Evidence that endogenous vasopressin plays a protective role in circulatory shock. Role for reticuloendothelial system using Brattleboro rats

Altura, Bella T.

doi:10.1007/bf01965981

Cited by 25 publications

(8 citation statements)

References 6 publications

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“…rats which also showed that these animals are much more susceptible to blood loss than l.e. rats (Altura, 1980). Altura suggested that the absence of the constrictor effect of the hormone on the microcirculation in b.d.i.…”

Section: Resultsmentioning

confidence: 99%

The cardiovascular effects of vasopressin after haemorrhage in anaesthetized rats.

Chapman¹,

Hreash²,

Laycock³

et al. 1986

The Journal of Physiology

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SUMMARY1. The cardiovascular effects of an acute haemorrhage (2 % of the body weight)were studied over a 60 min period in three groups of rats: (a) Brattleboro rats with hereditary hypothalamic diabetes insipidus (b.d.i.) lacking circulating vasopressin, (b) control rats of the parent Long Evans (l.e.) strain, and (c) l.e. rats treated with an antagonist of the vascular action of vasopressin.2. Prior to the haemorrhage there were no significant differences between the three groups of rats with respect to mean arterial blood pressure, cardiac output, stroke volume or total peripheral resistance.3. Following the haemorrhage cardiac output and stroke volume were severely reduced in all three groups of rats. Total peripheral resistance was relatively unaffected in antagonist-treated l.e. rats and b.d.i. rats, but rose substantially in response to the loss of blood in the control l.e. group. Both total peripheral resistance and mean arterial blood pressure were markedly greater in the untreated l.e. control rats than in the other two groups of animals during the first 20 min after haemorrhage.4. The mean heart rate measured in Brattleboro rats was elevated compared with that of control l.e. rats throughout the experiment and, in addition, significantly greater than that of antagonist-treated l.e. rats during the first 40 min after the haemorrhage.5. Survival rate for the b.d.i. rats following the 2 % haemorrhage was lower than that for l.e. control rats and antagonist-treated l.e. rats.6. The results indicate that the recovery of the blood pressure following an acute arterial haemorrhage is significantly influenced by vasopressin, particularly during the first 20 min, and that the predominant effect of the hormone is to increase the total peripheral resistance. The higher mortality associated with volume depletion in the b.d.i. rats is unlikely to be directly related to the absence of the vascular action of vasopressin, since administration of the vasopressin antagonist to normal l.e. rats does not reduce their survival rate.

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Section: Resultsmentioning

confidence: 99%

The cardiovascular effects of vasopressin after haemorrhage in anaesthetized rats.

Chapman¹,

Hreash²,

Laycock³

et al. 1986

The Journal of Physiology

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“…Arginine vasopressin could exert a positive influence on the water balance system (195), the cardiovascular system (196), the immune system (197)(198)(199)(200), the adrenal system (20 1,202), and the respiratory system (203,204). Now, as a result of these exhaustive studies, it is clear that this neurohormone acts centrally on the thermoregulatory system in a manner which may be quite beneficial to the animal during a febrile episode.…”

Section: Avp: Its Role As An Endogenous Antipyreticmentioning

confidence: 99%

Peptide neurohormones: their role in thermoregulation and fever

Ruwe¹,

Veale²,

Cooper³

1983

Can. J. Biochem. Cell Biol.

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The neural elements of the rostral diencephalon in the mammal have been implicated in the regulation of body temperature. Moreover, it may be the neural elements within this region of the brain which activate the febrile mechanisms in response to pyrogen. Is it possible that the neuropeptides located within this area of the brain serve as neurochemical intermediaries involved in temperature regulation, fever, and (or) antipyresis? Central administration of several neuropeptides can elicit marked changes in the core temperature of an animal. Although most of these purative neuroregulators exert only a very minor influence on thermoregulation, a small number of the neuropeptides have been shown to have a profound effect on the system controlling this basic vegetative function. One of these peptides, arginine vasopressin (AVP) may play a role as an endogenous antipyretic. The neuroanatomical localization of this peptide, as well as its axonal projections, are consistent with such a role for this neurohypophyseal peptide in the mediation of antipyresis. In addition, current evidence suggests that AVP does function as a neurotransmitter. Examination of the febrile response to pyrogen in both the periparturient animal and the neonate indicates that an elevation in plasma levels of AVP is closely correlated with the diminution in the febrile response. Also, when AVP is perfused into punctate regions of the brain, a pyrogen-induced fever may be markedly suppressed AVP appears to act primarily within the septal area, 2- to 3-mm rostral to the anterior commissure. During the development of fever, the release of AVP is altered within these same loci. As body temperature decreases during the febrile state, there is a concomitant increase in the amount of AVP released into the extracellular fluid of these septal sites. Very recent findings suggest that AVP may have additional central neurochemical functions. For example, this peptide may be involved in the etiology of some forms of convulsive disorders. The precise manner in which body temperature is regulated by the central nervous system normally and during fever is not well understood.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…Таким образом, хотя выявленное повышение уровня ВП у пациентов с ХСН в сравнении со здоровыми представителями контрольной группы в целом соответствовало данным литературы [10,15,16], установленное нами относительное снижение уровня ВП у пациентов с ХСН III стадии и IV ФК ранее мало описано в литературе. Так, по данным S. Masson и соавт., уровень копептина (является С-концевой частью прогормона ВП, производимой организмом в эквимолярном ВП количестве) в группе пациентов с III и IV ФК ХСН статистически значимо выше, чем в группе пациентов со II ФК [17].…”

Section: Discussionunclassified

“…С одной стороны, изменение О р и г и н а л ь н ы е и с с л е д о в а н и я уровня ВП у пациентов с ростом тяжести ХСН может иметь двоякий характер. Так, на начальной и клинически выраженной стадии ХСН повышение уровня ВП играет негативную роль, стимулируя задержку жидкости и прогрессирование сердечной недостаточности [9,10]; однако на последних стадиях оно может сменяться истощением нейронов гипоталамуса и относительным дефицитом ВП, который может как являться одной из причин негативного прогноза у таких пациентов, так и быть лишь одним из симптомов истощения организма и нарушения регуляции гипоталамо-гипофизарно-надпочечниковой оси у пациентов с терминальной и декомпенсированной ХСН [20].…”

Section: Discussionunclassified

“…При этом, если у здорового человека уровень ВП подвержен обратной регуляции под воздействием как осмотических факторов, так и рефлексов с барорецепторов (синокаротидной зоны, дуги аорты, левого предсердия), то у пациентов с ХСН эффективность данных регуляторных механизмов существенно снижается [6][7][8]. Это приводит к длительной нерегулируемой гиперпродукции ВП у пациентов с ХСН, задержке жидкости и развитию у них так называемой гиперволемической гипонатриемии, приводящей к ухудшению прогноза и росту смертности пациентов с ХСН [9,10].…”

Section: Introductionunclassified

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Correlation Between Vas Opressin Concentration and Chronic Heart Failure Seve Rity: Charac Teristics of Pa Tients With Terminal and Decompe Nsa Ted Heart Failure

2018

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Objective: to evaluate vasopressin (VP) concentration in patients with varying severity of chronic heart failure (CHF), intensity of clinical symptoms, and decreased level of left ventricular ejection fraction (LVEF). Materials and methods. In total, 120 patients (44 males, 76 females) with CHF of varying genesis (mean age 72.12 ± 10.18 years) and 30 clinically healthy individuals (18 males, 12 females) as a control group (mean age 33.4 ± 6.23 years) were examined. All patients underwent comprehensive clinical and instrumental examination in accordance with the standards for patients with CHF. The VP level was determined using ELISA. Statistical analysis was performed using the IBM SPSS Statistics v. 23 software.Results. The patients with CHF had significantly higher blood VP levels compared to the control group (72.91 ± 53.9 pg/ml versus 6.6 ± 3.2 pg/ml respectively; p <0.01). At the same time, patients with stage III CHF had significantly lower VP levels than patients with stages IIВ and IIА (35.61 ± 21.53 pg/ml versus 71.67 ± 48.31 pg/ml and 86.73 ± 59.78 pg/ml respectively; p<0.01). A similar picture was observed for the functional classes (FC). For instance, for CHF FC II and III, the VP level was 91.93 ± 67.13 pg/ml and 77.95 ± 54.01 pg/ml respectively, while for FC IV it decreased to 50.49 ± 28.18 pg/ml (p <0.01). The VP concentration in patients who subsequently perished was significantly lower than in patients who survived (48.79 ± 26.30 pg/ml versus 79.72 ± 57.73 pg/ml; p = 0.012). Moreover, in patients with LVEF <50 %, the VP level was significantly lower than in patients with LVEF >50 % (59.43 ± 42.51 pg/ml versus 86.43 ± 62.46 pg/ml respectively; p <0.05).Conclusion. The observed significant differences in VP in patients with stage III and IV CFH can indicate depletion of neurohumoral mediators in this patient category. However, a correlation between the VP level and the level of LVEF decrease can indicate a significant difference in the role of VP in CHF pathogenesis in patients with preserved and decreased LVEF. This observation requires further research.

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Evidence that endogenous vasopressin plays a protective role in circulatory shock. Role for reticuloendothelial system using Brattleboro rats

Cited by 25 publications

References 6 publications

The cardiovascular effects of vasopressin after haemorrhage in anaesthetized rats.

The cardiovascular effects of vasopressin after haemorrhage in anaesthetized rats.

Peptide neurohormones: their role in thermoregulation and fever

Correlation Between Vas Opressin Concentration and Chronic Heart Failure Seve Rity: Charac Teristics of Pa Tients With Terminal and Decompe Nsa Ted Heart Failure

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