Regulation of the cardiac rhythm at rest and in orthostasis.
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The morphology of the first spontaneous post-pacing P wave was assessed in 106 patients who underwent electrophysiological study for various arrhythmias. An overall number of 589 atrial pacing sessions, from 60-200 b/min, were analyzed (mean 5.55 +/- 1.3 session per patient). After cessation of 138 (23.42%) of them, spontaneous post-pacing P wave arose from extrasinus foci. Nonsinus spontaneous post-pacing P waves were recorded after 1 or more pacing rates (from 1 to 7) in 58 patients (54.7%, Group 1). In the remaining 48 patients the spontaneous post-pacing P waves were sinus after all pacing sessions (45.3%, Group 2). Sinus node disease (SND) was present in 32.7% of Group 1 patients and in 2% of Group 2 (p = 0.002). Spontaneous post-pacing P wave of extrasinus origin was recorded in 19/20 of SND patients (95%) compared to 39/86 of patients with normal sinus function (45.34%, p < 0.001). SND patients had a greater number of pacing sessions resulting in nonsinus spontaneous post-pacing P waves. Pacing rate associated with nonsinus spontaneous post-pacing P waves was lower in SND patients compared to patients with normal sinus node function. In the SND group, nonsinus spontaneous post-pacing P waves were recorded beyond the first spontaneous one in 9 patients compared to only 1 in patients with normal sinus node function (p < 0.005). Extrasinusal first spontaneous post-pacing P waves at a pacing rate of 140 b/min had the highest sensitivity (75%). Increasing of pacing rate from 60 to 140 b/min was associated with progressive arousal of secondary foci with highest value of 36.8% in pacing rate of 140 b/min. Further increase of pacing rate resulted in a slight reduction of spontaneous post-pacing firing from secondary foci. Atropine was administered in 12 Group 1 patients and abolished all measurable morphological changes of spontaneous post-pacing P waves compared to pre-pacing. Autonomic blockade was performed in 14 Group 1 patients and 16 Group 2 patients. In 35.7% of Group 1 patients autonomic blockade abolished the appearance of nonsinus spontaneous post-pacing P waves, while in the remaining patients increased the lowest pacing rate resulting in nonsinus spontaneous post-pacing P waves. In 12.5% Group 2 patients autonomic blockade resulted in nonsinus spontaneous post-pacing P waves after cessation of atrial pacing. In conclusion, the extrasinus spontaneous rise of atrial impulse is a very frequent phenomenon after atrial pacing especially in patients with SND. Pacing rate has different quantitative effects on sinus and secondary atrial pacemakers. Secondary pacemakers are less under autonomic control compared to sinus node.
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The authors evaluated regional skin temperatures of the foot following the administration of a variety of local anesthetic nerve blocks with either Xylocaine (lidocaine hydrochloride) or Sensorcaine (bupivacaine hydrochloride). The study was carried out on ten randomized parallel groups of five subjects, each group being tested with one drug and one regional nerve block. The results indicated that both Xylocaine and Sensorcaine, when administered as a posterior tibial block, result in a significantly increased blood flow to the foot. Nerve blockade of the remaining nerves of the foot did not significantly increase the sympatholytic effect obtained by posterior tibial nerve block alone.
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Autonomic dysreflexia is a condition that develops after spinal cord injury in which potentially life-threatening episodic hypertension is triggered by stimulation of sensory nerves in the body below the site of injury. Central sprouting of small-diameter primary afferent fibers in the dorsal horn of the spinal cord occurs concurrently with the development of this condition. We propose a model for the development of autonomic dysreflexia in which increased nerve growth factor (NGF) in the injured cord stimulates small-diameter primary afferent fiber sprouting, thereby magnifying spinal sympathetic reflexes and promoting dysreflexia. We identified this population of afferent neurons using immunocytochemistry for calcitonin gene-related peptide. Blocking intraspinal NGF with an intrathecally-delivered neutralizing antibody to NGF prevented small-diameter afferent sprouting in rats 2 weeks after a high thoracic spinal cord transection. In the same rats, this anti-NGF antibody treatment significantly decreased (by 43%) the hypertension induced by colon stimulation. The extent of small-diameter afferent sprouting after cord transection correlated significantly with the magnitude of increases in arterial pressure during the autonomic dysreflexia. Neutralizing NGF in the spinal cord is a promising strategy to minimize the life-threatening autonomic dysreflexia that develops after spinal cord injury.
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