Alternating Wenckebach Periods in Acute Inferior Myocardial Infarction: Clinical, Electrocardiographic, and Therapeutic Characterization

We report on twelve patients with alternating Wenckebach periods (AWP) occurring during an acute inferior myocardial infarction (AIMI). There were nine males and three females, with a mean age of 61 years (range, 43 to 75). AWP appeared during the first 48 hours of the AIMI in 10 patients and on the fourth day of hospitalization in two patients. AWP occurred spontaneously in nine patients and following the administration of atropine in the remaining three patients. Mean systolic blood pressure significantly decreased during AWP as compared to the period preceding or following the bradyarrhythmia (93 ± 42 mmHg vs 123 ± 37 mmHg, p < 0.02). Killip functional class was significantly higher during AWP as compared to the period preceding or following the bradyarrhythmia (2.1 ± 1.2 vs 1.5 ± 0.8, p < 0.02). Pacemaker therapy was initiated prophylactically in two patients, because of syncope in six, because of hemodynamic deterioration in two, and for syncope and hemodynamic deterioration in two. Three patients died in cardiogenic shock despite pacemaker therapy. No evidence of right ventricular infarction was seen in the patients.
Atropine administration during AWP significantly increased the sinus rate and significantly decreased the ventricular rates and the systolic blood pressure. In addition, three patients developed long bouts of paroxysmal AV block. Isoproterenol administration improved AV conduction in one patient, caused no change in two patients and induced non-sustained ventricular tachycardia in three patients.
In conclusion, AWP occurring during AIMI is a symptomatic bradyarrhythmia associated with hemodynamic deterioration. Drug therapy for this bradyarrhythmia is usually ineffective and sometimes paradoxical responses are observed. Pacemaker therapy is usually needed to correct symptoms and the worsening hemodynamic status. We recommend prophylactic pacemaker implantation in patients developing AWP during AIMI.     

The influence of atropine premedication on the induction of anaesthesia with isoflurane in children

Airway irritability often occurs during induction of anaesthesia with isoflurane and may be accompanied by substantial reductions in oxygen saturation. The aim of this study was to determine the influence of atropine pre-anaesthetic medication on the induction characteristics of isoflurane. The incidence and severity of airway complications were significantly reduced in children who received atropine, both the oral and intra-muscular routes being equally effective. However, almost half the children receiving no premedication had saturation levels less than 90%.     

Muscarinic cholinergic receptors mediate the cerebrovasodilation elicited by stimulation of the cerebellar fastigial nucleus in rat

We have investigated the effects of systemic administration of atropine sulfate on the global cerebrovascular vasodilation elicited by electrical stimulation of the cerebellar fastigial nucleus (FN) in chloralose-anesthetized rat. Atropine (0.3 mg/kg, i.v.) abolished the cerebrovasodilation elicited from FN but did not affect the concomitant elevation in arterial pressure and the EEG changes. We conclude that the cerebrovascular effect of FN stimulation, but not the peripheral cardiovascular or EEG changes, are mediated by cholinergic muscarinic receptors associated with cerebral vessels and/or intrinsic neural pathways.     

山莨菪碱对肾移植术后并发症的治疗

目的：研究山莨菪碱对移植肾术后并发症的治疗作用。方法：肾移植术后３２人。术后１４人未发生少尿时ｉｖ山莨菪碱４７±ｓ１２（３０～６０）ｍｇ／ｄ，连续给药７．１±２．９ｄ（４～１０ｄ）（预防组）。术后１８人出现少尿时ｉｖ山莨菪碱９１±２７（６０～１２０）ｍｇ／ｄ、呋塞米与免疫抑制剂（治疗组）。结果：预防组多尿期缩短１～３ｄ，２４ｈ尿量明显少于治疗组，血肌酐达正常值较治疗组提前１．５ｄ，无继发少尿或无尿。治疗组亦全部恢复正常，肾功能达显效所需时间为２．５±１．０ｄ（１～４ｄ）。结论：山莨菪碱具有改善和保护移植肾功能，预防和治疗移植肾术后出现的少尿或无尿的作用。     

刺激家兔额叶皮层影响尾核痛单位放电机制的初步探讨

目的：探讨额叶皮层对尾核痛单位放电的影响及其可能机制。方法：参照Ｓａｗｙｅｒ兔脑图谱，用ＳＮ－２型推进器以２μｍ／ｓ速度将玻璃微电极插入尾核头部Ａ３～５，Ｒ３．５～５，Ｈ３．５～５处引导神经元自发放电。结果：引导了尾核单位放电３７９个，其中痛单位８６个，占引导总数的２２．６８％，包含痛兴奋单位（ＰＥＮ）５７个，占痛单位的６６．２８％；痛抑制单位（ＰＩＮ）２９个，占３３．７２％。尾核有７４．４２％的痛单位对刺激额叶皮层起反应。刺激额叶皮层可易化尾核ＰＩＮ的电活动（６２．５２％出现增频反应），抑制ＰＥＮ的电活动（６４．９１％出现减频反应）。脑室注射阿托品或氟哌啶醇均可不同程度的阻断刺激额叶皮层对尾核痛单位的影响。结论：额叶皮层参与对尾核痛单位的调制，乙酰胆碱，多巴胺及相应的受体可能参与其调制过程     

褐藻氨酸对M-胆碱受体的作用

本文以离体豚鼠回肠作标本,乙酰胆碱作对照剂,阿托品作对抗剂,观察了褐藻氨酸对肠管平滑肌的作用。结果表明,褐藻氨酸使汤平滑肌产生了剂量依赖性的兴奋作用,该作用可被阿托品竞争性对抗。褐藻氨酸的PD_2为3.86,阿托品的PA_2为9.6.提示褐藻氨酸对M-胆碱受体有激动作用。     

Autoradiographic identification of muscarinic receptors in human iris smooth muscle

We have used the specific, irreversible muscarinic ligand [³H]-propylbenzilylcholine mustard to localize putative muscarinic cholinergic receptors in the smooth muscle tissue of the human iris. Analysis of autoradiograms from labeled irides reveals high grain densities over the iris sphincter muscle, consistent with the well-known pharmacology of this muscle. In addition, a smaller but significant population of muscarinic binding sites was seen in the iris dilator muscle as well. Grain densities in both muscles are substantially reduced in control tissue treated with relatively high concentrations of the muscarinic antagonists quinuclidinyl benzilate (QNB) and atropine. This is, to our knowledge, the first report of autoradiographic localization of putative muscarinic receptors in the human iris.     

Mechanisms of late decelerations in the fetal heart rate. A study with autonomic blocking agents in fetal lambs.

Fetal heart rate decelerations resembling the late deceleration FHR pattern were produced in fetal sheep by periodic occlusion of the maternal common hypogastric artery for 30-60 sec. Transient fetal hypertension also occurred during the occlusions. Alpha-adrenergic blockade with phentolamine eliminated or markedly reduced the hypertensive response. FHR decelerations still occurred intermittently with some occlusions; however, their character was greatly altered. After parasympathetic blockade with atropine, the decelerations were replaced by periodic FHR accelerations during the occlusions. These accelerations were, in turn, eliminated by the beta-adrenergic blocking agent, propranolol. In the presence of combined parasympathetic, alpha- and beta-adrenergic blockade, the FHR remained essentially constant during the hypogastric artery occlusions in non-acidemic fetuses. FHR decelerations persisted after parasympathetic or total autonomic blockade when the fetuses were significantly hypoxic, as judged by depressed arterial blood pH and base excess values. Beat-to-beat variability of the baseline FHR persisted in the face of severe hypoxia and acidosis. These observations demonstrate that reflex mechanisms are involved importantly in the genesis of late deceleration FHR patterns in the acutely hypoxemic fetus, but that direct depression of myocardial rhythmicity becomes a factor as hypoxic acidosis develops.