Ontogeny of canine intrathoracic cardiac nervous system

1991 ◽  
Vol 261 (4) ◽  
pp. R920-R927 ◽  
Author(s):  
C. Haddad ◽  
J. A. Armour

The functional cardiac innervation of 61 puppies from nine different litters (2-8 littermates), ranging in age from 1 day to 7 wk, was investigated. The efferent sympathetic nervous system exerted minimal effects on the heart of 1-day-old puppies, gradually influencing the heart more thereafter such that by 7 wk of life it was functionally mature. In contrast, efferent parasympathetic cardiac innervation was well developed at birth, maturing thereafter such that by 4-7 wk of age its capacity to modulate the heart was similar to that found in adults. The right- and left-sided efferent sympathetic and parasympathetic intrathoracic nervous systems induced similar cardiac modulation throughout this period of development. Cardiac myocyte beta-adrenergic receptors were partially functional at birth, as determined by responses elicited by supramaximal doses of the beta-agonist isoproterenol. Responses elicited by isoproterenol became greater over the following 7 wk of life, when they were found to be similar to those elicited in adults. By 1 wk of age, synaptic mechanisms in intrathoracic sympathetic ganglia involved in cardiac regulation were relatively well developed, with cardiopulmonary-cardiac reflexes present but not functionally mature at that age. It is concluded that maturation of the efferent sympathetic nervous system modulating the canine heart depends to a large extent on the ontogeny of cardiac beta-adrenergic receptors rather than the ontogeny of synapses in intrathoracic ganglia. Furthermore, even though functional cardiac efferent parasympathetic innervation is present before efferent sympathetic innervation, both reach maturity at about the same age.

1985 ◽  
Vol 63 (4) ◽  
pp. 340-343 ◽  
Author(s):  
Betty P. Vogh ◽  
David R. Godman

Administration iv of 50 mg∙kg−1 acetazolamide (A) and 3 mg∙kg−1 timolol (T) causes the formation of cerebrospinal fluid (f-CSF) to be reduced to 43.7% of the control rate compared with a reduction to 82.5% of control by T alone and to 52.6% of control by A alone. The effect of combined drugs is the same when A is combined with T initially, when A is added to T after studying T alone, or when T is added to A after studying A alone. In contrast, in rats f-CSF is not influenced by T, either alone or when in combination with A. The rate in rats is reduced to 55% of control by treatments with A or A and T. Decrease in formation of cerebrospinal fluid by A occurs through inhibition of carbonic anhydrase, but the means whereby T (a known blocker of beta-adrenergic receptors) causes a reduction in f-CSF is not established; it is known that it does not inhibit carbonic anhydrase. Control of f-CSF by the sympathetic nervous system is discussed.


1987 ◽  
Vol 253 (4) ◽  
pp. G531-G539 ◽  
Author(s):  
R. A. Gillis ◽  
J. Dias Souza ◽  
K. A. Hicks ◽  
A. W. Mangel ◽  
F. D. Pagani ◽  
...  

The purpose of this study is to determine whether or not the sympathetic nervous system provides a tonic inhibitory input to the colon in chloralose-anesthetized cats. Proximal and midcolonic motility were monitored using extraluminal force transducers. An intravenous bolus injection of 5 mg of phentolamine in 14 animals elicited a pronounced increase in proximal colon contractility. The minute motility index changed from 0 +/- 0 to 26 +/- 4 after phentolamine administration. Midcolonic motility also increased in response to phentolamine. Specific blockade of alpha 2-receptors, but not alpha 1-receptors, caused the same response seen with phentolamine. alpha-Adrenergic blockade increased colon contractility after spinal cord transection but not after ganglionic blockade. Blockade of alpha-adrenergic receptors was also performed before vagal and pelvic nerve stimulation and in both cases increased colonic motility. Vagal stimulation alone had no effect on colonic contractility, while pelvic nerve stimulation increased motility at the midcolon. alpha-Receptor blockade did not alter the ineffectiveness of vagal stimulation but did unmask excitatory effects of pelvic nerve stimulation on the proximal colon. All excitatory colonic responses were prevented by blocking muscarinic cholinergic receptors. These data indicate that tonic sympathetic nervous system activity exerts an inhibitory effect on colonic motility. The inhibitory effect is mediated through alpha 2-adrenergic receptors. Based on these findings, we suggest that alterations in sympathetic nervous system activity may be extremely important for the regulation of circular muscle contractions in the colon.


1982 ◽  
Vol 10 (3) ◽  
pp. 221
Author(s):  
Bart Chernow ◽  
Michael Ziegler ◽  
Joseph Coyle ◽  
David Cruess ◽  
Pat Hughes ◽  
...  

2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
VA Aleksandrenko ◽  
EA Kuzheleva ◽  
AA Garganeeva

Abstract Funding Acknowledgements Type of funding sources: None. Introduction. Abnormalities in the cardiac sympathetic nervous system have been documented in myocardial infarction (MI) and have been directly implicated in pathogenesis and progression of MI. Assessment of the autonomic nervous system activity in acute stage of MI allowed us to identify groups of high-risk patients. Purpose. To investigate the sympathetic nervous system activity in patients with MI by assessing the condition of beta-adrenergic reactivity of erythrocytes. To analyze ADRB1 Arg389Gly associations with the state of beta-adrenergic reactivity of erythrocytes in patients with MI. Methods. During the study period, 62 patients were enrolled. The patients were divided into 2 groups. The first group consisted of 11 patients (nine women and two men, median age of 54.0 [49.0;61.0] years) with normal beta-adrenergic reactivity of erythrocytes, the second group consisted of 51 patients (40 women and 11 man, median age of 61.0 [48.0;72.0] years) with abnormal beta-adrenergic reactivity of  erythrocytes. The research of beta-adrenergic reactivity of erythrocytes was conducted by analysis of changing erythrocyte osmoresistance under the influence of beta blocker in the first 6 hours from the onset of the heart attack. The genetic research was conducted by PСR method in real time. Results. Groups of patients were comparable in main clinical indicators (anamnesis of ischemic heart disease and chronic heart failure, frequency of beta blockers administration before and during of MI, electrocardiography features: elevation of ST-segment, Q-wave and etc.). The second group presented with a higher occurrence of acute left ventricular failure (33.3% vs 0%, p = 0.026) and arterial hypertension (90.2% vs 63.6%, p = 0.044). Parameters of myocardial damage were significantly higher in the second group than the first group. Primarily, this manifested in the presence of a greater number of hypokinesis zones on echocardiography (p = 0.015). In addition, patients of the second group had a lower ejection fraction according to echocardiography (51.0 [46.5;59.0]% vs 58.0 [52.0;63.0]%, p = 0.042). Levels of blood necrosis biomarkers were significantly higher in the second group, e.g. Troponin I (24.1 [9.9;68.0] ng/ml vs 1.3 [0.2;1.8] ng/ml, p = 0.001). At the same time statistically significant distinctions of the severity of coronary atherosclerosis in groups were not revealed. The analysis of ADRB1 Arg389Gly demonstrated association of CC-genotype with abnormal beta-adrenergic reactivity of erythrocytes [OR 5.9, 95% СI 1.16-30.25, p = 0.043]. Conclusion. Patients with an abnormal beta-adrenergic reactivity were characterized by a greater volume of damage to the heart muscle. Moreover, association of CC-genotype of gene ADRB1 Arg389Gly with abnormal beta-adrenergic reactivity of erythrocytes was identified.


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