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At least 19 recordsLinked to original sources
PubMed1990

Treatment of uncontrolled hemorrhagic shock with hypertonic saline solution.

Hypertonic saline solution (HTS) treatment of uncontrolled hemorrhagic shock (UCHS) induced by incision of three major branches of the ileocolic artery, leading to free intra-abdominal bleeding, was studied in rats. The rats were divided into two groups. In group 1, the abdominal wall was closed immediately after induction of hemorrhage and the rats were divided into six subgroups--1a, five untreated; 1b, 14 treated with 5 milliliters per kilogram of sodium chloride 7.5 per cent (HTS) after five minutes; 1c, eight had HTS infused after 15 minutes; 1d, nine had HTS infused after 30 minutes; 1e, nine had HTS infused after 60 minutes, and 1f, nine had HTS infused after 120 minutes. In rats in group 2, the abdominal wall was kept open during HTS therapy and bleeding was estimated by the amount of sponges used to absorb shed blood. These rats were also divided into six subgroups--2a, five untreated; 2b, nine had HTS infused after five minutes; 2c, six had HTS infused after 15 minutes; 2d, six had HTS infused after 30 minutes; 2e, eight had HTS infused after 60 minutes, and 2f, six had HTS infused after 120 minutes. UCHS in group 1 was followed by a fall in the mean arterial pressure (MAP) from 99 to 46 torr (p less than 0.001) in five minutes and a gradual rise to 63 torr (p less than 0.01) after 30 minutes, with a survival rate of 80 per cent. HTS infusion five minutes after hemorrhage was followed by a further fall in MAP to 37 torr (p less than 0.01) after 30 minutes and a mortality rate of 85.7 per cent (p less than 0.01). HTS treatment after 15, 30, 60 and 120 minutes also led to a further fall in MAP and increased mortality. In group 2, the hemodynamic response to intra-abdominal vessel injury in untreated rats was similar to that of those in group 1 and the amount of sponges used to absorb shed blood was 2.4. After five, 60 and 120 minutes of HTS treatment, the hemodynamic response was similar to that in group 1. Five and one-half (p less than 0.01), 3.5 and 3.0 sponges, respectively, were used to absorb shed blood.(ABSTRACT TRUNCATED AT 400 WORDS)

Abdominal Muscles↗
PubMed1990

Influence of preinduction methoxamine, lactated Ringer solution, or hypertonic saline solution infusion or postinduction dobutamine infusion on anesthetic-induced hypotension in horses.

A controlled study of the cardiovascular responses in horses anesthetized with acepromazine (0.05 mg/kg of body weight, IV), guaifenesin (100 mg/kg, IV), thiamylal (5.0 mg/kg, IV), and halothane in O2 (1.2 to 1.4% end-expired concentration) was performed to determine whether hypotension could be prevented by use of various treatments. Six horses were given 5 treatments in a randomized sequence: no treatment (control), methoxamine (0.04 mg/kg, IV), lactated Ringer solution (20.0 ml/kg, IV), 7.5% hypertonic saline solution (4.0 ml/kg, IV), or constant infusion of dobutamine (5.0 mg/kg/min, IV) during anesthesia. Heart rate, ECG, blood pressure, central venous pressure, cardiac output, blood gas analysis, PVC, and plasma total protein concentration were measured during the study. Compared with the control value, an increase in blood pressure during halothane administration was observed after administration of lactated Ringer solution, hypertonic saline solution, or dobutamine (P less than 0.05). The improved blood pressure response to hypertonic saline solution and dobutamine was related to an increase in cardiac output, which was statistically significant (P less than 0.05). Other statistically significant differences in cardiopulmonary responses among treatments were not observed during anesthesia. The PCV was increased in response to dobutamine infusion, and plasma total protein concentration was reduced in response to administration of hypertonic saline or lactated Ringer solution.

Acepromazine↗
PubMed1996

Influence of hypertonic saline solution infusion on defibrillation efficacy.

Hypertonic saline solution may enhance cardiac conduction via the fast inward sodium channel and alter transmembrane Ca+2 conductance via the sodium-calcium exchanger. Evidence suggests that both Ca+2 conductance and myocardial conduction velocity may affect ventricular defibrillation. Since hypertonic saline solution solutions (ie, sodium bicarbonate) may be administered to patients who have conditions that often require ventricular defibrillation (ie, cardiac arrest or hypovolemic shock), we studied the effect of hypertonic saline solution on the defibrillation threshold (DFT) in 16 pentobarbital-anesthetized domestic farm swine (20 to 30 kg). Defibrillation was performed using two interfaced epicardial electrode patches. DFTs were determined at baseline and during treatment phase. Pigs were randomly assigned to treatment consisting of either hypertonic saline solution (6 mmol/kg load, 2.0 to 3.0 mmol/kg infusion) to maintain serum sodium concentrations 10 to 15 mmol/L above baseline or control (D5W given in equal volume). DFT values (joules) that predicted 50% success were modeled from a best-fit histogram. Hypertonic saline solution did not change DFT values from baseline values (10.2 +/- 4.3 vs 10.8 +/- 7.0, respectively). Likewise, placebo (D5W) did not change DFT values from baseline values (10.1 +/- 4.5 vs 11.3 +/- 4.3). During treatment phase, DFT values were 99 +/- 28% of baseline values in the hypertonic saline solution group and 116 +/- 23% of baseline values in the D5W groups (p = 0.21). The administration of hypertonic saline solution also did not affect ventricular conduction velocity, right ventricular action potential duration, or right ventricular effective refractory period. These data indicate that hypertonic saline solution does not appreciably affect defibrillation efficacy or electrical treatment of ventricular fibrillation.

Animals↗
PubMed2005

Use of exhaled breath condensate in the study of airway inflammation after hypertonic saline solution challenge.

STUDY OBJECTIVES: Hypertonic saline solution inhalation is suspected to produce airway inflammation. DESIGN: The aim of this study was to verify this hypothesis by measuring inflammatory markers in exhaled breath condensate (EBC) collected before and after sputum induction with hypertonic and isotonic saline solution. PATIENTS AND METHODS: We enrolled 10 patients with asthma, 10 patients with COPD, and 7 healthy subjects with no history of lung disease. Levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha were measured in EBC by a specific enzyme immunoassay kit. Exhaled pH was measured after deaeration/decarbonation by bubbling with argon (350 mL/min) for 10 min by means of a pH meter. MEASUREMENTS AND RESULTS: Exhaled IL-6 and TNF-alpha concentrations were greater and pH was decreased compared to baseline after hypertonic saline solution inhalation in each group of subjects studied. No changes were observed following isotonic saline solution inhalation. Concentrations of IL-6, TNF-alpha, and pH in EBC correlated. CONCLUSIONS: These findings suggest that hypertonic saline solution inhalation could cause a low-grade inflammation in airways, and levels of inflammatory markers such as IL-6, TNF-alpha, and pH in EBC may be a useful noninvasive way to assess and monitor airway inflammation.

Aged↗
PubMed1997

[Hemodynamic effects of hypertonic saline solutions].

Haemodynamic effects of hypertonic saline solutions (HSS) have been extensively studied in animals and humans. Hypertonic sodium chloride (7.5%, 2,500 mOsm.L-1) either alone or combined with colloids, remains the standard solution. The haemodynamic response of HSS observed during treatment of hypovolaemic shock is explained by 1) an increase in preload due to the expansion of the plasma volume and a musculocutaneous vasoconstriction and 2) a decrease in systemic vascular resistance and afterload. A myocardial stimulation has been shown in various experimental conditions and in humans. However, the clinical relevance of this inotropic effect is questionable. Haemorrhagic shock is the main indication for small volume resuscitation with HSS. Other potential situations for the use of HSS are volume replacement in perioperative period, septic shock or burn injury and cardiopulmonary resuscitation. Before recommending the clinical use of HSS, additional clinical studies are required to substantiate the benefits of HSS over colloids.

Burns↗
PubMed1994

RETRACTED: Volume loading with hypertonic saline solution: endocrinologic and circulatory responses.

Hypertonic saline solution appears to be an attractive method of volume expansion. In 45 patients undergoing elective aorto-coronary bypass grafting, endocrinologic and circulatory responses to volume loading with hypertonic saline solution prepared in low molecular weight (MW) hydroxyethyl starch (HES) solution (72 g/L NaCl, HES concentration: 6%; MW: 200,000 D; degree of substitution [DS]: 0.5) (HS-HES) was compared randomly to patients who had received low molecular weight HES solution (LMW-HES). A group of patients without volume loading served as a control. Volume was infused to double the low pulmonary capillary wedge pressure (PCWP < 5 mmHg) after induction of anesthesia. Plasma levels of atrial natriuretic peptide (ANP), endothelin, vasopressin, and catecholamines were measured before, during, and after cardiopulmonary bypass (CPB) until the first postoperative day. In addition to systemic circulatory changes, capillary skin blood flow was measured by laser Doppler flowmetry. ANP plasma concentration increased in both volume groups (HS-HES: +79%; HES: +32%), whereas it decreased in the control (-20%). Infusion of HS-HES resulted in an increase in plasma endothelin concentration before and after CPB (from 3 to 6 pg/mL). Five hours after CPB, both treatment groups had higher endothelin plasma concentrations than the control patients (P < 0.05). Epinephrine and norepinephrine plasma levels increased most markedly in the control patients and were highest in the postbypass period in these patients. CI increased most after infusion of HS-HES (+65%) (P < 0.05). In the postbypass period, CI remained significantly higher in both volume groups than in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed2004

Hypertonic saline solutions in brain injury.

PURPOSE OF REVIEW: Hypertonic saline solutions have received renewed attention as effective agents for the treatment of cerebral edema and in brain resuscitation in a variety of brain injury paradigms. Although evidence of the beneficial action of hypertonic saline solutions in traumatic brain injury is robust, data supporting use in other conditions are only now mounting. RECENT FINDINGS: Osmotic properties of hypertonic saline solutions have been well studied in laboratory-based studies in animal models and in patients with acute brain injury. There are, in addition, emerging data on the extraosmotic actions on brain pathophysiology. This review cites baseline literature and provides new evidence of actions of hypertonic saline solutions: (a). in augmenting cerebral blood flow after subarachnoid hemorrhage, (b). as an antiinflammatory adjunct, and (c). utility in chemonucleolysis for intervertebral disc disease and treatment of seizures associated with severe hyponatremia. SUMMARY: Brain injury from diverse etiologies including trauma, ischemic stroke, global cerebral ischemia from cardiac arrest, intraparenchymal or subarachnoid hemorrhage, infection, or toxic-metabolic derangements are commonly encountered in the clinical setting. Many of these conditions are associated with cerebral edema with or without elevated intracranial pressure. Osmotherapy constitutes the cornerstone of medical therapy for such patients. Hypertonic saline solutions have received renewed attention in clinical practice as osmotic agents for cerebral resuscitation. This article reviews experimental and clinical evidence of the efficacy of hypertonic saline solutions and elaborates on their use in patients with acute neurologic injury. Important areas for current and future research are highlighted before the use of hypertonic saline solutions can be accepted for widespread use.

Brain Injuries↗
PubMed1991

Hemodynamic response of endotoxemic calves to treatment with small-volume hypertonic saline solution.

The hemodynamic effects of hypertonic saline solution (HSS) resuscitation on endotoxic shock were examined in pentobarbital-anesthetized calves (8 to 20 days old). Escherichia coli (055:B5) endotoxin was infused IV at dosage of 0.1 microgram/kg of body weight for 30 minutes. Endotoxin induced large decreases in cardiac index, stroke volume, maximal rate of change of left ventricular pressure (+dP/dtmax), femoral and mesenteric arterial blood flow, glomerular filtration rate, urine production, and mean aortic pressure. Severe pulmonary arterial hypertension and increased pulmonary vascular resistance were evident at the end of endotoxin infusion. Treatment with HSS (2,400 mosm of NaCl/L, 4 ml/kg) or an equivalent sodium load of isotonic saline solution (ISS: 300 mosm of NaCl/L, 32 ml/kg) was administered 90 minutes after the end of endotoxin administration. Both solutions were infused IV over a 4- to 6-minute period. Administration of HSS induced immediate and significant (P less than 0.05) increase in stroke volume and central venous pressure, as well as significant decrease in pulmonary vascular resistance. These effects were sustained for 60 minutes, after which all variables returned toward preinfusion values. The hemodynamic response to HSS administration was suggestive of rapid plasma volume expansion and redistribution of cardiac output toward splanchnic circulation. Plasma volume expansion by HSS was minimal 60 minutes after resuscitation. Administration of ISS induced significant increase in cardiac index, stroke volume, femoral arterial blood flow, and urine production. These effects were sustained for 120 minutes, at which time, calves were euthanatized. Compared with HSS, ISS induced sustained increase in mean pulmonary arterial pressure and only a small increase in mesenteric arterial blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Induced sputum: comparison between isotonic and hypertonic saline solution inhalation in patients with asthma.

BACKGROUND: Sputum induction by hypertonic saline solution inhalation is widely used to study airways secretions in patients with asthma. However, hypertonic saline solution is a potent indirect bronchoconstrictor. STUDY OBJECTIVES: We studied the validity of isotonic saline solution (0.9%) inhalation as a means to induce sputum by comparing it to hypertonic saline solution (4.5%) inhalation. PATIENTS: Sixteen patients with moderate-to-severe asthma reporting a clinical history of mucus hypersecretion. METHODS: Subjects underwent sputum induction twice at 1-week intervals. Saline solution (hypertonic or isotonic) was inhaled for three periods of 5 min. The parameters assessed in sputum samples were cell counts, sodium, eosinophil cationic protein (ECP), and albumin concentrations, osmolality, and pro-matrix metalloproteinase (MMP)-9 activity by zymography. RESULTS: The maximal fall in peak expiratory flow during sputum induction was greater after inhalation of hypertonic saline solution than after inhalation of isotonic saline solution (p < 0.01). Each subject produced analyzable sputum on both visits. There were no statistically significant differences in total and differential sputum cell counts, and the reproducibility coefficients were high for eosinophils and neutrophils when comparing the two methods. Likewise, sputum levels of ECP and albumin as well as sputum pro-MMP-9 activity were not different between the two methods, and were highly reproducible as shown by high intraclass coefficients (Ri) of correlation (0.72, 0.74, and 0.77 for ECP, albumin, and pro-MMP-9, respectively). Sputum sodium concentrations and osmolality were higher after inhalation of hypertonic saline solution (p < 0.05). CONCLUSION: In patients with moderate-to-severe asthma reporting a clinical history of mucus hypersecretion, inducing sputum by isotonic or hypertonic saline solution inhalation leads to comparable results in eosinophil and neutrophil cell counts and fluid phase mediators/proteins.

Administration, Inhalation↗
PubMed1991

[Use of hypertonic saline solutions in intensive care and emergency medicine--developments and perspectives].

The primary factor rendering patients at risk of developing multiple system organ failure after shock and trauma is the persistence of impaired microcirculation along with its sequelae for cellular and organ function. Bolus infusion (2-5 min) of 4 ml/kg hypertonic/hyperoncotic saline solution through a peripheral vein is a new concept for primary resuscitation from severe hypovolemia associated with trauma and hemorrhage and is termed "small-volume resuscitation". The experimental data obtained by various research groups have demonstrated the efficacy of 7.2%-7.5% saline solution in restoring central hemodynamics and organ blood flow. The simultaneous application of a hyperoncotic colloid (6%-10% dextran 60/70; 6%-10% hydroxyethylstarch 200,000) aims at prolonging the circulatory effect of saline. Of particular importance are the data obtained in experiments on traumatic-hemorrhagic hypovolemia in beagles, which proved that the infusion of 10% dextran 60 in 7.2% saline (hypertonic-hyperoncotic solution) restores nutritional blood flow within less than 5 min, thereby enhancing the circulatory effect of hypertonic saline alone. In the pre-clinical setting, small-volume resuscitation by means of hypertonic saline/dextran solution is aimed at the rapid normalization of the compromised microcirculation and, thus, at the prevention of late complications such as sepsis and multiple system organ failure. The novelty of hypertonic saline/dextran resuscitation lies in its operational mechanism at the microcirculatory level, which also renders this concept attractive for volume support in endotoxemia and septic shock.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Volume↗
PubMed2005

Comparison of a small volume of hypertonic saline solution and dextran 40 on hemodynamic alternations in conscious calves.

The hemodynamic effects of rapid intravenous (IV) administration of 10% dextran 40 in saline solution (D40) and 7.2% hypertonic saline solution (HSS) in calves were compared. Calves received isotonic saline solution (ISS), HSS or D40 (3 calves/group) and were monitored of blood pressure, and cardiac output (CO) for 180 min. HSS and D40 infusions induced a significant increase in relative plasma volume reaching 134.9+/-2.8 and 125.0+/-1.9%, respectively at the end of fluid infusion. In the HSS group, CO, cardiac index (CI) and stroke volume (SV) remained constant at low levels after 90 minutes despite the maximal values of CO, CI and SV at the end of infusion, reaching 21.0+/-6.3 l/min (p<0.05), 177.8+/-14.2 ml/min/kg (p<0.001) and 0.20+/-0.03 l/beat (at t=10 min, p<0.001), respectively. In contrast, CI and SV in the D40 group showed significant increases to 14.7+/-2.9 l/min and 153.5+/-17.2 ml/min/kg, respectively, at the end of fluid infusion. And those values remained constant at higher levels than those of the before infusions values throughout the experimental periods. Positive effects for hemodynamic alternations of D40 in calf practice were milder and longer than those of HSS. Therefore, the D40 infusion should be explored as a possible treatment for dehydrated calves, since rapid infusion of D40 may be safe and more beneficial for rehydrating more than HSS treatment.

Animals↗
PubMed2003

Resuscitation from hemorrhagic shock: experimental model comparing normal saline, dextran, and hypertonic saline solutions.

OBJECTIVE: To compare the effectiveness of normal saline, dextran, hypertonic, and hypertonic-hyperoncotic solutions in hemorrhagic shock. DESIGN: Laboratory investigation. SETTING: University hospital, Emergency Surgery and Intensive Care staff. SUBJECTS: Thirty-two large white female pigs. INTERVENTIONS: Routine care included: anesthesia and sedation (ketamine 10 mg/kg, droperidol 0.25 mg/kg, diazepam 0.7 mg/kg, fentanyl 0.006 mg/kg, 2% enflurane, 20% nitrous oxide, pancuronium bromide 0.13 mg/kg); volume-controlled ventilation (Paco(2) 35-40 torr; 4.7-5.4 kPa); cannulation of right carotid artery and pulmonary artery. Three flow probes (subdiaphragmatic aorta, superior mesenteric artery, right renal artery) and regional venous catheters (superior mesenteric vein, right renal vein) were positioned. Animals were bled to 45 mm Hg for 1 hr and resuscitated with four different fluids and blood to normal aortic blood flow and hemoglobin. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure and blood flow through abdominal aorta ([OV0312](aor)), mesenteric artery ([OV0312](mes)), and renal artery ([OV0312](ren)) were continuously monitored. Cardiac output, systemic and regional oxygen delivery ([U1E0A]o(2), [U1E0A]o(2mes), [U1E0A]o(2ren)), and consumption ([OV0312]o(2), [OV0312]o(2mes), [OV0312]o(2ren)) were recorded every 30 mins. Baseline [OV0312](aor) was restored with different amounts of fluids in the four groups: normal saline (91.35 +/- 22.18 mL/kg); dextran (16.24 +/- 4.42 mL/kg); hypertonic (13.70 +/- 1.44 mL/kg); and hypertonic-hyperoncotic (9.11 +/- 1.20 mL/kg). The amount of sodium load was less using dextran and hypertonic-hyperoncotic and sodium levels were only transiently increased after hypertonic infusion. Mean arterial pressure and cardiac output were normalized in all groups. Animals resuscitated with normal saline and dextran showed increased pulmonary artery pressures. [U1E0A]o(2) was significantly higher after hypertonic-hyperoncotic infusion, because of reduced hemodilution. Hypertonic and hypertonic-hyperoncotic normalized [OV0312](mes), [U1E0A]o(2mes), [OV0312]o(2mes), [OV0312](ren), and [U1E0A]o(2ren), whereas normal saline and dextran did not achieve this result. At the end of the experiment, hypertonic-hyperoncotic maintained mean arterial pressure, cardiac output, and [U1E0A]o(2) until the end of observation in contrast to normal saline, dextran, and hypertonic. CONCLUSIONS: Resuscitation with a small volume of hypertonic-hyperoncotic solution allows systemic and splanchnic hemodynamic and oxygen transport recovery, without an increase in pulmonary artery pressure. It only transiently increased sodium concentration.

Animals↗
PubMed1995

Effect of hypertonic saline solution on left ventricular afterload in normovolumic dogs.

The effects of hypertonic saline solution (HSS) and hyperosmotic dextrose (HD; 2,400 mosm/L, 4 ml/kg of body weight) on left ventricular afterload were determined in normovolumic, chloralose-anesthetized, autonomically blocked dogs (n = 8). Solutions were infused IV over 3 minutes. Left ventricular afterload was assessed by use of a dual-tipped micromanometer catheter with an electromagnetic fluid-velocity sensor located in the ascending aorta, and the impedance spectrum was calculated after Fourier analysis of signal-averaged aortic pressure and flow signals. Hypertonic saline solution and HD decreased peripheral resistance, reflection coefficient at zero frequency, and frequency of the first zero crossing of the phase angle for 3 to 5 minutes after either fluid was administered. Characteristic impedance was not altered by HSS or HD. These impedance spectrum changes indicate transient vasodilatation and afterload reduction. We conclude that the vascular effect of an ionic hyperosmotic solution (HSS) is similar to that of a nonionic hyperosmotic solution (HD), and that HSS and HD transiently decrease afterload in normovolumic dogs. The duration of the afterload reduction after HSS administration appeared to be too short to be of great clinical benefit.

Animals↗
PubMed1993

The effect of heat load and dehydration on hypertonic saline solution treatment of controlled hemorrhagic shock.

Small volume hypertonic saline solution has been suggested for initial effective resuscitation of hemorrhagic shock. The effect of hypertonic saline solution in controlled hemorrhagic shock was studied in rats subjected to dehydration or heat, or both. The rats were randomly divided into four groups--group 1 (n = 19), normal rats; group 2 (n = 21), water deprivation for 12 hours; group 3 (n = 20), heating at 37 degrees C. for five hours, and group 4 (n = 19), water deprivation for 12 hours and heating at 37 degrees C. for five hours. Controlled hemorrhagic shock was induced in all rats by arterial bleeding of 15 milliliters per kilogram and the rats were divided into three treatment subgroups--group a was untreated, group b was treated with 5 milliliters per kilogram 0.9 percent NaCl and group c was treated with 5 milliliters per kilogram 7.5 percent NaCl. Arterial bleeding of 15 milliliters per kilogram in group 1 resulted in decrease in mean arterial pressure (MAP) to 44 +/- 2 millimeters of mercury (p < 0.001) and pulse rate to 280 +/- 13 per minute (p < 0.01). A similar decrease in MAP and pulse rate was observed in all four groups. Infusion of hypertonic solution (HTS) in group 1c was followed by an increase in MAP to 89.0 +/- 9.7 milliliters of mercury (p < 0.01) in 15 minutes. This was significantly higher than infusion of normal saline solution in group 1b (p < 0.01) or untreated group 1a (p < 0.01). This difference remained significant also after 45 minutes from infusion (p < 0.05 and p < 0.05, respectively). The increase in MAP in response to HTS in group 1c after 15 minutes was significantly higher than the rise in groups 2c (p < 0.05), 3c (p < 0.05) and 4c (p < 0.05). This difference in response to HTS remained significant 45 minutes from infusion in groups 3c (p < 0.05) and 4c (p < 0.05), but not in dehydrated rats in group 2c. Arterial bleeding did not alter serum sodium significantly in all four groups. Infusion of HTS in group 1c was followed by an increase in serum sodium from 149.1 +/- 1.4 to 161.1 +/- 2.4 milliequivalent per liter (p < 0.001), while infusion of HTS in group 4c, where serum sodium was initially elevated to 157.1 +/- 3.0 milliequivalent per liter, did not further elevate the serum sodium level.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

The effect of heat load and dehydration on hypertonic saline solution treatment of uncontrolled hemorrhagic shock.

Hypertonic saline solution treatment of uncontrolled hemorrhagic shock (UCHS) leads to increased bleeding from injured vessels, fall in arterial blood pressure, and increased mortality. The effect of dehydration induced by either water deprivation or heating on this response was studied in rats. The animals were divided into four groups: group 1 (n = 32), normal rats; group 2 (n = 30), water deprivation for 12 hours; group 3 (n = 30), heating at 37 degrees C for 5 hours; and group 4 (n = 30), heating as in group 3 and water deprivation as in group 2. UCHS was induced in all rats by 20% resection of the animals' tail. The rats were then divided into four treatment subgroups: group a was untreated, group b was treated after 15 minutes with 5 mL/kg NaCl 7.5% hypertonic saline (HTS), group c was treated after 15 minutes with 41.5 mL/kg NaCl 0.9% large volume normal saline (LNS) and group d was treated after 15 minutes with HTS + LNS. Tail resection in group 1a resulted in bleeding of 4.9 +/- 0.3 mL, and fall in mean arterial pressure (MAP) to 50 +/- 3 mm Hg (p < 0.001). Blood loss and fall in hematocrit in groups 2, 3, and 4 was significantly lower than in group 1. The fall in MAP and pulse rate was similar in all four groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Qualitative evaluation of the blood-brain barrier after the use of hypertonic saline solution in young rats.

The blood-brain barrier (BBB) controls the biochemical environment of the brain with variable permeability when comparing adults to children. Based on the knowledge that there is a greater vulnerability in the BBB of young subjects submitted to biochemical variations in the blood and in the brain, an experimental model was designed to study small volume resuscitation. Young Wistar rats were submitted to hemorrhage and resuscitated with 7.5% NaCl solution before undergoing a qualitative evaluation of their BBB. Thirty male rats were anesthetized and divided into four groups: Group 1 - submitted to hemorrhagic shock restored with hypertonic saline solution (HSS); Group 2 - submitted to hemorrhagic shock without volume restoration; Group 3 - receiving only HSS, and Group 4 - control. The data analyzed were: mean arterial blood pressure, base excess, sodium, chloride, urea, blood osmolarity and blood glucose levels. After infusing a 2% Evans blue solution, qualitative analysis of the BBB was carried out. Group 1 presented final mean blood pressure levels equivalent to groups 3 and 4. Group 2 had a significant difference in the final base excess when compared to the other groups. In groups 1 and 3, mean sodium and chloride, as well as serum osmolarity, were more elevated than groups 2 and 4. Macroscopic examination of the brain did not reveal any changes in color, which could be attributed to the opening of the BBB. It was concluded that the 7.5% NaCl solution in this experimental model did not promote qualitative changes in the BBB.

Animals↗
PubMed1993

Resuscitation of anesthetized endotoxemic pigs by use of hypertonic saline solution containing dextran.

We evaluated the biochemical and hemodynamic response to hypertonic saline solution plus dextran in isoflurane-anesthetized pigs infused IV with Escherichia coli endotoxin (5 micrograms/kg of body weight for 0 to 1 hour + 2 micrograms/kg for 1 to 4 hours). After 120 minutes of endotoxemia, pigs were treated with a bolus (4 ml/kg over 3 minutes) of either normal saline solution (NSS; 0.9% NaCl), or hypertonic saline solution plus dextran (HSSD; 7.5% NaCl + 6% dextran-70). Administration of HSSD significantly (P < 0.05) increased serum osmolality and concentrations of sodium and chloride for approximately 2 hours during endotoxemia. Plasma total protein concentration decreased significantly (P < 0.05) for 2 hours after treatment with HSSD, indicating hemodilution and increased plasma volume. Although HSSD transiently increased cardiac index (CI) for approximately 15 minutes, this effect was not sustained; however, the endotoxin-induced decrease in CI was ameliorated from 120 to 180 minutes. In pigs of the endotoxin + NSS group from 180 to 240 minutes, CI decreased significantly (P < 0.05), compared with baseline and control values. The endotoxin-induced increases in mean pulmonary arterial pressure and pulmonary vascular resistance were not attenuated by HSSD. At 135 minutes, total peripheral vascular resistance was transiently lower (for approx 15 minutes) in pigs treated with HSSD, compared with control pigs. The endotoxin-induced increase in plasma lactate concentration was not attenuated by HSSD, indicating continued peripheral O2 debt. We conclude that, despite sustained increases in serum osmolality and concentrations of sodium and chloride, HSSD has only transiently beneficial cardiopulmonary effects during endotoxemia in pigs.

Anesthesia↗