Understanding Organisms Using Ecological Observatory Networks.

Human activities are rapidly changing ecosystems around the world. These changes have widespread implications for the preservation of biodiversity, agricultural productivity, prevalence of zoonotic diseases, and sociopolitical conflict. To understand and improve the predictive capacity for these and other biological phenomena, some scientists are now relying on observatory networks, which are often composed of systems of sensors, teams of field researchers, and databases of abiotic and biotic measurements across multiple temporal and spatial scales. One well-known example is NEON, the US-based National Ecological Observatory Network. Although NEON and similar networks have informed studies of population, community, and ecosystem ecology for years, they have been minimally used by organismal biologists. NEON provides organismal biologists, in particular those interested in NEON's focal taxa, with an unprecedented opportunity to study phenomena such as range expansions, disease epidemics, invasive species colonization, macrophysiology, and other biological processes that fundamentally involve organismal variation. Here, we use NEON as an exemplar of the promise of observatory networks for understanding the causes and consequences of morphological, behavioral, molecular, and physiological variation among individual organisms.

Paired comparisons of efficacy of intravenous and oral procainamide in patients with inducible sustained ventricular tachyarrhythmias.

Thirty-eight patients who had inducible sustained ventricular tachycardia during baseline programmed electrical stimulation underwent electrophysiologic testing after both intravenous and oral administration of procainamide. Each had presented clinically with documented sustained ventricular tachycardia or out of hospital cardiac arrest not associated with acute myocardial infarction. In 23 patients (61%) (Group I) the arrhythmia became noninducible during an intravenous infusion of procainamide. Oral procainamide was subsequently administered and retesting was carried out after dose titration to match plasma concentration at the end of the intravenous study. Among the 23 patients in Group I the mean (+/- SD) plasma procainamide level was 7.2 +/- 2.8 micrograms/ml after intravenous dosing and 7.9 +/- 2.5 micrograms/ml after oral dosing (p = 0.09). In 15 (65%) of the 23 patients, sustained ventricular arrhythmia was inducible on oral therapy with comparable plasma procainamide levels (intravenous = 6.3 +/- 2.1 micrograms/ml, oral = 7.5 +/- 2.1 micrograms/ml). The other eight patients (35%) had concordant responses to repeat testing with comparable intravenous (mean 9.0 +/- 3.3 micrograms/ml) and oral (8.8 +/- 3.1 micrograms/ml) plasma procainamide levels. In the additional 15 patients (Group II) sustained ventricular tachyarrhythmia remained inducible on intravenous procainamide therapy and the patients were retested on oral therapy with similar plasma concentration (p = 0.05). In seven patients (47%) sustained ventricular tachyarrhythmia was noninducible on treatment with oral procainamide (mean plasma level 7.6 +/- 2.7 micrograms/ml) after failure of intravenous procainamide (mean plasma level 10.3 +/- 2.3 micrograms/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Entrainment of circus movement tachycardia utilizing an accessory pathway with long retrograde conduction times during ventricular and atrial stimulation.

An unusual case is presented in which a circus movement tachycardia incorporating an accessory pathway with long retrograde conduction time was transiently entrained. Overdrive high right atrial stimulation produced entrainment without atrial fusion since collision of anterograde and retrograde impulses took place within the accessory pathway. Tachycardia termination occurred when, at a faster pacing rate, an atrial impulse that collided in the accessory pathway was blocked at the atrioventricular (AV) node. In contrast, the entrainment seen during right ventricular apical stimulation was characterized by the occurrence of both fusion and collision within the ventricles. The tachycardia was terminated when a pure paced impulse that collided in the normal pathway was blocked in a retrograde direction in the accessory pathway. These data indicate that: 1) transient entrainment of this arrhythmia (circus movement tachycardia) can be identified by the classical criteria used to diagnose it, provided that fusion and collision occur within the ventricles; and 2) the accessory pathway is the weak link for tachycardia termination only during ventricular pacing since the AV node is the weak link during atrial stimulation.

Cardiac arrest in an adolescent with atrial fibrillation and hypertrophic cardiomyopathy.

A 15 year old youth, who presented with out-of-hospital cardiac arrest due to documented ventricular fibrillation, was found to have nonobstructive hypertrophic cardiomyopathy. Electrophysiologic study demonstrated inducible sustained atrial fibrillation with a rapid ventricular response. This rhythm, associated with hypotension and evidence of myocardial ischemia, spontaneously degenerated into ventricular fibrillation. No ventricular arrhythmias were inducible by programmed ventricular stimulation. Therapy with metoprolol and verapamil slowed the ventricular rate during atrial fibrillation and maintained hemodynamic stability, both during follow-up electrophysiologic study and during a subsequent spontaneous episode.

Changes in spontaneous sinus node rate as an estimate of cardiac autonomic tone during stable and unstable ventricular tachycardia.

Changes in sinus node rate were measured as an estimate of reflex control of cardiac autonomic tone during 32 episodes of stable ventricular tachycardia (without loss of consciousness) and 21 episodes of unstable ventricular tachycardia (loss of consciousness requiring electrical cardioversion) in 32 patients without retrograde ventriculoatrial conduction. Sinus node rate was measured before induction of ventricular tachycardia (at 5 s intervals during tachycardia) and 5 s after termination of ventricular tachycardia. It increased from 85 +/- 12 beats/min to a maximum of 109 +/- 25 beats/min during stable ventricular tachycardia (p less than 0.001) and from 82 +/- 15 beats/min to a maximum of 105 +/- 34 beats/min during unstable ventricular tachycardia (p less than 0.001). During unstable ventricular tachycardia, the increase in sinus rate was more abrupt and was followed by a sharp decrease beginning before termination of the tachycardia and resulting in a slower rate after termination (56 +/- 15 beats/min) than before tachycardia (p less than 0.001). Stable ventricular tachycardia resulted in a continuous increase of sinus node rate, which remained higher after termination (102 +/- 15 beats/min) than before tachycardia (p less than 0.001). Autonomic mechanisms responsible for changes in sinus rate were evaluated by reinducing the ventricular tachycardia after beta-adrenergic blockade by propranolol in 10 patients. Intravenous propranolol (mean dose 11 +/- 4 mg) had no effect on the magnitude of increase in sinus rate (+18 +/- 6 beats/min before and +17 +/- 7 beats/min after propranolol).(ABSTRACT TRUNCATED AT 250 WORDS)

Outcome of resuscitation from bradyarrhythmic or asystolic prehospital cardiac arrest.

Previous studies of outcome as a function of the initial electrophysiologic mechanisms recorded at the scene of prehospital cardiac arrest have demonstrated that bradyarrhythmias and asystole have the worst prognosis. In this report, our observations in bradyarrhythmic and asystolic arrests occurring from 1980 to 1982 are compared with those from 1975 to 1978. From 1980 to 1982, 61 (27%) of 225 cardiac arrest events meeting entry criteria for the study were bradyarrhythmic or asystolic. Only 2 (8%) of 24 patients with asystole and 1 (20%) of 5 patients with sinus bradycardia survived prehospital intervention. Only 1 of these 29 patients was discharged from the hospital alive. In contrast, 15 (47%) of 32 patients who presented with idioventricular rhythm at initial contact survived prehospital intervention and were hospitalized, and 8 (25%) of these 32 were ultimately discharged alive. When compared with the 1975 to 1978 patients with bradyarrhythmia and asystole, both prehospital survival (8 versus 30%, p less than 0.001) and survival after hospitalization (0 versus 15%, p less than 0.05) significantly improved, but the improvement occurred predominantly in the subgroup with idioventricular rhythm. Survivors within this subgroup tended to have a prompt response to prehospital pharmacologic interventions that were not available to the 1975 to 1978 group. The response was manifested by return to a sinus mechanism or increase in the rate of idioventricular rhythm. In conclusion, outcome has improved for a specific subgroup of victims of prehospital cardiac arrest with bradyarrhythmia or asystole; the improved outcome may relate to field interventions by rescue personnel at the scene of arrest but the mortality rate is still high.

Time to first shock and clinical outcome in patients receiving an automatic implantable cardioverter-defibrillator.

The relation between time to first shock and clinical outcome was studied in 60 patients who received an automatic implantable cardioverter-defibrillator (AICD) from August 1983 through May 1988. The mean (+/- SD) patient age was 64 +/- 10 years, 82% were men and the mean ejection fraction was 33 +/- 13%. During follow-up, 38 patients (63%) had one or more shocks; there were no differences in age, gender distribution or ejection fraction at entry between the shock and no shock groups. Among 51 patients with coronary artery disease, 31 (61%) had one or more shocks, whereas all seven patients with cardiomyopathy had one or more shocks (p less than 0.05). Neither of the two patients with idiopathic ventricular fibrillation had shocks. Of the 13 deaths, 12 occurred during post-hospital follow-up and 1 during the index hospitalization. Of the four sudden post-hospital deaths, only one was due to tachyarrhythmia in the absence of acute myocardial infarction. All four sudden deaths and five of eight post-hospital nonsudden deaths occurred in patients who had had one or more appropriate shocks during follow-up. Eight of the nine first appropriate shocks among patients who subsequently died occurred within the first 3 months of follow-up, but the actual deaths were delayed to a mean of 14.1 +/- 13.9 months (p less than 0.05). The mean time to all deaths was 14.8 +/- 13.1 months. The ejection fraction was significantly lower among patients who died than among patients who survived (25 +/- 7% versus 35 +/- 14%, p less than 0.02), but it did not distinguish risk of first shocks.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic effects of diltiazem hydrochloride on supraventricular tachycardia.

The effects of intravenous diltiazem hydrochloride (0.25 mg/kg body weight) were studied in eight patients with nine episodes of supraventricular tachycardia. Five episodes of tachycardia were due to atrioventricular (A-V) nodal reentry (group A), two were due to retrograde utilization of a concealed A-V accessory pathway (group B) and two were episodes of atrial fibrillation (group C). Intravenous administration of diltiazem slowed the ventricular rate in eight of nine episodes of tachycardias. Supraventricular tachycardia was terminated within 2 minutes after intravenous diltiazem in four of five patients in group A, and one of two in group B. Cycle length alternation was observed before termination of the arrhythmia in two patients from group A. In group C the ventricular response slowed but also became regular during atrial fibrillation. Although diltiazem depressed both anterograde and retrograde conduction as assessed by programmed stimulation, tachycardia termination or slowing or alternation of cycle length all occurred because of the effects of diltiazem predominantly on anterograde A-V nodal properties during supraventricular tachycardia. Although no statistical conclusions can be made from this limited study, it appears that diltiazem has significant depressant electrophysiologic effects on both anterograde and retrograde A-V nodal function as assessed by programmed stimulation during sinus rhythm. Further electrophysiologic studies are needed before determining the clinical efficacy of this agent for treatment or prophylaxis of recurrent supraventricular tachycardias.

Quintuple pathways participating in three distinct types of atrioventricular reciprocating tachycardia in a patient with Wolff-Parkinson-White syndrome.

Electrophysiologic studies were performed in a patient with recurrent supraventricular tachyarrhythmias. Sinus and paced atrial beats had QRS complexes characteristic of atrioventricular (A-V) conduction through a manifest left lateral accessory pathway (Wolff-Parkinson-White syndrome, type A). Three distinct types of A-V reciprocating tachycardia and three different modes of retrograde atrial activation were demonstrated. Type 1 tachycardia involved the slow A-V nodal pathway and a second (left lateral or left paraseptal) accessory A-V pathway capable of retrograde conduction only. Type 2 tachycardia was of the slow-fast A-V nodal pathway type. Type 3 tachycardia involved in heretofore undescribed circuit in that retrograde conduction occurred through an accessory A-V pathway with long retrograde conduction times and anterograde conduction through both the manifest left lateral accessory A-V pathway and fast A-V nodal pathway. Premature ventricular beats delivered late in the cycle of this tachycardia advanced (but did not change) the retrograde atrial activity without affecting the timing of the corresponding anterograde H deflection. In summary, this patient had five (three accessory and two intranodal) pathways participating in three different types of A-V reciprocating tachycardia; the recurrence of these were prevented with oral amiodarone therapy.

Characteristics of entrainment during autodecremental atrial and ventricular stimulation.

The entrainment characteristics of orthodromic circus movement tachycardias occurring during autodecremental atrial and ventricular stimulation were studied in 9 patients with manifest Wolff-Parkinson-White syndrome. The phenomenon occurred in 34 of 38 episodes of tachycardia during autodecremental atrial stimulation. It was not seen in 4 episodes because the first impulse penetrating the circuit terminated the arrhythmia. Invariably, the HH and VV intervals were not equal to, but longer than, the stimulus-stimulus intervals, thus not fulfilling the definition of "classic" (constant cycle length) entrainment postulated by Okumura et al. Furthermore, the first 2 of the 3 diagnostic criteria were not demonstrated and the third only could be demonstrated in 7 episodes. Tachycardia termination was achieved in all 38 episodes. Entrainment occurred during autodecremental ventricular stimulation in 79 of 80 episodes, with the AA and H-H- intervals (when visible) being equal to the corresponding paced cycle lengths. Moreover, the intervals between the last paced ventricular beat and the first ventricular beat of the resumed tachycardia were invariably longer than the last stimulus-stimulus intervals. These characteristics were those which Okumura et al attributed to "concealed" entrainment. Tachycardia termination was achieved in 77 of 80 episodes. In summary: (1) autodecremental atrial pacing produced a specific form of entrainment that did not fulfill the "classic" definition of Okumura et al; (2) autodecremental ventricular pacing consistently produced "concealed" entrainment; and (3) autodecremental stimulation was very effective in terminating 115 of 118 (98%) of episodes of circus movement tachycardias.

Entrainment of atrioventricular nodal reentrant tachycardias during overdrive pacing from high right atrium and coronary sinus. With special reference to atrioventricular dissociation and 2:1 retrograde block during tachycardias.

Entrainment was attempted during electrophysiologic evaluation of 8 patients with atrioventricular (AV) nodal reentrant tachycardia. Entrainment could be performed while pacing from the high right atrium in 35 of 35 episodes, from proximal coronary sinus in 9 of 21 episodes and from distal coronary sinus in 10 of 20 episodes. The minimal rates required were 8 to 40 beats/min faster than those of the tachycardias. That the atria (as defined in electrophysiologic studies) were not a necessary component of the reentry circuit was suggested by the occurrence, during tachycardia, of short episodes of AV dissociation and of 1 episode of 2:1 retrograde block. For the tachycardia to be interrupted, the pacing rate usually had to be slightly faster than that required to entrain, as well as sufficiently rapid to produce anterograde block of an atrial impulse in the slow AV nodal pathway. Moreover, termination of tachycardia apparently was a function of the pacing site. In some episodes, either because of a proximity effect or because of a preferential input into the upper common pathway, coronary sinus pacing terminated the tachycardia at slower rates or with fewer stimuli than high right atrial pacing. Thus, patients with drug-resistant AV nodal reentrant tachycardias may benefit from recently introduced pacing techniques for termination of tachycardia through entrainment.

Linking phenomenon during atrial stimulation with accessory pathways.

Linking is an electrophysiologic phenomenon in which each successive impulse entering a macroreentry circuit propagates preferentially along 1 limb because of the functional impedance to conduction in the contralateral limb produced by the previous impulse. Electrophysiologic studies were performed in 12 patients with a bidirectionally conducting accessory pathway. Linking was analyzed while 1:1 atrioventricular conduction took place through the normal pathway. When atrial pacing (at the same cycle length) could be initiated during sinus rhythm in patients with rapidly conducting accessory pathways, linking was dynamically maintained by repetitive local refractoriness (interference). When it could be initiated during the usual type of orthodromic circus movement tachycardia, linking was sustained by actual impulse collision, the underlying mechanism having also been called entrainment. When it could be initiated during sinus rhythm in a patient with a slowly conducting accessory pathway, linking was maintained by impulse collision, but the underlying mechanism could not be called entrainment because stimulation had not been started during tachycardia. This study showed that 2 terms--linking and entrainment--may be applied to the same mechanism and, conversely, that the same name could not be used in reference to the same mechanism when pacing was initiated under different circumstances. However, using the proposed conceptual formulation for linking, it is apparent that seemingly diverse mechanisms associated with macroreentry circuits involving accessory pathways are, in fact, variations on a common electrophysiologic theme.

Significance of pacing cycle lengths in manifest entrainment of orthodromic circus movement tachycardia by ventricular pacing.

The physiology of entrainment of orthodromic circus movement tachycardia (CMT) was studied using ventricular pacing during 18 episodes of induced CMT in 7 patients with atrioventricular (AV) accessory pathways. The first paced impulse was delivered as late as possible in the tachycardia cycle (mean 88 +/- 5% of the spontaneous cycle length [CL]). Entrainment was demonstrated by the following criteria: 1:1 retrograde conduction via the accessory pathway; capture of atrial, ventricular and His bundle electrograms at the pacing rate; and resumption of tachycardia at its previous rate after cessation of pacing. The number of ventricular paced impulses ranged from 5 to 14 (mean 8 +/- 3), and entrainment occurred in 2 to 7 paced cycles (mean 4 +/- 2). Orthodromic activation of a major part of the reentry circuit (manifest entrainment) was demonstrated during 9 episodes by the occurrence of His bundle electrogram preceding the first CMT QRS at the time anticipated from the last paced beat. In the 9 other episodes, persistent retrograde His bundle activation and AV nodal penetration by each paced impulse caused a delay (mean 79 +/- 25 ms) in activation of the His bundle preceding the first CMT QRS after the last paced beat. The mean pacing CL achieving manifest entrainment was 92 +/- 3% of the tachycardia CL, compared with 84 +/- 3% for retrograde AV nodal penetration (p less than 0.01). In conclusion, manifest entrainment of orthodromic CMT can be demonstrated by ventricular pacing at very long CLs; shorter CLs may cause CMT termination due to retrograde AV nodal penetration.

QRS morphology-dependent pharmacodynamics in multiform ventricular ectopic activity.

The effect of an infusion of intravenous procainamide on the frequency of ventricular premature complexes (VCPs) of differing QRS morphologies was studied in 20 patients with multiform ectopic activity. In 17 of 20 patients, there was differential suppression of single VPCs with different QRS morphologies. VPCs of the most frequent QRS morphology and the second most frequent QRS morphology were compared with respect to the procainamide level at the escape of VPCs from 85% suppression and the duration of suppression measured from the onset of the procainamide infusion. In 8 patients, VPCs of the most frequent QRS morphology remained suppressed at lower procainamide concentrations and for longer times than did VPCs of the second most frequent QRS morphology (escape procainamide concentration = 2.8 +/- 1.7 versus 5.4 +/- 2.3 micrograms/ml, p less than 0.025; time to escape 244 +/- 138 versus 98 +/- 114 min; p less than 0.05). In 9 other patients, VPCs of the second most frequent QRS morphology remained suppressed at lower procainamide concentrations and for longer times than did VPCs of the most frequent QRS morphology (escape procainamide concentration 2.9 +/- 1.4 versus 8.3 +/- 6.3 micrograms/ml, p less than 0.025; time to escape 317 +/- 114 versus 63 +/- 80 min; p less than 0.001). Thus, in individual patients there are specific patterns of suppression of VPCs of different QRS morphologies which are independent of the frequency of each morphology. There is apparently a differential pharmacologic effect of procainamide on the foci or pathways responsible for the different QRS morphologies of multiform VPCs.

Annihilation, entrainment and modulation of ventricular parasystolic rhythms.

Annihilation and one-to-one entrainment of modulated parasystolic rhythms in humans has not been previously discussed. In 9 nonmedicated patients, it was possible to measure the intrinsic, parasystolic ectopic cycle length given by the intervals between 2 consecutive parasystolic beats without any interposed nonparasystolic beat. The corresponding values varied between 960 and 2,350 ms (corresponding to rates between 62 and 26 beats/min). In addition, modulation could be determined, because nonparasystolic beats falling during the initial 59% of the cycle prolonged the parasystolic cycle length (by 12 to 37.5%), whereas those that fell later in the cycle shortened it (by 9 to 25%). Plotting this prolongation or shortening as a function of the temporal position of the nonparasystolic beats in the cycle yielded biphasic response curves, of which 7 were symmetric and 2 asymmetric. In 2 patients, episodes of concealed one-to-one entrainment were initiated by late nonparasystolic (sinus) beats and, later on, terminated by early ventricular extrasystoles. In 2 other patients (and in 2 separate occasions) nonparasystolic beats, falling in part of the cycle located in between those of maximal delay and acceleration, produced pacemaker annihilation (cessation of automatic activity for the remaining monitoring time). Parasystolic annihilation and concealed entrainment may be one of the causes that can explain the large, spontaneous, day-to-day variability in the incidence of ectopic ventricular beats reported in Holter recordings. Nevertheless, future prospective studies performing interventions that can change the sinus and ectopic rates are required to corroborate our finding.

Concealment of manifest, and exposure of concealed, ventricular parasystole produced by isoproterenol.

Few studies have dealt with the effects of isoproterenol on ventricular parasystole. Intravenous isoproterenol (2 to 4 micrograms/min) was administered to 11 nonmedicated patients with ventricular parasystole. At the onset of the drip infusion, 8 patients had continuous parasystole, 2 had intermittent parasystole, and 1 patient (in whom intermittent parasystole was documented 2 to 5 days earlier) showed no manifest parasystolic activity. In all patients, whose control parasystolic cycle length varied between 960 and 2,530 ms, isoproterenol caused a decrease of the parasystolic cycle lengths ranging from 12 to 36%. Therefore, isoproterenol produced a consistent increase of the parasystolic rate. In 4 patients, parasystolic activity ceased to be manifest when the concomitantly enhanced (by isoproterenol) sinus cycle lengths became shorter than 430 ms. This phenomenon reflected a tachycardia-dependent parasystolic concealment, presumably as a result of interference in the parasystolic-ventricular junction. In every case, the arrhythmia reappeared at its initial rate upon stopping the drip infusion. In no patient did parasystolic ventricular tachycardia develop. In the patient without manifest parasystolic beats, isoproterenol unmasked the intermittent parasystole that previously had been intrinsically manifest. The latter effect reflected a true exposure, or unmasking of a latent, rate-independent concealed, parasystolic focus.(ABSTRACT TRUNCATED AT 250 WORDS)

Surgical management of post-myocardial infarction ventricular tachyarrhythmia by myocardial debulking, septal isolation, and myocardial revascularization.

Sustained ventricular tachycardia or ventricular fibrillation, associated with severely depressed left ventricular function after myocardial infarction, carries a poor prognosis. We have used an extensive surgical procedure in 18 patients (15 men and three women) with a mean age of 63 years who had more than three episodes of recurrent, hemodynamically significant ventricular tachycardia or fibrillation and congestive heart failure. The operation consisted of complete myocardial revascularization and myocardial debulking by extensive infarctectomy with unguided endocardial resection and septal isolation with support of the necrotic wall with a Teflon patch. Implantable defibrillator patches were placed in eight patients. Blood cardioplegia and intra-aortic balloon assist (12 patients) were used for perioperative myocardial preservation. Postoperative studies demonstrated a significant increase in ejection fraction (n = 16) and a decline in pulmonary wedge pressure. Hospital mortality was 16% (three patients). Two deaths were due to congestive heart failure and one to arrhythmia. During postoperative electrophysiologic studies, ventricular tachycardia was not inducible in six of eight patients (75%). During a mean follow-up of 24 months, 11 of 15 patients who survived operation are alive and are in New York Heart Association Class I or II. Three of four late deaths were due to congestive heart failure and drug toxicity and one was arrhythmia related. This procedure is effective for preventing recurrent ventricular tachycardia or fibrillation in a majority of patients who cannot have intraoperative mapping.

Occurrence of paralytic shellfish poison in Bangladeshi freshwater puffers.

Two species of freshwater puffer fish, Tetraodon cutcutia and Chelonodon patoca, collected from several locations in Bangladesh, showed lethal potency in mice ranging from 2.0 to 40.0 MU/g tissue as paralytic shellfish poison. In both species, toxicity of the skin was generally higher than the other tissues examined (muscle, liver and ovary). Water-soluble toxins from T. cutcutia were partially purified by activated charcoal treatment followed by column chromatographies using Bio-Gel P-2 and Bio-Rex 70. Analyses by cellulose acetate membrane electrophoresis and high-performance liquid chromatography with fluorometric detection demonstrated that the toxins were composed of saxitoxin, decarbamoylsaxitoxin, gonyautoxins 2 and 3, decarbamoylgonyautoxins 2 and 3, and three unidentified components which are possibly related to paralytic shellfish poison.

Occurrence of a methyl derivative of saxitoxin in Bangladeshi freshwater puffers.

A new component of paralytic shellfish poison was isolated from a Bangladeshi freshwater puffer Tetraodon cutcutia. Its structure was deduced to be carbamoyl-N-methylsaxitoxin based on electrospray ionization mass spectrometry, [1H] NMR, and conversion experiments.

Two new isomers of domoic acid from a red alga, Chondria armata.

Isodomoic acids G and H, two new isomers of the neurotoxin domoic acid, along with isodomoic acids A, B, E and F, were isolated from a red alga, Chondria armata, collected at the southern tip of Kyushu Island. The structures of two of these were deduced to be (E, E) and (Z, E) isomers of 2-carboxy-4-(5-carboxy-l-methyl-2-hexenylidene)-3-pyrro- lidineacetic acid, based on electrospray ionization mass and [1H]nuclear magnetic resonance spectral analyses including [1H-1H]correlation spectroscopy and nuclear Overhauser effect correlation spectroscopy.