Follow-up X Rays Play a Key Role in Detecting Implantable Cardioverter Defibrillator Lead Fracture:

MORISHIMA, I., et al .: Follow-up X Rays Play a Key Role in Detecting Implantable Cardioverter Defibrillator Lead Fracture: A Case of Incessant Inappropriate Shocks Due to Lead Fracture. A patient with an implantable cardioverter defibrillator (ICD) received incessant inappropriate shocks due to a lead fracture 3 years after implantation. Routine lead measurements at 3-month intervals had shown no abnormal findings even at the most recent measurement performed 2 months prior to the event. In contrast, serial observation of chest X rays clearly disclosed progressive lead narrowing starting 11 months prior to the event. This case indicates the importance of the routine chest X rays in long-term follow-up of ICDs and sets a precedent for interpreting lead narrowing in such X rays. (PACE 2003; 26[pt. I]:911–913)     

Potentiation of Acute Toxicity of 2-sec-Butylphenyl N-Methylcarbamate (BPMC) by Fenthion in Mice

Potentiation of Acute Toxicity of 2-sec-Butylphenyl N-methylcarbamate(BPMC) by Fenthion in Mice. MIYAOKA, T., TAKAHASHI, H., TSUDA,S., AND SHIRASU, Y. (1984). Fundam. Appl. Toxicol. 4, 802–807.This study was undertaken to determine whether interactionsof toxicologic importance might occur during combined exposureof male mice to 2-sec-butylphenyl N-methylcarbamate (BPMC) andO,O-dimethyl O-(3-methyl-4-methylthiophenyl)phosphorothioate(fenthion). The equitoxic (administration of BPMC and fenthionresulted in only a 1.6-fold potentiation compared to the expectedLD50. However, 1 hr oral pretreatment with 3 (1/100 LD50), 7.5,15, and 30 mg/kg of fenthion resulted in 5-, 9-, 12-, and 15-foldpotentiation of the acute oral toxicity of BPMC, respectively.This fenthion pretreatment caused significant increases in theBPMC plasma concentrations and in the area under the concentration-timecurve. The increase of the plasma concentrations of BPMC dependedupon the fenthion dose and was associated with that of the potencyratio. The pretreatment of fenthion prolonged the hexobarbitalsleeping time. The plasma concentrations of BPMC after the administrationof a dose of LD2.5 (20 mg/kg) in fenthion-pretreated mice wereclearly lower than those of a dose of LD2.5 (195 mg/kg) in nontreatedmice. These results suggested that fenthion pretreatment causedthe potentiation of the acute toxicity of BPMC partially bythe inhibition of detoxification of BPMC.     

A case of pseudo-Bartter's syndrome due to intestinal malrotation

Intestinal malrotation presenting beyond the neonatal period is associated with a multiplicity of symptoms, which are often non-specific and, consequently, are associated with delays in diagnosis. Pseudo-Bartter's syndrome, which mimics the manifestations of Bartter's syndrome, can be caused by a severe chloride deficiency secondary to vomiting, diarrhea, perspiration, diuretic abuse and so on. We describe a 6 year old boy who had been admitted to hospital three times during the preceding year. The patient lapsed into a critical condition with profound hypochloremia and hypokalemic metabolic alkalosis induced by extremely massive vomiting. The attacks of vomiting were spasmodic and self-limited. During the episodes of vomiting he fulfilled the criteria of pseudo-Bartter's syndrome, including hyperreninemia, hyperaldosteronism and normal blood pressure, but in the intervals between attacks he was completely asymptomatic. At the third admission, examination supported an overall clinical picture of bowel obstruction, which was confirmed by radiographic examination. Laparotomy revealed a midgut volvulus with intestinal malrotation. After surgery he made a good recovery and was symptom-free. In this patient, the high degree of hypochloremia and hypovolemia activated the renin-angiotensin-aldosterone system, then aldosterone promoted intensive reabsorption of sodium and excretion of potassium into the urine. Consequently the diagnosis of pseudo-Bartter's syndrome was established on the basis of an extreme decrease in urinary chloride and an increase in urinary potassium concentration. It is relatively rare for vomiting due to intestinal malrotation to induce pseudo-Bartter's syndrome. The importance of considering this rare diagnosis in such cases is discussed.     

Drug Metabolism: Intestinal Bacterial Hydrolysis is Required for the Appearance of Compound K in Rat Plasma after Oral Administration of Ginsenoside Rb1 from Panax ginseng

Ginsenoside Rb₁ from Panax ginseng root is transformed into compound K via ginsenosides Rd and F₂ by intestinal bacterial flora. Among 31 defined intestinal strains from man, only Eubacterium sp. A-44 transformed ginsenoside Rb₁ into compound K via ginsenoside Rd. The ginsenoside Rb₁-hydrolysing enzyme isolated from Eubacterium sp. A-44 was identical to a previously purified geniposide-hydrolysing β-D-glucosidase. When ginsenoside Rb₁ (200 mg kg^?1) was administered orally to germ-free rats, neither compound K nor any other metabolite was detected in the plasma, intestinal tract or cumulative faeces 7 or 15 h after administration. Most of the ginsenoside Rb₁ administered was recovered from the intestinal tract, especially the caeca, and cumulative faeces indicating poor absorption of ginsenoside Rb₁. When ginsenoside Rb₁ was administered orally to gnotobiote rats mono-associated with Eubacterium sp. A-44, a significant amount of compound K was detected in the plasma and considerable amounts were found in the caecal contents and cumulative faeces 7 and 15 h after administration. A small amount of ginsenoside Rb₁ was detected in the caecal contents only 7 h after administration. These results indicate that orally administered ginsenoside Rb₁ is poorly absorbed from the gut but that its metabolite compound K, produced by ginsenoside Rb₁-hydrolysing bacteria such as Eubacterium sp. A-44 in the lower part of intestine, is absorbed.     

Survey of conformational role of ester bonds in a cyclic depsipeptide

The effect of ester bond on the conformation of peptide molecule was studied by designing and synthesizing a model tetradepsipeptide cyclo(-l -Ala-l -Hmb-)z and by analyzing the conformation both theoretically and experimentally. Theoretical analysis showed that both ester and peptide bonds in the calculated low-energy conformations within 3 kcal/mol of the global minimum take a trans but distorted configuration. The distortion is larger in ester bonds than in peptide bonds. Further, the four carbonyls project from one side of the plane of the cyclic backbone, whereas the side chains project from the other side. These results are consistent with the experimental results obtained by NMR measurement; first, the coupling constant deduced from ¹H-NMR species in DMSO-d₆ is consistent with the dihedral angles of the calculated low-energy conformations; second, results of NOE measurement can reproduce the calculated configuration of the carbonyls and side chains. From the consistency between theoretical and experimental results, it is concluded that this model tetradepsipeptide takes an all-trans backbone conformation in solution and this backbone conformation is stabilized by large distortion in the ester bond, which compensates the strain resulted from the 12-membered cyclic backbone structure consisting only of L-residues.     

Vagal Enhancement as Evidence of Residual Ischemia After Inferior Myocardial Infarction

Background: Acute inferior myocardial infarction (MI) often induces transient sinus bradycardia through vagal enhancement, known as Bezold-Jarisch reflex, which is explained by preferential distribution of vagal nerve in the inferior wall. We examined vagal activity in relation to the occurrence of residual ischemia in patients with old inferior MI and assessed its diagnostic usefulness.
Methods: Exercise myocardial scintigraphy was performed in 15 patients with old inferior MI, 19 angina pectoris (AP) patients with inferior ischemia but no MI, and 32 control subjects who had no evidence of cardiac disease. We analyzed the connection of residual ischemia in old MI with ST-segment response to exercise and with vagal activity as determined by coefficient of component variance of high frequency (CCV_HF).
Results: Exercise-induced percentage change in CCV_HF was higher in patients with old MI and residual ischemia (18.8 ± 13.5%) and AP (5.5 ± 9.7%) than old MI but no residual ischemia (–24.1 ± 4.9%) or control (–22.8 ± 4.5%, P = 0.006). Percentage change in CCV_HF > –5% had a good diagnostic value for the detection of residual ischemia in patients with old inferior MI with sensitivity of 83%, specificity of 89%, accuracy of 87%, and positive likelihood ratio of 7.50, which was higher than that of ST-segment depression (67%, 50%, 56%, and 1.33).
Conclusions: Vagal enhancement was associated with residual ischemia in old inferior MI as well as inferior AP. Measurement of CCV_HF is useful in improving the diagnostic reliability of exercise electrocardiography in patients with old inferior MI.