PubMed · 7383095
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K P Price. 1980-07-24. Headache.. https://pubmed.ncbi.nlm.nih.gov/7383095/
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We studied heart rate variability in ambulatory electrocardiographic recordings from 312 patients with significant coronary artery disease and a left ventricular ejection fraction of > or = 30%. Only those patients who had both episodes of ischemia and nonsustained ventricular arrhythmias showed diminished values for parasympathetic nonspectral and spectral heart rate (HR) variability parameters. The root mean square of difference of successive R-R intervals (RMSSD) and high-frequency (HF) power in this group were 28 +/- 3 msec and 9 +/- 1 msec, respectively. The highest values of these HR variability parameters were found in patients with nonsustained ventricular tachycardia and no ischemia (81 +/- 21 msec and 14 +/- 1 msec, respectively, p < or = 0.05). A relation was seen between transient myocardial ischemia and low-frequency power and between transient ischemia and ventricular tachycardia. These data suggest that the autonomic nervous system may play a role in ischemia and in ischemia-related ventricular arrhythmias.
BACKGROUND & AIMS: The roles of hyperglycemia in diabetic gastroparesis and gastric delivery in postprandial hyperglycemia of diabetic patients are unclear. The aims of this study were to assess gastric emptying and its relation to postprandial glucose metabolism in patients with asymptomatic non-insulin-dependent diabetes mellitus (NIDDM) and no autonomic neuropathy and to identify motor mechanisms responsible for any accelerated gastric emptying. METHODS: Autonomic function, gastric emptying, postprandial glucose metabolism, and hormone levels (glucagon, insulin, cholecystokinin, glucose-dependent insulinotropic polypeptide, neurotensin, and peptide YY) were assessed in healthy volunteers and patients with NIDDM. In a second study, gastric tone and motility were measured in patients with accelerated gastric emptying and in controls. RESULTS: Gastric emptying of solids did not differ in the two groups, but liquids emptied faster in patients with NIDDM (P < 0.02). The rate of entry of ingested glucose into the systemic circulation was similar, but higher postprandial glucagon and lower insulin concentrations led to greater (P < 0.01) postprandial hepatic glucose release. Levels of other enteropeptides, gastric accommodation, and antral motility were similar, but patients with NIDDM had greater proximal gastric phasic contractions than controls (P < 0.05). CONCLUSIONS: Excessive hepatic glucose release, not rapid entry of ingested glucose, is the primary cause of postprandial hyperglycemia in patients with NIDDM. Accelerated gastric emptying in patients with nonneuropathic NIDDM is associated with increased proximal stomach phasic contractions.