Hypophysectomy alters cardiorespiratory variables: central effects of pituitary endorphins in shock

1981 ◽  
Vol 241 (4) ◽  
pp. H479-H485 ◽  
Author(s):  
J. W. Holaday ◽  
M. O'Hara ◽  
A. I. Faden
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Mean Arterial Pressure ◽  
Hypovolemic Shock ◽  
Cardiovascular Effects ◽  
Central Effects ◽  
Hypophysectomized Rats ◽  
The Central Nervous System

The possible involvement of pituitary endorphins in the pathophysiology of shock was evaluated by measuring cardiorespiratory variables after naloxone injection in conscious hypophysectomized and sham-hypophysectomized rats subjected to controlled hemorrhage. Additionally, the role of the central nervous system (CNS) in mediating the cardiodepressant effects of endorphins in shock was studied. After the induction of hypovolemic shock (20 min at below 40 mmHg), hypophysectomized and sham-hypophysectomized rats received intraventricular (ivt) injections of naloxone HCl (10 micrograms) or an equivalent volume of saline (20 microliters over 20 s). In sham-hypophysectomized rats, both injections significantly elevated mean arterial pressure and pulse pressure; however, the increase produced by naloxone was significantly greater than that produced by saline. By contrast, hypophysectomized rats showed no response to naloxone or saline. Intravenous (iv) administration of naloxone HCl (3 mg/kg) or saline to these same hypophysectomized rats 15 min after ivt administration had no additional cardiovascular effects; as before, only animals with intact pituitaries responded to naloxone. Heart rate and respiration rate were unaffected by ivt or iv naloxone. From these data we suggest that pituitary endorphins contribute to the pathophysiology of hypovolemic shock, at least in part through actions within the CNS.

Central nervous system cardiovascular effects of bombesin in conscious rats

1985 ◽  
Vol 248 (4) ◽  
pp. H425-H431 ◽  
Author(s):  
L. A. Fisher ◽  
C. R. Cave ◽  
M. R. Brown
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Effects ◽  
Peripheral Circulation ◽  
Alpha Adrenergic Receptors ◽  
The Central Nervous System ◽  
Atropine Methyl Nitrate

The effects of intracerebroventricular administration of bombesin on mean arterial pressure and heart rate were studied in conscious, freely moving rats. Injection of bombesin produced dose-dependent elevations of mean arterial pressure and reductions of heart rate. These effects were not caused by leakage of bombesin into the peripheral circulation. Adrenalectomy abolished the pressor action of bombesin but did not alter bombesin-induced bradycardia. Systemic phentolamine pretreatment prevented bombesin-induced changes of mean arterial pressure, whereas rats treated intravenously with captopril or a vasopressin antagonist still exhibited pressor responses to bombesin administration. Bombesin-induced bradycardia was partially antagonized by intravenous atropine methyl nitrate administration, whereas systemic injections of propranolol did not modify this response. It is concluded that bombesin acts within the central nervous system to elevate mean arterial pressure through an adrenal-dependent mechanism involving alpha-adrenergic receptors and to reduce heart rate through an adrenal-independent mechanism involving, at least in part, cardiac parasympathetic nervous activation.

Central and Peripheral Mechanisms in the Maintenance of Experimental Hypertension in the Rabbit

1973 ◽  
Vol 45 (5) ◽  
pp. 701-709 ◽  
Author(s):  
John L. Reid ◽  
Peter J. Lewis ◽  
Colin T. Dollery
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renal Hypertension ◽  
Experimental Hypertension ◽  
Large Contribution ◽  
Neurogenic Hypertension ◽  
The Central Nervous System

1. The role of the central nervous system (CNS) in maintaining arterial pressure was investigated in two types of experimental hypertension in rabbits. 2. In rabbits with neurogenic hypertension produced by baroreceptor denervation, anaesthesia followed by injection of clonidine (1 μg/kg) into the cisterna magna lowered mean arterial pressure (MAP) from 100·5 ± 1·5 mmHg to 45·0 ± 2·5 mmHg. In normal animals treated similarly MAP fell from 79·1 ± 2·3 mmHg to 49·1 ± 3·9 mmHg. 3. In renal hypertensive rabbits with cellophane perinephritis, intracisternal clonidine decreased MAP from 117·9 ± 4·7 mmHg to 73·0 ± 4·2 mmHg. 4. Acute ganglion blockade with intravenous pentolinium (3 mg/kg) caused a maximum fall in MAP in renal hypertensive animals to 75·8 ± 5·5 mmHg. Combination of intracisternal clonidine and intravenous pentolinium did not significantly augment this fall. 5. The raised arterial pressure in neurogenic hypertension is mediated by the CNS. In renal hypertension, there is a large contribution from the CNS but there are additional non-neurogenic factors elevating the pressure.

Role of a nurse in the rehabilitation of children using ReviMotion hardware and software complex

2020 ◽  
pp. 49-56
Author(s):  
T. Shirshova
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
School Age Children ◽  
Equipment Management ◽  
School Age ◽  
Rehabilitation Process ◽  
Software Complex ◽  
Trained Personnel ◽  
The Central Nervous System

Disorders of the musculoskeletal system in school-age children occupy 1-2 places in the structure of functional abnormalities. Cognitive impairment without organic damage to the central nervous system is detected in 30-56% of healthy school children. Along with the increase in the incidence rate, the demand for rehabilitation systems, which allow patients to return to normal life as soon as possible and maintain the motivation for the rehabilitation process, is also growing. Adaptation of rehabilitation techniques, ease of equipment management, availability of specially trained personnel and availability of technical support for complexes becomes important.

The Role of Neuropeptide Y and Peptide YY in the Development of Obesity via Gut-brain Axis

2019 ◽  
Vol 20 (7) ◽  
pp. 750-758 ◽  
Author(s):  
Yi Wu ◽  
Hengxun He ◽  
Zhibin Cheng ◽  
Yueyu Bai ◽  
Xi Ma
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuropeptide Y ◽  
Metabolic Diseases ◽  
Peptide Yy ◽  
Vital Role ◽  
Gut Peptides ◽  
Nonalcoholic Fatty Liver ◽  
The Central Nervous System

Obesity is one of the main challenges of public health in the 21st century. Obesity can induce a series of chronic metabolic diseases, such as diabetes, dyslipidemia, hypertension and nonalcoholic fatty liver, which seriously affect human health. Gut-brain axis, the two-direction pathway formed between enteric nervous system and central nervous system, plays a vital role in the occurrence and development of obesity. Gastrointestinal signals are projected through the gut-brain axis to nervous system, and respond to various gastrointestinal stimulation. The central nervous system regulates visceral activity through the gut-brain axis. Brain-gut peptides have important regulatory roles in the gut-brain axis. The brain-gut peptides of the gastrointestinal system and the nervous system regulate the gastrointestinal movement, feeling, secretion, absorption and other complex functions through endocrine, neurosecretion and paracrine to secrete peptides. Both neuropeptide Y and peptide YY belong to the pancreatic polypeptide family and are important brain-gut peptides. Neuropeptide Y and peptide YY have functions that are closely related to appetite regulation and obesity formation. This review describes the role of the gutbrain axis in regulating appetite and maintaining energy balance, and the functions of brain-gut peptides neuropeptide Y and peptide YY in obesity. The relationship between NPY and PYY and the interaction between the NPY-PYY signaling with the gut microbiota are also described in this review.

The Yin and Yang of BK Channels in Epilepsy

2018 ◽  
Vol 17 (4) ◽  
pp. 272-279 ◽  
Author(s):  
Yudan Zhu ◽  
Shuzhang Zhang ◽  
Yijun Feng ◽  
Qian Xiao ◽  
Jiwei Cheng ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Bk Channels ◽  
Bk Channel ◽  
Potential Shape ◽  
Yin And Yang ◽  
The Central Nervous System ◽  
Action Potential Shape ◽  
Excitability Of Neurons

Background & Objective: The large conductance calcium-activated potassium (BK) channel, extensively distributed in the central nervous system (CNS), is considered as a vital player in the pathogenesis of epilepsy, with evidence implicating derangement of K+ as well as regulating action potential shape and duration. However, unlike other channels implicated in epilepsy whose function in neurons could clearly be labeled “excitatory” or “inhibitory”, the unique physiological behavior of the BK channel allows it to both augment and decrease the excitability of neurons. Thus, the role of BK in epilepsy is controversial so far, and a growing area of intense investigation. Conclusion: Here, this review aims to highlight recent discoveries on the dichotomous role of BK channels in epilepsy, focusing on relevant BK-dependent pro- as well as antiepileptic pathways, and discuss the potential of BK specific modulators for the treatment of epilepsy.

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