α_2受体阻滞后肾上腺素诱导的心衰病人血小板的聚集功能

先前的研究表明血小板α_2受体变化表征交感神经突触前α_2受体的变化。为了解心衰病人血小板α_2受体功能状况,我们观察了10例Ⅲ、Ⅳ级心功能的心衰病人及10例配对正常人由肾上腺素诱导的血小板聚集率在α_2受体阻滞前后的变化。结果表明肾上腺素诱导的血小板聚集率在两组无显著性差异,但应用α_2阻滞剂Rauwolscine(0.25mg/L)后,0.25,0.5,1.0mg/L E诱导的心衰病人血小板聚集率显著低于对照组,提示血小板α_2受体在心衰时有数量的减少或(和)功能的降低,表征交感神经突触前NE释放的负反馈机制被抑制。     

Altered neuropeptide Y Y1 responses in mesenteric arteries in rats with congestive heart failure

The aim of the present study was to elucidate if the potentiating effect of neuropeptide Y on various vasoactive agents in vitro is (1) altered in mesenteric arteries from rats with congestive heart failure and (2) mediated by the neuropeptide Y Y₁ receptor. The direct vascular effects of neuropeptide Y and its modulating effects on the contractions induced by endothelin-1-, noradrenaline-, 5-hydroxytryptamine (5-HT)-, U46619-(9, 11-dideoxy-11, 9-epoxymethano-prostaglandin F₂) and ATP, and acetylcholine-induced dilatations were studied in the presence and absence of the neuropeptide Y Y₁ antagonist, BIBP3226 (BIBP3226{(R)-N2-(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]- -arginine-amide}). Neuropeptide Y, per se, had no vasoactive effect in the arteries. The potency of endothelin-1 was significantly decreased in congestive heart failure rats. Neuropeptide Y and neuropeptide Y-(13–36) potentiated the endothelin-1-induced contraction in congestive heart failure mesenteric arteries. In 20% of the congestive heart failure rats, sarafotoxin 6c induced a contraction of 31±4%. Neuropeptide Y also potentiated U46619- and noradrenaline-induced contractions but not 5-HT-induced contractions in congestive heart failure arteries. In sham-operated animals neuropeptide Y potentiated noradrenaline- and 5-HT-induced contractions. These potentiations were inhibited by BIBP3226. Acetylcholine induced an equipotent relaxation in both groups which was unaffected by neuropeptide Y. In conclusion, neuropeptide Y responses are altered in congestive heart failure rats. The potentiating effect differs between vasoactive substances. Neuropeptide Y Y₁ and non-neuropeptide Y₁ receptors are involved.     

Block of the endplate acetylcholine receptor channel by the sympathomimetic agents ephedrine, pseudoephedrine, and albuterol

Recent observations suggest that some patients with congenital myasthenic syndromes respond favorably to ephedrine, pseudoephedrine, or albuterol. Conventional microelectrode studies, however, provide no clear explanation for a beneficial effect of ephedrine in endplate diseases. To gain further insight into how these drugs affect neuromuscular transmission, we investigated their effects on the kinetic properties of the acetylcholine (ACh) receptor. Single channel currents were recorded from rat lumbrical muscles endplates using low concentrations of ACh and 2.5–100 μM of drugs. Between 10–100 μM, each drug progressively increased the rate of channel closure in a concentration dependent manner, consistent with an open-channel block. Albuterol acted as a sequential fast-acting channel blocker, increasing the mean burst duration in a concentration dependent manner without altering the total open time per burst or the duration of intraburst blockages. Increasing concentrations of ephedrine and pseudoephedrine also increased the number of intraburst closures but decreased the total open time per burst. None of the drugs altered single channel conductance. The channel blocking effects of ephedrine and pseudoephedrine might reduce the synaptic overactivity that occurs in the slow-channel myasthenic syndromes or in endplate ACh esterase deficiency, but these effects occur at concentrations not attainable in clinical practice.     

Regional myocardial oxygen tension: 19F MRI of sequestered perfluorocarbon

A novel noninvasive method of measuring local myocardial oxygen tension (pO₂) In the perfused rat heart using ¹⁹F MRI is demonstrated. Tissue pO₂ was determined on the basis of the ¹⁹F spin-lattice relaxation rate (R1) of perflubron (perfluorooctyl bromide) sequestered in the heart after IV infusion of an emulsion. Spectroscopic measurement of R1 was previously used to measure a global weighted average of oxygen status. ¹⁹F MRI now provides 3D spatial resolution indicating local cardiac pO₂ under normally perfused, globally ischemic, and regionally ischemic conditions.     

Right internal thoracic artery through the transverse sinus in myocardial revascularization

Background. A major concern in evaluating dynamic cardiomyoplasty has been whether the synchronous stimulation of latissimus dorsi muscle is essential for benefit or not. We studied 10 patients to determine the efficacy of the systolic augmentation generated by the synchronous electrical stimulation of the latissimus dorsi muscle.

Methods. Left ventricular ejection fraction, end-systolic and end-diastolic volume indexes, and stroke volume index obtained during resting, peak exercise, and recovery periods (“on” values) were compared with those obtained 1 week after cessation of electrical stimulus (“off” values). Double product and estimated total body oxygen consumption at peak exercise were also calculated and compared.

Results. Higher ejection fractions (0.36 ± 0.07 versus 0.33 ± 0.06 at rest, 0.40 ± 0.07 versus 0.33 ± 0.07 peak exercise, and 0.37 ± 0.06 versus 0.31 ± 0.06 at recovery) and lower end-systolic volume indexes with relatively constant end-diastolic volume indexes were observed with the cardiomyostimulator on. Further, exercise response was better with the cardiomyostimulator on. Double product indirectly reflected better myocardial oxygen supply/demand ratio when on at peak exercise (17 ± 2.2 mm Hg × beats/min × 10⁻³ for on versus 19 ± 2.6 mm Hg × beats/min × 10⁻³ for off). Estimated total body oxygen consumption was improved at peak exercise when the cardiomyostimulator was functional (12 ± 2.7 mL · kg⁻¹ · min⁻¹ versus 11 ± 2.6 mL · kg⁻¹ · min⁻¹).

Conclusions. Current data suggest a true systolic assist during synchronous contractions of the latissimus dorsi muscle. It is thought, therefore, that synchronous electrical stimulation is essential for maximum benefit and all the beneficial effect of cardiomyoplasty certainly cannot be attributed to simple wrapping itself.     

Short and long term effects of exercise training on the tonic autonomic modulation of heart rate variability after myocardial infarction

We studied the effects of cardiac rehabilitation on the sympathovagalcontrol of heart rate variability in 30 patients after a first,uncomplicated myocardial infarction. Twenty-two patients completed8 weeks of endurance training (trained), while eight decidednot to engage in the rehabilitation programme for logisticalreasons, and were taken as untrained controls. Age, site ofinfarction, ejection fraction, ventricular diameter and stresstest duration were similar in the two groups at baseline. Heartrate variability was evaluated 4 weeks after infarction beforestarting rehabilitation, and repeated 8 weeks and one year laterin both trained and untrained patients. Measures of heart ratevariability, obtained from both time- and frequency- domainanalysis of a 15 min ECG recording in resting conditions, wereas follows: mean RR interval and its standard deviation (RRSD),the mean square successive differences (MSSD), the percent ofRR intervals differing >50 ms from the preceding RR (pNTN50),the low and high frequency components of the autoregressivepower spectrum of the RR intervals and their ratio (LF/HF).At baseline, heart rate variability was similar in trained anduntrained patients. In the short term (8 weeks after infarction),training increased RRSD by 25% (P<0·01), MSSD by 69%(P<0·01), pNN50 by 120% (P<0·01), and reducedLF/HF ratio by 30% (P<0·01). The effects persistedafter one year in trained patients. In untrained patients, theautonomic control of heart rate variability did not change 8weeks after myocardial infarction and was only slightly modifiedby time. Thus, exercise training, performed for 8 weeks aftera myocardial infarction, modifies the sympathovagal controlof heart rate variability toward a persistent increase in parasympathetictone, known to be associated with a better prognosis. This maypartly account for the favourable outcome of patients who undergorehabilitation.     

Lipids and lipoproteins as risk factors for coronary heart disease in men with abnormal glucose tolerance: the Honolulu Heart Program

Abstract. Objectives. To evaluate lipids and lipoproteins as risk factors for coronary heart disease (CHD) in older men with non-insulin-dependent diabetes (NIDDM) or abnormal glucose tolerance compared with normoglycaemic men. Design. A prospective, population-based cohort study based on the lipoprotein examination (1970–72) of the Honolulu Heart Program. Follow-up was through to December 1988. Setting. Honolulu, Hawaii. Subjects. Japanese-American men, ages 51–72 at baseline: 2042 with 1 h glucose < 12.5 mmol l^?1 (normal group); 376 on oral hypoglycaemic agents or with 1 h glucose ≥ 12.5 mmol l^?1 after 50 g oral glucose challenge (abnormal glucose tolerance group). None had prevalent coronary heart disease (CHD) or stroke at baseline. Main outcome measures. Incident CHD: definite nonfatal myocardial infarction (MI) or fatal CHD. Results. There were 221 incident cases in the normal group, and 65 in the abnormal glucose tolerance group. Total and high-density lipoprotein (HDL) cholesterol were significant predictors of incident CHD in men with NIDDM or abnormal glucose tolerance after controlling for age, body-mass index, systolic blood pressure, pack-years of cigarettes and alcohol consumption (P < 0.05). Total, low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) cholesterol were significant predictors in normal men, and HDL cholesterol was of borderline significance. Conclusions. Abnormal lipids and lipoproteins are significant, independent predictors of CHD in subjects with NIDDM or abnormal glucose tolerance. Attention to lipid and lipoproteins as CHD risk factors should be part of clinical management of these patients.     

Effects of trapidil-derivatives on calcium channel currents in isolated ventricular cells from mice

Summary A single glass micropipette voltage clamp technique with intracellular dialysis was used to study the effects of the trapidil derivatives AR 12–456 and AR 12–463 on Ca channel currents carried by Bat+ in isolated ventricular cells from mice hearts. Inspite of a more potent inhibition of the cAMP phosphodiesterase from heart (Bartel et al. 1985) a reversible Ca channel blocking action of both compounds could be observed. The concentration of half maximal block was calculated to about 50 mol/l for both derivatives tested. Neither a shift in the current-voltage relationships nor a significant change in the potential for half maximal activation was found. The maximal Ba²⁺ -conductance was reduced. The steady state inactivation was shifted towards more negative potentials by application of 100 mol/l AR 12–463. The decay of the Ba currents was accelerated in the range of the applied test potentials between –20 and +20 mV. It is concluded that the new trapidil derivatives with more potent inhibitory action on cardiac phosphodiesterase than trapidil can block myocardial Ca channels. Send offprint requests to B. Nilius     

Radiologic search for embolized leaflets of prosthetic heart valves: A report of two cases

In a radiologic search for embolized leaflets of Edwards-Duromedics bileaflet valves in 2 patients, the embolized fragments were localized in the iliac vessels using computed tomography. Sonography was successful in one case and standard X-ray films of the abdomen were negative in both cases.In vitro investigations with Björk-Shiley and Edwards-Duromedics leaflets suggested that standard X-ray films of the abdomen and pelvis should be considered as the first investigational technique. If negative, computed tomography of the lower abdomen should be done.