site of origin, and 11 (10%) had a continuous loop of electrical activity around an aneurysm. All patients had at least one tachycardia having the centrifugal spread pattern. Tachycardias with a continuous loop pattern had a shorter mean cycle length than those with a centrifugal spread pattern (260 +/- 33 versus 338 +/- 81 ms, p less than 0.002) and a longer duration of endocardial activation relative to the tachycardia cycle length (100 +/- 0 versus 58 +/- 19%, p less than 0.001). There was no difference in preoperative patient characteristics, operative survival or cure of tachycardia between patients having any tachycardias of the continuous loop pattern and those having only centrifugal spread tachycardias. Thus, the vast majority of ventricular tachycardias in this group of patients are characterized by a centrifugal spread of endocardial activation from a site of origin less than 6 cm2 in size. Mapping-guided ablative surgery may remove the entire tachycardia circuit in these patients and a critical portion of the circuit in the minority of patients with continuous loop tachycardias.

Continuous infusion of oxytocin prevents induction of uterine oxytocin receptor and blocks luteal regression in cyclic ewes.

Continuous intravenous infusion of oxytocin (3 micrograms/h) between Days 13 and 21 after oestrus delayed return to oestrus by 7 days (length of cycle 23.3 +/- 0.6 days compared to 16.6 +/- 0.2 days in control ewes). At a lower infusion rate (0.3 micrograms/h) oxytocin delayed luteolysis in only 2 of 5 ewes. Treatment from Day 14, when luteolysis had already begun, was ineffective. Delay of luteal regression by oxytocin had no effect on the length of subsequent cycles. Measurement of circulating progesterone concentrations and luteal weight showed that prolongation of the oestrous cycle was due to prevention of luteal regression. Luteal regression and behavioural oestrus were induced during continuous oxytocin administration begun on Day 13 when cloprostenol was given on Day 15 (mean cycle length, 17.3 +/- 0.21 days). Continuous oxytocin infusion from Day 13 blocked the rise in uterine oxytocin receptor concentrations which normally precedes oestrus. Mean receptor concentrations in caruncular and intercaruncular endometrium and in myometrium were 76, 36 and 9 fmol/mg protein on Day 17 in ewes receiving continuous oxytocin (3 micrograms/h); in control ewes these values were 675, 638 and 130 fmol/mg protein respectively at oestrus. Receptor concentrations on the day of oestrus in ewes receiving oxytocin and cloprostenol were not significantly different from those in control ewes (649, 852, and 109 fmol/mg protein respectively). Since cloprostenol, a PGF-2 alpha analogue, overcame the antiluteolytic action of oxytocin, it is suggested that continuous oxytocin treatment may inhibit uterine production of PGF-2 alpha, possibly by down regulating the uterine oxytocin receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Usefulness of programmed stimulation in predicting efficacy of propafenone in long-term antiarrhythmic therapy for paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous (i.v.) and oral propafenone were evaluated in 14 patients with Wolff-Parkinson-White syndrome and in 10 patients with atrioventricular (AV) nodal reentrant tachycardia. The effective refractory periods of the right atrium and the AV node increased after both preparations. In patients with Wolff-Parkinson-White syndrome, i.v. propafenone blocked anterograde accessory pathway conduction in 2 patients and retrograde conduction in 1; during oral therapy, accessory pathway conduction block occurred in 2 additional patients. The mean cycle length of the supraventricular tachycardia (SVT) increased from 338 ± 60 ms to 387 ± 56 ms (p < 0.05) after i.v. application, and from 336 ± 65 ms to 367 ± 65 ms (p < 0.05) during oral propafenone. The shortest pacing interval maintaining a 1:1 AV conduction increased from 325 ± 65 ms to 368 ± 81 ms (p < 0.05) after i.v. infusion, and from 333 ± 57 ms to 369 ± 75 ms (p < 0.05) during oral therapy. There was no difference in the electrophysiologic effects between i.v. and oral propafenone. The induction of SVT was prevented by i.v. propafenone in 10 of 20 patients and in 4 additional patients with oral propafenone. During follow-up, 6 of 7 patients, whose SVT could not be initiated by electrophysiologic drug testing, remained free from recurrences, whereas 5 of 7 patients with inducible tachycardia had recurrences of SVT. Thus, in patients with SVT, propafenone prolonged accessory pathway and AV nodal conduction and had a beneficial effect on circus movement tachycardia. Electrophysiologic drug testing with propafenone predicts its efficacy during chronic therapy in most patients.

Suppression of prostaglandin F-2 alpha release and delay of luteolysis after active immunization against oxytocin in the goat.

Active immunization against oxytocin significantly prolonged the oestrous cycle in 3 out of 4 goats; the mean (+/- s.e.m.) cycle length was 29.1 +/- 1.7 days (n = 12) compared to 19.4 +/- 0.6 days (n = 9) in control animals. During Days 10-21 of the cycle in the 3 responsive goats, peripheral plasma concentrations of progesterone and oxytocin were steady and those of 13,14-dihydro-15-keto-prostaglandin F-2 alpha were very low (50-100 pg X ml-1) with no marked pulsatile activity. The major effect of immunization would appear to be suppression of the synthesis of the uterine luteolysin PGF-2 alpha, thus confirming that endogenous oxytocin has a facilitatory role in luteolysis via prostaglandin production.