Chronotropic response to intravenous infusion in the anesthetized dog

1963 ◽  
Vol 204 (3) ◽  
pp. 423-426 ◽  
Author(s):  
Gulzar Ahmad ◽  
Paul A. Nicoll

Ninety-four anesthetized dogs at normal body temperature received 293 intravenous saline infusions by gravity flow through either a femoral or jugular vein. Also nine dogs with body temperature lowered to 27 C received 30 similar infusions. Heart rate and blood pressure were monitored by transducer and oscillographic recording. The chronotropic response of the normothermic group varied with the preinfusion heart rate, with those below 140/min generally showing increases and those above showing no response or a decrease. Negative results with hypothermic animals also having slow preinfusion rates indicate the Bainbridge effect requires the slow preinfusion heart rate to be under vagal inhibition.

Children ◽  
2020 ◽  
Vol 7 (8) ◽  
pp. 89
Author(s):  
Woori Bae ◽  
Kyunghoon Kim ◽  
Bongjin Lee

To effectively use vital signs as indicators in children, the magnitude of deviation from expected vital sign distribution should be determined. The purpose of this study is to derive age-specific centile charts for the heart rate and respiratory rate of the children who visited the emergency department. This study used the Korea’s National Emergency Department Information System dataset. Patients aged <16 years visiting the emergency department between 1 January 2016 and 31 December 2017 were included. Heart rate and respiratory rate centile charts were derived from the population with normal body temperature (36 to <38 °C). Of 1,901,816 data points retrieved from the database, 1,454,372 sets of heart rates and 1,458,791 sets of respiratory rates were used to derive centile charts. Age-specific centile charts and curves of heart rates and respiratory rates showed a decline in heart rate and respiratory rate from birth to early adolescence. There were substantial discrepancies in the reference ranges of Advanced Paediatric Life Support and Pediatric Advanced Life Support guidelines. Age-based heart rate and respiratory rate centile charts at normal body temperature, derived from children visiting emergency departments, serve as new evidence-based data and can be used in follow-up studies to improve clinical care for children.


2010 ◽  
Vol 298 (5) ◽  
pp. R1333-R1342 ◽  
Author(s):  
Kevin J. Cummings ◽  
Aihua Li ◽  
Evan S. Deneris ◽  
Eugene E. Nattie

Neonatal rodents deficient in medullary serotonin neurons have respiratory instability and enhanced spontaneous bradycardias. This study asks if, in Pet-1−/− mice over development: 1) the respiratory instability leads to hypoxia; 2) greater bradycardia is related to the degree of hypoxia or concomitant hypopnea; and 3) hyperthermia exacerbates bradycardias. Pet-1+/+, Pet-1+/−, and Pet-1−/− mice [postnatal days (P) 4–5, P11–12, P14–15] were held at normal body temperature (Tb) and were then made 2°C hypo- and hyperthermic. Using a pneumotach-mask system with ECG, we measured heart rate, metabolic rate (V̇o2), and ventilation. We also calculated indexes for apnea-induced hypoxia (total hypoxia: apnea incidence × O2 consumed during apnea = μl·g−1·min−1) and bradycardia (total bradycardia: bradycardia incidence × magnitude = beats missed/min). Resting heart rate was significantly lower in all Pet-1−/− animals, irrespective of Tb. At P4–5, Pet-1−/− animals had approximately four- to eightfold greater total bradycardia ( P < 0.001), owing to an approximately two- to threefold increase in bradycardia magnitude and a near doubling in bradycardia incidence. Pet-1−/− animals had a significantly reduced V̇o2 at all Tb; thus there was no genotype effect on total hypoxia. At P11–12, total bradycardia was nearly threefold greater in hyperthermic Pet-1−/− animals compared with controls ( P < 0.01). In both genotypes, bradycardia magnitude was positively related to the degree of hypopnea ( P = 0.02), but there was no genotype effect on degree of hypopnea or total hypoxia. At P14–15, genotype had no effect on total bradycardia, but Pet-1−/− animals had up to seven times more total hypoxia ( P < 0.001), owing to longer and more frequent apneas and a normalized V̇o2. We infer from these data that 1) Pet-1−/− neonates are probably not hypoxic from respiratory dysfunction until P14–15; 2) neither apnea-related hypoxia nor greater hypopnea contribute to the enhanced bradycardias of Pet-1−/− neonates from approximately P4 to approximately P12; and 3) an enhancement of a temperature-sensitive reflex may contribute to the greater bradycardia in hyperthermic Pet-1−/− animals at approximately P12.


1988 ◽  
Vol 8 (3) ◽  
pp. 385-394 ◽  
Author(s):  
Jeffrey R. Kirsch ◽  
Daniel F. Hanley ◽  
David A. Wilson ◽  
Richard J. Traystman

(D-ala2)-met5-encephalinamide (AM encephalinamide) and (D-ala2)-leu5-encephalinamide (AL encephalinamide) were administered into the cisterna magna in anesthetized dogs to determine whether these opiates effected the neurohypophyseal circulation differently than the circulation of other brain areas. At the beginning of the experimental protocol, animals were given either mock cerebral spinal fluid (CSF) or 5 or 25 mg of AM encephalinamide or 5 mg of AL encephalinamide in equal volumes of mock CSF into the cisterna magna. By 60 min after intracisternal injection, radiolabeled AM encephalinamide distributed throughout the brain with the highest concentration being in the area of the brainstem. Sixty minutes after intracisternal injection, heart rate was decreased 29.0 ± 5.1%, 41.3 ± 4.4%, and 36.0 ± 3.6%, and MABP was decreased 25.2 ± 8.0%, 26.4 ± 2.4%, and 32.3 ± 2.6% in animals treated with AL encephalinamide (5 mg), AM encephalinamide (5 mg), and AM encephalinamide (25 mg), respectively. Neither AL encephalinamide or AM encephalinamide altered CBF or CMRO2 when compared with animals treated with mock CSF, whereas both AL encephalinamide and AM encephalinamide reduced neurohypophyseal blood flow by 30 min (43 ± 11%, AL encephalinamide; 35 ± 7%, AM encephalinamide, 5 mg; 46 ± 8%, AM encephalinamide, 25 mg); the reduction was sustained throughout the 60-min protocol (34 ± 10%, AL encephalinamide; 37 ± 3%, AM encephalinamide, 5 mg; 38 ± 4% AM encephalinamide, 25 mg). Plasma arginine vasopressin was transiently elevated 15 (326 ± 75%, AL encephalinamide; 323 ± 109%, AM encephalinamide, 25 mg) and 30 min (271 ± 68%, AL encephalinamide; 368 ± 136%, AM encephalinamide, 25 mg) in animals treated with AL encephalinamide or AM encephalinamide (25 mg). Intravenous naloxone administered at the end of the 60-min encephalinamide protocol was associated with a rise toward control values in heart rate and MABP in the AL encephalinamide group and in heart rate, MABP, and neurohypophyseal blood flow in both the AM encephalinamide 5 mg and 25 mg groups. These data suggest that encephalinamides may play a role in the regulation of neurohypophyseal blood flow through their actions on opiate receptors.


1983 ◽  
Vol 245 (5) ◽  
pp. H721-H724 ◽  
Author(s):  
C. Chassaing ◽  
P. Duchene-Marullaz ◽  
M. J. Veyrac

The influence of isoproterenol, norepinephrine, and dopamine on the cardiomoderator effects of moderate vagal stimulation was studied in anesthetized dogs. The drugs were administered at increasing doses in successive perfusions. Stimulation of the vagus nerve, the parameters of which remained constant throughout each experiment, was performed immediately before each sequence of perfusion and after 10-min perfusion. Isoproterenol at 0.025, 0.05, 0.1, and 0.2 microgram X kg-1 X min-1 raised heart rate dose relatedly but did not alter heart rate under vagal stimulation. Thus the amplitude of vagal bradycardic effects increased dose relatedly. Norepinephrine at 0.125, 0.25, 0.5, and 1 microgram X kg-1 X min-1 lowered heart rate through reflex hypertension. Heart rate under vagal stimulation remained constant. Thus the effects of vagal stimulation decreased as dose increased, finally becoming null. Dopamine at 0.5, 1, 2.5, and 5 micrograms X kg-1 X min-1 did not significantly alter heart rate, but at 10 and 20 micrograms X kg-1 X min-1, like norepinephrine, it raised blood pressure, causing a reflex fall in heart rate. At all doses, heart rate under vagal stimulation remained stable. Consequently, at the highest doses, the net effects of vagal stimulation were slight. These results suggest the simultaneous involvement of sympathetic-parasympathetic interactions both post- and prejunctionally. In the latter case, different mechanisms of regulation of neurotransmitter release are involved during vagal stimulation according to the sympathomimetic used. With isoproterenol, norepinephrine release seems more particularly affected, whereas with norepinephrine and dopamine, acetylcholine release is apparently inhibited.


1962 ◽  
Vol 17 (5) ◽  
pp. 833-836 ◽  
Author(s):  
John Salzano ◽  
F. G. Hall

Anatomical and physiological dead spaces were enlarged as a result of reduction in body temperature to 28 C in spontaneously respiring anesthetized dogs. Respiratory dead space at 32 C was not significantly different from that at normal body temperature. Vagal blockade resulted in an increase in tidal volume and decrease in respiratory frequency and increased anatomic and physiologic dead space at normal and reduced temperatures. Alveolar ventilation and cardiac output declined equally (percentagewise) with reduction in body temperature to 32 C; at 28 C alveolar ventilation fell more precipitously so that alveolar ventilation-cardiac output ratio (ventilation-perfusion) at 28 C was approximately one-half that at 37 and 32 C. Arterial-alveolar carbon dioxide pressure differences were independent of temperature and vagal blockade. The results indicate no impairment of gas transport or gas exchange at 32 or 28 C in spontaneously respiring anesthetized dogs. Submitted on January 11, 1962


2021 ◽  
Vol 7 (1) ◽  
pp. e000907
Author(s):  
Giovanni Polsinelli ◽  
Angelo Rodio ◽  
Bruno Federico

IntroductionThe measurement of heart rate is commonly used to estimate exercise intensity. However, during endurance performance, the relationship between heart rate and oxygen consumption may be compromised by cardiovascular drift. This physiological phenomenon mainly consists of a time-dependent increase in heart rate and decrease in systolic volume and may lead to overestimate absolute exercise intensity in prediction models based on heart rate. Previous research has established that cardiovascular drift is correlated to the increase in core body temperature during prolonged exercise. Therefore, monitoring body temperature during exercise may allow to quantify the increase in heart rate attributable to cardiovascular drift and to improve the estimate of absolute exercise intensity. Monitoring core body temperature during exercise may be invasive or inappropriate, but the external auditory canal is an easily accessible alternative site for temperature measurement.Methods and analysisThis study aims to assess the degree of correlation between trends in heart rate and in ear temperature during 120 min of steady-state cycling with intensity of 59% of heart rate reserve in a thermally neutral indoor environment. Ear temperature will be monitored both at the external auditory canal level with a contact probe and at the tympanic level with a professional infrared thermometer.Ethics and disseminationThe study protocol was approved by an independent ethics committee. The results will be submitted for publication in academic journals and disseminated to stakeholders through summary documents and information meetings.


1998 ◽  
Vol 85 (1) ◽  
pp. 204-209 ◽  
Author(s):  
John W. Castellani ◽  
Andrew J. Young ◽  
Michael N. Sawka ◽  
Kent B. Pandolf

This study examined whether serial cold-water immersions over a 10-h period would lead to fatigue of shivering and vasoconstriction. Eight men were immersed (2 h) in 20°C water three times (0700, 1100, and 1500) in 1 day (Repeat). This trial was compared with single immersions (Control) conducted at the same times of day. Before Repeat exposures at 1100 and 1500, rewarming was employed to standardize initial rectal temperature. The following observations were made in the Repeat relative to the Control trial: 1) rectal temperature was lower and heat debt was higher ( P < 0.05) at 1100; 2) metabolic heat production was lower ( P < 0.05) at 1100 and 1500; 3) subjects perceived the Repeat trial as warmer at 1100. These data suggest that repeated cold exposures may impair the ability to maintain normal body temperature because of a blunting of metabolic heat production, perhaps reflecting a fatigue mechanism. An alternative explanation is that shivering habituation develops rapidly during serially repeated cold exposures.


1972 ◽  
Vol 50 (5) ◽  
pp. 381-388
Author(s):  
Victor Elharrar ◽  
Reginald A. Nadeau

The importance of the level of adrenergic tone in the determination of the dose–response curve to noradrenaline (NA) and in the evaluation of β-adrenergic blocking agents was studied in open-chest sodium pentobarbital anesthetized dogs by injecting drugs directly into the sinus node artery. Changes in the level of adrenergic tone by stimulating the right stellate ganglion resulted in variation of the observed chronotropic response to NA and of its ED50. The chronotropic responses were corrected by taking into account the underlying adrenergic tone. The negative chronotropic effect of dl-propranolol (1 and 10 μg) appeared to be related to its β-blocking properties and not to its quinidine-like effects as shown by the lack of effect of d-propranolol injected at the same doses. The magnitude of the negative chronotropic effects of 10 μg of propranolol and 100 μg of practolol, oxprenolol, and sotalol was shown to be related to the initial heart rate and consequently to the level of adrenergic tone. The comparison of these four β-blocking agents was carried out on corrected dose-response curves to NA. Their relative potencies were found to be: propranolol > oxprenolol > practolol > sotalol, corresponding to ratios of 1, [Formula: see text], [Formula: see text], and [Formula: see text]


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