Effects of <scp>l</scp>-NAME on cerebral metabolic, vasopressin,  oxytocin, and blood pressure responses in hemorrhaged rats

Kadekaro, Massako; Terrell, Mary Lee; Liu, Hanwu; Gestl, Shelley A.; Bui, Vuong; Summy-Long, Joan Y.

doi:10.1152/ajpregu.1998.274.4.r1070

Cited by 36 publications

(40 citation statements)

References 21 publications

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“…The decrease found in the other metabolic acid-base-independent variable ([A tot ]) was probably a consequence of hemodilution. Previous studies have found decreases in plasma proteins during hemorrhage (18). However, the decrease was insufficient (ϳ2 meq/l) to have a relevant effect on [H ϩ ] changes that could significantly counteract SID changes.…”

Section: Discussionmentioning

confidence: 94%

“…This latter may increase the activity of the anaerobic energyproducing systems or decrease aerobic energy-producing systems during hemorrhagic shock, thus raising lactic acid concentration of extracellular fluid and reducing plasma HCO 3 Ϫ concentration ([HCO 3 Ϫ ]) (17). However, hemorrhage also results in changes in the main plasma inorganic ions and proteins (6,10,16,18,(37)(38)(39)41).…”

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confidence: 99%

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Acid-base disturbance during hemorrhage in rats: significant role of strong inorganic ions

Alfaro

Pesquero

Palacios

1999

Journal of Applied Physiology

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Alfaro, V., J. Pesquero, and L. Palacios. Acid-base disturbance during hemorrhage in rats: significant role of strong inorganic ions. J. Appl. Physiol. 86(5): 1617-1625, 1999.-The present study tests the hypothesis that changes in the strong inorganic ion concentrations contribute significantly to the acid-base disturbance that develops during hemorrhage in the arterial plasma of rats in addition to lactate concentration ([Lac Ϫ ]) increase. The physicochemical origins for this acid-base disorder were studied during acute, graded hemorrhage (10, 20, and 30% loss of blood volume) in three groups of rats: conscious, anesthetized with ketamine, and anesthetized with urethan. The results support the hypothesis examined: strong-ion difference (SID) decreased in the arterial plasma of all groups studied because of an early imbalance in the main strong inorganic ions during initial hemorrhagic phase. Moreover, changes in plasma [Lac Ϫ ] contributed to SID decrease in a later hemorrhagic phase (after 10% hemorrhage in urethan-anesthetized, after 20% hemorrhage in ketamine-anesthetized, and after 30% hemorrhage in conscious group). Inorganic ion changes were due to both dilution of the vascular compartment and ion exchange with extravascular space and red blood cells, as compensation for blood volume depletion and hypocapnia. Nevertheless, anesthetized rats were less able than conscious rats to preserve normal arterial pH during hemorrhage, mainly because of an impaired peripheral tissue condition and incomplete ventilatory compensation. strong-ion difference; ion imbalance; metabolic acidosis; anesthesia; ketamine; urethan METABOLIC ACIDOSIS IN BLOOD is common during hemorrhage (8, 17). Reduction in blood volume during hemorrhagic shock results in decreased cardiac output and decreased O 2 delivery to tissues (8,10,17,29). This latter may increase the activity of the anaerobic energyproducing systems or decrease aerobic energy-producing systems during hemorrhagic shock, thus raising lactic acid concentration of extracellular fluid and reducing plasma HCO 3 Ϫ concentration ([HCO 3 Ϫ ]) (17). However, hemorrhage also results in changes in the main plasma inorganic ions and proteins (6,10,16,18,(37)(38)(39)41).In 1983, Stewart (35) designed an approach for the study of acid-base changes in body fluids, which assumes that ion and protein changes influence the acid-base balance in a physiological compartment, arterial plasma in the present study. Several authors have used this physicochemical approach to quantify mixed acid-base disorders (3-5, 21, 25, 27, 40). The physicochemical analysis is done by combining the state of electroneutrality with the state of equilibrium for all incompletely dissociated substances and the solvent, water. Three sets of variables that are relevant to the acid-base balance can be changed primarily and/or individually in vivo. They can be regarded as independent variables and are the PCO 2 , the strong-ion difference (SID), and the total concentration of weak acids ([A tot ]). PCO 2 represents t...

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Section: Discussionmentioning

confidence: 94%

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confidence: 99%

Acid-base disturbance during hemorrhage in rats: significant role of strong inorganic ions

Alfaro

Pesquero

Palacios

1999

Journal of Applied Physiology

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“…Hypovolaemia and hypotension are known to be powerful stimuli increasing the release of arginine vasopressin (AVP) and oxytocin (OXY) in the rat (Schiltz et al 1997, Kadekaro et al 1998. The reduction of blood volume is mainly detected by cardiac stretch (volume) receptors whilst the reduction of blood pressure affects the activity of arterial baroreceptors (Renaud 1996, Share 1996, Thrasher & Keil 2000.…”

Section: Introductionmentioning

confidence: 99%

“…Numerous neurotransmitters and neuromodulators have been shown to influence the function of magnocellular hypothalamic neurons under conditions of hypovolaemia (Yokoi et al 1996, Kadekaro et al 1998, Ueta et al 1998, Yamaguchi et al 1998. In this respect, it is of interest to investigate possible effects of another brain peptide, glucagon-like peptide 1(7-36) amide (tGLP-1), postulated to be a neuromodulator of the autonomic nervous system, on the hypovolaemia-induced release of neurohypophysial hormones.…”

Section: Introductionmentioning

confidence: 99%

Effects of glucagon-like peptide-1(7-36) amide on neurohypophysial and cardiovascular functions under hypo- or normotensive hypovolaemia in the rat

Bojanowska

Stempniak²

2002

Journal of Endocrinology

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To date, glucagon-like peptide 1(7-36) amide (tGLP-1) has been found to affect the neurohypophysial and cardiovascular functions in normotensive and normovolaemic rats. The aim of the present study was to investigate possible effects of tGLP-1 on the mean arterial blood pressure and the release of vasopressin and oxytocin under conditions of blood volume depletion in the rat. In the first series of experiments, the animals were injected i.p. with either 0·15 M saline or 30% polyethylene glycol (PEG). PEG caused an 18% reduction of blood volume 1 h after injection. No significant changes in the mean arterial blood pressure were found in either normo-or hypovolaemic rats during the experiment. tGLP-1 injected i.c.v. at a dose of 1 µg/5 µl 1 h after the i.p. injection increased similarly the arterial blood pressure in normoand hypovolaemic rats. The plasma vasopressin/oxytocin concentrations were markedly elevated in hypovolaemic animals and tGLP-1 further augmented the release of both hormones. In the second study, hypovolaemia was induced by double blood withdrawal. The haemorrhage resulted in a marked decrease of the mean arterial blood pressure and in the elevated plasma vasopressin/oxytocin concentrations. tGLP-1 injected immediately after the second blood withdrawal increased the arterial blood pressure. In parallel, tGLP-1 enhanced significantly vasopressin and oxytocin secretion when compared with haemorrhaged, saline-injected rats. The results of this study indicate that tGLP-1 may affect the arterial blood pressure and the secretion of neurohypophysial hormones under pathological conditions brought about by blood volume depletion.

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“…The mechanism responsible for this suppression has not been identified; however, one molecule that may be involved is nitric oxide (NO). When administered centrally, nitric oxide synthase (NOS) inhibitors such as N-nitro-L-arginine methyl ester (L-NAME) increase blood pressure (25) and T b (31). However, these increases can be blocked by the nonspecific COX inhibitor indomethacin (31,44), indicating interactions between COX and NO activity.…”

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confidence: 99%

Suppression of endotoxin-induced fever in near-term pregnant rats is mediated by brain nitric oxide

Begg¹,

Kent²,

Mathai³

2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Begg DP, Kent S, McKinley MJ, Mathai ML. Suppression of endotoxin-induced fever in near-term pregnant rats is mediated by brain nitric oxide. Am J Physiol Regul Integr Comp Physiol 292: 2174-2178, 2007. First published March 1, 2007; doi:10.1152/ajpregu.00032.2007.-Over the last three decades, experiments in several mammalian species have shown that the febrile response to bacterial endotoxin is attenuated late in pregnancy. More recent evidence has established that the expression of nitric oxide synthase (NOS) enzymes is increased in the brain late in pregnancy. The current study investigated the possible role of brain nitric oxide in mediating the phenomenon of fever suppression. Core body temperature (T b) of near-term pregnant rats (day 19 and 20) was measured following inhibition of brain NOS and intraperitoneal injection of LPS (50 g/kg); they were compared with both day 15 pregnant and virgin animals. Intracerebroventricular injection with an inhibitor of NOS, N G -monomethyl-L-arginine citrate (L-NMMA; 280 g), in near-term pregnant rats restored the febrile response to LPS. As expected, near-term dams that received intracerebroventricular vehicle ϩ IP LPS did not increase T b, in contrast to the 1.0 Ϯ 0.2°C rise in Tb in dams treated with ICV L-NMMA ϩ IP LPS (P Ͻ 0.01). In virgin females and day 15 pregnant controls receiving this treatment, the increases in T b were 1.5 Ϯ 0.3°C and 1.6 Ϯ 0.4°C, respectively. Thus, blockade of brain NOS restored the febrile response to LPS in near-term dams; at 5 h postinjection, T b was 60 -70% of that observed in virgins and day 15 pregnant animals. Intracerebroventricular L-NMMA alone did not induce a significant change in Tb in any group. These results suggest that the mechanism underlying the suppression of the febrile response in near-term pregnancy is mediated by nitric oxide signaling in the brain. nitric oxide synthase; N G -monomethyl-L-arginine citrate; lipopolysaccharide; core body temperature; thermoregulation FEVER IS A REGULATED INCREASE in core body temperature (T b ) caused by initiation of heat-conserving and heat-producing systems. It plays a crucial role in the physiological response to infection by pathogens, improving the efficiency of lymphocytes and reducing the replication of many microorganisms (23). Fever can be caused by a number of different stimuli, such as infection with bacteria and viruses (27) or by stress (13,17). It has been widely documented that these factors result in the release of proinflammatory cytokines from macrophages (11). This results in the stimulation of central and peripheral cyclooxygenase (COX) enzymes that catalyze the synthesis of PGs (10). The enzymes COX-1 and COX-2 are the ratelimiting step in the production of PGs, and inhibition of COX blocks the febrile response (39). PGE 2 has been seen traditionally as the final step in the process of fever generation. The febrile response is integral to the body's defense against infection; however, if T b becomes excessively high, it endangers the host, as these temperatu...

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Effects of l-NAME on cerebral metabolic, vasopressin, oxytocin, and blood pressure responses in hemorrhaged rats

Cited by 36 publications

References 21 publications

Acid-base disturbance during hemorrhage in rats: significant role of strong inorganic ions

Acid-base disturbance during hemorrhage in rats: significant role of strong inorganic ions

Effects of glucagon-like peptide-1(7-36) amide on neurohypophysial and cardiovascular functions under hypo- or normotensive hypovolaemia in the rat

Suppression of endotoxin-induced fever in near-term pregnant rats is mediated by brain nitric oxide

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