Heart-Rate Response to Sustained Hand Grip: Comparison of the Effects of Cardiac Autonomic Blockade and Diabetic Autonomic Neuropathy

1979 ◽  
Vol 56 (3) ◽  
pp. 287-291 ◽  
Author(s):  
L. Hume ◽  
D. J. Ewing ◽  
I. W. Campbell ◽  
S. R. Reuben ◽  
B. F. Clarke

1. The heart-rate response during sustained hand grip was studied in four normal subjects before and after intravenous atropine, propranolol and combined cardiac autonomic blockade with both drugs. The results suggest that the increase in heart rate during the first 30 s is due to parasympathetic withdrawal, whereas the further increase between 30 s and 180 s is probably mediated by a combination of parasympathetic withdrawal and sympathetic stimulation. 2. The increases in heart rate during each minute of sustained hand grip were compared in 26 normal subjects, 37 diabetic subjects without and 24 diabetic subjects with proven autonomic neuropathy. In the diabetic subjects with autonomic neuropathy the increase in heart rate during the first minute was impaired, whereas the increases during the second and third minutes were similar in all three groups. 3. The initial increase in heart rate over the first 30 s of hand grip and the later increase between 30 s and 180 s were compared in nine normal subjects, ten diabetic subjects without and six diabetic subjects with autonomic neuropathy. The increase during the first 30 s was impaired in the diabetic subjects with autonomic neuropathy, whereas the later phase of the response was similar in all three groups. 4. It is concluded that impairment of the heart-rate response to sustained hand grip in diabetic autonomic neuropathy is mainly due to impairment of the early parasympathetic phase, but that the presence of cardiac sympathetic damage can also be detected.

1987 ◽  
Vol 72 (1) ◽  
pp. 55-60 ◽  
Author(s):  
Claudio CaRdone ◽  
Federico Bellavere ◽  
Marcello Ferri ◽  
Domenico Fedele

1. To differentiate between the possible reflex and mechanical components in the heart rate response to cough, eight healthy subjects performed a standardized cough test before and after pharmacological autonomic blockade; to test the clinical usefulness of the cough manoeuvre two groups of diabetic patients (without and with autonomic neuropathy) were compared with a group of age-matched normal subjects. 2. Because of the use of abdominal and expiratory muscles during cough, the cardioacceleratory response was compared with that induced by an intense contraction of the arm muscles (handgrip). 3. The cardioacceleratory response was completely abolished by atropine while propranolol failed to affect it. The diabetic patients with autonomic neuropathy showed a response similar to that after cholinergic blockade. The response was similar to that induced by muscular contraction for 4 s, after which it differed showing a continued cardioacceleration. The patterns of recovery were not different. 4. The cough-induced cardioacceleration is essentially reflex in nature and under cholinergic control; initially the mechanism may be partially related to the intense contraction of abdominal and expiratory muscles; later, the arterial hypotension related to the cough may contribute to the more sustained shortening of the R–R interval. 5. The cough test may be useful for the evaluation of cardiac parasympathetic integrity.


1976 ◽  
Vol 51 (s3) ◽  
pp. 681s-685s ◽  
Author(s):  
G. Nyberg

1. Sustained hand-grip exercise and mental arithmetic were performed by normal and hypertensive subjects. Blood pressure and heart rate were recorded with a device which allows blind and unbiased measurements, based on the conventional cuff method. 2. Both stimuli caused increases in heart rate and systolic and diastolic blood pressure, which were greater for isometric exercise than for mental arithmetic. 3. Normal females had a greater response to repeated exercise, and had a smaller systolic pressure elevation during mental arithmetic than the other groups. 4. Repeated testing showed good reproducibility in normal subjects.


1982 ◽  
Vol 63 (1) ◽  
pp. 17-22 ◽  
Author(s):  
P. M. A. Calverley ◽  
D. J. Ewing ◽  
I. W. Campbell ◽  
P. K. Wraith ◽  
H. M. Brash ◽  
...  

1. Unexplained cardiorespiratory arrests have been reported in patients with diabetic autonomic neuropathy and these could be due to denervation of the carotid chemoreceptors. 2. We have studied the ventilatory response to transient hypoxia () during exercise in 22 male diabetic patients, six with symptomatic and cardiovascular evidence to suggest diabetic autonomic neuropathy (DAN+) and 12 without these features (DAN−). 3. There was no difference in the ventilatory response to transient hypoxia between the different groups of diabetic patients ( in DAN+ patients = −0·9 ± 0·2 litre min−1 kPa−1; in DAN− patients = −1·2 ± 0·6 litres min−1 kPa−1) even allowing for differences in the level of exercise achieved (CO2 production in DAN+ patients = 743 ± 103 ml/min; CO2 production in DAN– patients = 800 ± 144 ml/min). These results fell within our normal range for ventilatory response to transient hypoxia at this level of exercise. 4. The heart rate response to transient hypoxia varied within the groups but was significantly (P < 0·05) less in the patients with established diabetic autonomic neuropathy. 5. We conclude that the peripheral chemoreceptors are intact in diabetic autonomic neuropathy and that other mechanisms must be implicated in the unexpected cardiorespiratory arrests seen in these patients.


1995 ◽  
Vol 115 (3) ◽  
pp. 460-465
Author(s):  
Toshihiro Nishimura ◽  
Souzaburou Yoshihara ◽  
Kazuyuki Nagatsuka ◽  
Takeshi Inoue ◽  
Masao Saito ◽  
...  

2014 ◽  
Vol 116 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
James P. Mendoza ◽  
Rachael J. Passafaro ◽  
Santhosh M. Baby ◽  
Alex P. Young ◽  
James N. Bates ◽  
...  

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.


1990 ◽  
Vol 69 (3) ◽  
pp. 962-967 ◽  
Author(s):  
J. T. Sullebarger ◽  
C. S. Liang ◽  
P. D. Woolf ◽  
A. E. Willick ◽  
J. F. Richeson

Phenylephrine (PE) bolus and infusion methods have both been used to measure baroreflex sensitivity in humans. To determine whether the two methods produce the same values of baroreceptor sensitivity, we administered intravenous PE by both bolus injection and graded infusion methods to 17 normal subjects. Baroreflex sensitivity was determined from the slope of the linear relationship between the cardiac cycle length (R-R interval) and systolic arterial pressure. Both methods produced similar peak increases in arterial pressure and reproducible results of baroreflex sensitivity in the same subjects, but baroreflex slopes measured by the infusion method (9.9 +/- 0.7 ms/mmHg) were significantly lower than those measured by the bolus method (22.5 +/- 1.8 ms/mmHg, P less than 0.0001). Pretreatment with atropine abolished the heart rate response to PE given by both methods, whereas plasma catecholamines were affected by neither method of PE administration. Naloxone pretreatment exaggerated the pressor response to PE and increased plasma beta-endorphin response to PE infusion but had no effect on baroreflex sensitivity. Thus our results indicate that 1) activation of the baroreflex by the PE bolus and infusion methods, although reproducible, is not equivalent, 2) baroreflex-induced heart rate response to a gradual increase in pressure is less than that seen with a rapid rise, 3) in both methods, heart rate response is mediated by the vagus nerves, and 4) neither the sympathetic nervous system nor the endogenous opiate system has a significant role in mediating the baroreflex control of heart rate to a hypertensive stimulus in normal subjects.


1988 ◽  
Vol 255 (1) ◽  
pp. R149-R156 ◽  
Author(s):  
K. Sander-Jensen ◽  
J. Mehlsen ◽  
C. Stadeager ◽  
N. J. Christensen ◽  
J. Fahrenkrug ◽  
...  

Progressive central hypovolemia is characterized by a normotensive, tachycardic stage followed by a reversible, hypotensive stage with slowing of the heart rate (HR). We investigated circulatory changes and arterial hormone concentrations in response to lower-body negative pressure (LBNP) in six volunteers before and after atropine administration. LBNP of 55 mmHg initially resulted in an increase in HR from 55 +/- 4 to 90 +/- 5 beats/min and decreases in mean arterial pressure (MAP) from 94 +/- 4 to 81 +/- 5 mmHg, in central venous pressure from 7 +/- 1 to -3 +/- 1 mmHg, and in cardiac output from 6.1 +/- 0.5 to 3.7 +/- 0.11/min. Concomitantly, epinephrine and norepinephrine levels increased. After 8.2 +/- 2.3 min of LBNP, the MAP had decreased to 41 +/- 7 mmHg and HR had decreased to 57 +/- 3 beats/min. Vasopressin increased from 1.2 +/- 0.3 to 137 +/- 45 pg/ml and renin activity increased from 1.45 +/- 4.0 to 3.80 +/- 1.0 ng.ml-1.h-1 with no further changes in epinephrine, norepinephrine, and vasoactive intestinal polypeptide. A tardy rise in pancreatic polypeptide indicated increased vagal activity. After atropine. LBNP also caused an initial increase in HR, which, however, remained elevated during the subsequent decrease in MAP to 45 +/- 6 mmHg occurring after 8.1 +/- 2.4 min.(ABSTRACT TRUNCATED AT 250 WORDS)


1999 ◽  
Vol 9 (4) ◽  
pp. 377-383 ◽  
Author(s):  
Ruchir Sehra ◽  
Joyce E. Hubbard ◽  
Susan P. Straka ◽  
Naomi S. Fineberg ◽  
Douglas P. Zipes ◽  
...  

AbstractBackgroundRadiofrequency catheter ablation is standard treatment for children with re-entrant supraventricular tachycardias. Autonomic changes have been noted after such ablation for atrioventricular nodal re-entry tachycardia, but not as well documented with atrioventricular re-entry over an accessory pathway.Methods and resultsIn 10 normal paediatric volunteers and 12 children referred for electrophysiologic testing and radiofrequency ablation of supraventricular tachycardia, non-invasive autonomic function tests and tilt-table testing were performed, and the variability in 24-h heart rate was analysed. Patients with supraventricular tachycardia underwent these tests both 24–72 h before and 24 h after ablation. Patients with tachycardia underwent additional autonomic testing to assess the sensitivity of baroreceptors and the intrinsic heart rate with autonomic blockade immediately before and after ablation. One non-invasive autonomic function test, namely handgrip, demonstrated significant differences (p < 0.05) in diastolic blood pressure before and after ablation, though these values did not differ from controls. Significant decreases were noted in two indexes of the variability of heart rate before and after ablation (p < 0.05). Certain tilt test variables also demonstrated significant differences between controls and those with tachycardia subsequent to ablation. Intracardiac testing demonstrated changes (p < 0.05) in sinus cycle lengths, effective refractory periods and/or blood pressures at baseline and during testing of the sensitivity of baroreceptors before and after ablation. These changes were consistent with increased sympathetic or decreased parasympathetic tone. With autonomic blockade, these differences were abolished.ConclusionsCatheter ablation of accessory pathways in children was associated with changes consistent with increased sympathetic or decreased parasympathetic tone. These autonomic changes persisted 24 h after the ablation procedure.


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