Site of action of endotoxin in evoking bradycardia

1969 ◽  
Vol 47 (12) ◽  
pp. 999-1008
Author(s):  
B. Blattberg ◽  
M. N. Levy

Previous investigation of the mechanism responsible for the bradycardia evoked by the intravenous injection of bacterial endotoxin revealed that the primary site of action of the endotoxin must be some subdiaphragmatic structure. The present study was undertaken to localize more precisely this site of action. In anesthetized dogs, the renal pedicles or the intestinal arteries were ligated before endotoxin was administered. It was found that exclusion of the intestinal vascular bed prevented the fall in heart rate, whereas occlusion of the renal vasculature did not alter the cardiac response. To localize the mesenteric site of action of endotoxin more precisely, small doses of endotoxin were injected into each of the individual intestinal arteries and into the splenic artery and the portal vein. The response was compared with that evoked by the injection of an equivalent amount of endotoxin into a femoral artery. It was observed that when endotoxin was injected into the intestinal arteries, bradycardia resulted. However, when endotoxin was injected into the femoral artery or the portal vein, no significant change in heart rate was detected, indicating that the intestines probably are the site of action for evoking bradycardia.

1978 ◽  
Vol 235 (3) ◽  
pp. H345-H349 ◽  
Author(s):  
G. R. Hageman ◽  
F. Urthaler ◽  
T. N. James

Excitation of a cardiac chemoreceptor with 5-hydroxytryptamine (serotonin) produces a complex autonomic reflex which includes hypertension, changes in heart rate and contractile force, and disturbances of AV conduction. This study examines the afferent and efferent neural pathways of this autonomic reflex in 60 anesthetized dogs. We used cooling and sectioning techniques in 40 of these, and in 20 others recorded afferent neurograms. The most common afferent pathways for the reflex were found in the left and right recurrent cardiac nerves. No preferential efferent routes to the heart were found, although the nature of the reflex cardiac response could be altered by specific nerve interruption. Cyproheptadine (1 mg/kg iv) regularly abolished both the reflex and the chemoreceptor afferent neural traffic, but injection of a 10 times higher concentration of serotonin (1 mg/ml) readily surmounted the blockade and restored the chemoreceptor neural traffic. Thus cyproheptadine interdicts the reflex at the site of its initiation.


1992 ◽  
Vol 262 (5) ◽  
pp. E671-E678 ◽  
Author(s):  
S. Kowalyk ◽  
R. Veith ◽  
M. Boyle ◽  
G. J. Taborsky

To determine whether the gut or liver releases galanin during sympathetic neural activation, we performed bilateral thoracic splanchnic nerve stimulation (BTSNS) in halothane-anesthetized dogs. Using experimentally determined galanin extraction rates of 60% for gut and no extraction by liver, calculations demonstrated a minor increase in gut spillover during BTSNS (delta = +4.8 +/- 1.8 pmol/min), whereas liver spillover of galanin-like immunoreactivity (GLIR) increased markedly (delta = +27.9 +/- 9.5 pmol/min). To confirm the finding of liver galanin release, GLIR was measured in femoral artery, portal vein, and hepatic vein during hepatic nerve stimulation (HNS). GLIR spillover from gut was not increased by HNS (delta = +1.9 +/- 6.3 pmol/min). In contrast, liver GLIR spillover was greatly increased during HNS (delta = +53.3 +/- 16.4 pmol/min). Extracts of canine liver contained 2.7 +/- 0.4 pmol GLIR/g tissue. We conclude that, despite the known significant galanin content of the gut, little galanin is released from this organ during sympathetic activation. In contrast, the liver, heretofore not described to contain galanin, contains and releases significant amounts of the peptide during sympathetic activation.


2020 ◽  
pp. 81-85
Author(s):  
E. P. Popova ◽  
O. T. Bogova ◽  
S. N. Puzin ◽  
D. A. Sychyov ◽  
V. P. Fisenko

Spectral analysis of heart rate variability gives an idea of the role of the autonomic nervous system in the regulation of chronotropic heart function. This method can be used to evaluate the effectiveness of drug therapy. Drug therapy should be carried out taking into account the individual clinical form of atrial fibrillation. Information about the vegetative status of the patient will undoubtedly increase the effectiveness of treatment. In this study, spectral parameters were studied in patients with newly diagnosed atrial fibrillation. The effect of antiarrhythmic drug class III amiodarone on the spectral parameters of heart rate variability was studied.


1952 ◽  
Vol 30 (6) ◽  
pp. 561-570
Author(s):  
J. G. Aldous ◽  
D. K. R. Stewart

Suspensions of the cells of baker’s yeast were irradiated with ultraviolet light for sufficient times to produce populations of 75, 50, 30, and 5% viable cells. After washing and drying, various enzyme solutions were prepared from these cells. Enzymatic activities, on a nitrogen basis, were compared to those of solutions prepared from a nonirradiated population. At the 50% survival level, hexokinase, carboxylase, and zymase were inhibited to a degree roughly proportional to the viability. Carboxylase, and to a certain extent, hexokinase activity varied directly as the population viability. Catalase, alcohol dehydrogenase, and lactic dehydrogenase showed no diminution in activity even at the 5% survival level. These results suggest that although ultraviolet radiation may produce nuclear damage, the primary site of action may be certain enzymes of the cytoplasm.


Biomedicine ◽  
2021 ◽  
Vol 41 (2) ◽  
pp. 274-277
Author(s):  
Priya S.A. ◽  
R. Rajalakshmi

  Introduction and Aim: Mental stress may impact dramatically on dynamic autonomic control on heart. Many studies have demonstrated association of high body mass index (BMI) with greater risk for cardiovascular disease with disturbance in autonomic neuronal activity. Analysis of Heart rate variability (HRV)during acute mental stress assesses the autonomic status of the individual. Hence, we aimed to study the effect of acute mental stress on time domain measures in obese adults.   Materials and Methods:Sixty male volunteers of 30 each in study group (obese individuals) and control group (non-obese individuals) were recruited for the study. A basal recording of ECG in lead II was done on all the individuals. Then they underwent mental arithmetic stress task for 5 minutes during which again ECG was recorded. The change in time domain measures of HRV during rest and stress task was analyzed and compared between both the groups.   Results: Analysis of time domain measures of HRV revealed a statistically significant increase (p ? 0.001) in mean heart rate in both obese and non-obese individuals, while rMSSD(root mean square differences of successive RR interval) and SDNN (standard deviation of all NN intervals) showed a statistically significant (p? 0.001) decrease in obese individuals and non-obese individuals did not show any statistically significant change during the mental stress task.   Conclusion: In response to acute mental stress there was increased heart rate in both the groups. But the autonomic neuronal activity differed by way of sympathetic dominance in non-obese individuals and parasympathetic withdrawal in obese individuals.  


2021 ◽  
pp. 69-70
Author(s):  
Pakanati Sujana ◽  
Venkata Mahesh Gandhavalla ◽  
K. Prabhakara Rao

Introduction: COVID19 is caused by SARS-CoV-2 which is primarily transmitted through respiratory droplets and contact routes. WHO recommended the use of personal protective equipment (PPE) for prevention and N95 respirators are critical components of PPE. Breathing through N95 respirator will impart stress in the individual and that can be assessed by heart rate variability (HRV). HRV measures the variation in time between each heartbeat controlled by autonomic nervous system (ANS), which is a non invasive reliable index to identify the ANS imbalances. Aims And Objectives: This study is aimed at assessing the HRV of Interns working in COVID19 wards using N95 respirators. Methodology: This study included 100 interns in whom short term HRV was recorded using the standard protocol. Lead II of ECG was recorded using AD instruments (ADI) 8channel polygraph and HRV was analysed using Labchart 8pro software. The recordings were taken before and 1hour after wearing N95 respirator. Results: Overall HRV (SDRR) was found to decrease signicantly after wearing N95 respirator for 1hr (p=0.000). Similarly, indices representing the parasympathetic component ( RMSSD and HF ) were also found to decrease signicantly with the use of N95 respirator. Low frequency (LF) power and LF/HF ratio increased signicantly with N95 respirator use (p=0.000). Conclusion: We conclude that using N95 respirator increased sympathetic activity reecting decreased HRV in our subjects Hence we recommend that it is better to change the duty pattern for interns.


1959 ◽  
Vol 197 (5) ◽  
pp. 963-967 ◽  
Author(s):  
John T. Shepherd ◽  
David E. Donald ◽  
Erland Linder ◽  
H. J. C. Swan

5-Hydroxytryptamine (serotonin) was infused into anesthetized dogs at a rate of 20 µg/kg/min. In nine sets of observations on three dogs the increase in the difference of pressure between the pulmonary artery and the left atrium, which averaged 55%, consistently exceeded the increase in pulmonary blood flow, which averaged 16%. 5-HT therefore is a potent constrictor of pulmonary vessels, even in small concentrations. No changes in the pulmonary-artery wedge and pulmonary-vein pressures were detected during the infusions of 5-HT, nor was there any change in the volume of blood between the pulmonary artery and the root of the aorta. With this dose of 5-HT the principal site of the increased resistance to flow through the lungs appeared to be in the precapillary vessels. In the isolated perfused lung, moderate constriction of pulmonary veins also was produced by large doses of 5-HT.


1976 ◽  
Vol 230 (4) ◽  
pp. 893-900 ◽  
Author(s):  
ER Powers ◽  
Foster ◽  
Powell WJ

The modification by aortic pressure and stroke volume of the response in cardiac performance to increases in heart rate (interval-force relationship) has not been previously studied. To investigate this interaction, 30 adrenergically blocked anesthetized dogs on right heart bypass were studied. At constant low aortic pressure and stroke volume, increasing heart rate (over the entire range 60-180) is associated with a continuously increasing stroke power, decreasing systolic ejection period, and an unchanging left ventricular end-diastolic pressure and circumference. At increased aortic pressure or stroke volume at low rates (60-120), increases in heart rate were associated with an increased performance. However, at increased aortic pressure or stroke volume at high rates (120-180), increases in heart rate were associated with a leveling or decrease in performance. Thus, an increase in aortic pressure or stroke volume results in an accentuation of the improvement in cardiac performance observed with increases in heart rate, but this response is limited to a low heart rate range. Therefore, the hemodynamic response to given increases in heart rate is critically dependent on aortic pressure and stroke volume.


1991 ◽  
Vol 261 (3) ◽  
pp. H720-H727 ◽  
Author(s):  
F. L. Belloni ◽  
T. H. Hintze

The effects of the ATP-sensitive K(+)-channel blocker glibenclamide on the cardiovascular responses to adenosine in dogs were determined. Adenosine (0.01-20 mumol/kg iv) caused coronary vasodilatation, arterial hypotension, and bradycardia in dogs with either combined beta-adrenergic and muscarinic receptor blockade or with bilateral cervical vagotomy plus beta-adrenergic receptor blockade. The 50% effective dose for adenosine-induced coronary dilatation was increased from 0.13 +/- 0.04 mumol/kg in the control state to 1.1 +/- 0.5 mumol/kg after 2 mg/kg of glibenclamide (P less than 0.001). Adenosine at 5 mumol/kg reduced heart rate by 19 +/- 5% from a baseline of 158 +/- 6 beats/min in five anesthetized dogs. After glibenclamide (10 mg/kg), this dose of adenosine failed to cause a significant change in heart rate. The arterial hypotensive effects of adenosine were also attenuated by glibenclamide. Thus glibenclamide inhibited adenosine-induced bradycardia, hypotension, and coronary dilatation. On the other hand, glibenclamide did not affect the reductions in heart rate caused by vagus nerve stimulation. The mechanism of this adenosine antagonism is not known but, in the case of bradycardia, it does not appear to involve any of the steps shared in common by both adenosine-induced and vagal responses of the sinoatrial node.


1984 ◽  
Vol 246 (4) ◽  
pp. F447-F456 ◽  
Author(s):  
M. J. Camargo ◽  
H. D. Kleinert ◽  
S. A. Atlas ◽  
J. E. Sealey ◽  
J. H. Laragh ◽  
...  

The effects of rat atrial tissue extract on renal hemodynamics and fluid and electrolyte excretion were investigated in the isolated perfused rat kidney (IK). IK were perfused at a constant effective perfusion pressure of about 90 mmHg. After control clearance periods (C), extracts of rat atria (AE) or ventricles (VE) were added to the perfusate and three 10-min experimental periods followed. AE, but not VE, significantly increased (P less than 0.001) renal vascular resistance (RVR) to 133 +/- 8% of C, GFR to 201 +/- 34%, filtration fraction to 245 +/- 41%, urine flow (V) to 675 +/- 131%, fractional excretion (FE) of H2O to 336 +/- 29%, absolute Na excretion (UNaV) to 1,259 +/- 290%, FENa to 642 +/- 129%, UKV to 2,226 +/- 1,237%, and FEK to 542 +/- 119%. Despite the marked natriuresis, since GFR doubled, Na reabsorption rose from 78.3 +/- 36.3 in C to 132 +/- 36.3 mueq/min after AE. The effects of AE were immediate and lasted to the end of the perfusion. The lower the initial control GFR, the larger was the AE-induced increase in GFR. Perfusion with low [Ca] (0.2 mM) or verapamil (10(-5) M) severely blunted the hemodynamic, diuretic, kaliuretic, and natriuretic effects of AE. AE decreased rather than increased the RVR when IK were perfused with vasoconstrictors such as angiotensin II, norepinephrine, or vasopressin. The results demonstrate that AE acts directly on the kidney, eliciting powerful Ca-dependent hemodynamic and natriuretic responses. The natriuresis induced by AE can be accounted for, at least in part, by its renal hemodynamic effects rather than by the presence of a putative tubular natriuretic factor. The hypothesis is advanced that AE contains a substance(s) which behaves as a functional agonist/antagonist of endogenous vasoconstrictors with a preferential site of action on the efferent arterioles of the renal vasculature.


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