Hypertonic Saline Resuscitation Research Articles

3.5% Hypertonic saline produces sympathetic activation in hemorrhaged rabbits

The neural mechanisms for pressor effects after hypertonic saline infusion are still unclear. Using direct measurement of the renal sympathetic nerve activity (RNA), we tested the hypothesis that the autonomic nervous system is involved in an acute blood pressure elevation produced by hypertonic saline (HTS) in anesthetized rabbits subjected to hemorrhage. Twenty urethane-anesthetized rabbits were ventilated mechanically after a tracheostomy and paralyzed with gallamine triethiodide. Heart rate (HR), mean blood pressure (MBP) and central venous pressure (CVP) were measured simultaneously with RNA. The animals were divided into the following four groups: (1) animals with intact baroreceptors that received HTS (intact HTS group, N=5); (2) those with intact baroreceptors that received normal saline (intact NS group, N=5); (3) those that underwent selective cervical vagotomy (vagotomy group, N=5); (4) those with sino-aortic denervation (SAD group, N=5). The last two groups were given HTS only. After inducing hemorrhagic hypotension to 40 mmHg over 10 min, 3.5% HTS at half the volume of shed blood was infused over approximately 120 s. In the intact HTS group, sympathetic activation, associated with tachycardia and pressor effects, developed. This enhancement of RNA was followed by a return to the pre-infusion level, but the increased blood pressure and tachycardia lasted until the end of the experiment. These levels of MBP and HR were significantly higher than those of the intact NS group. In the vagotomized animals, HTS resuscitation also increased RNA and systemic blood pressure. In contrast, in the SAD group, neither sympathetic activation nor an early phase increase in systemic blood pressure occurred. These results indicate that in hemorrhaged rabbits, 3.5% HTS produces sympathetic activation along with an acute pressor effect and that this is likely to be mediated through the sino-aortic nerves, possibly the peripheral chemoreceptors, but not through the vagal nerves.

Hypertonic saline resuscitation decreases susceptibility to sepsis after hemorrhagic shock.

We hypothesized that improvements in cellular immune function after hypertonic saline (HTS) resuscitation will alter the outcome of sepsis after hemorrhage. To test this hypothesis, a two-hit model was used. Hemorrhage was induced in BALB/c mice by catheterizing the femoral artery and bleeding until a mean arterial pressure = 35 mm Hg was reached and maintained for 1 hour. Resuscitation was performed with HTS (NaCl 7.5%, 4 mL/kg) or lactated Ringer's (LR, twice the shed blood volume), plus the shed blood. Cecal ligation and puncture (CLP) was performed 24 hours after hemorrhage. Mortality was assessed for 72 hours, comparing HTS (n = 14) and LR (n = 13) resuscitation. Another set of animals (n = 10 in each group at each time point) were killed at 2 and 24 hours after blood collection. Liver and blood were cultured for the presence of bacteria, and lung and liver samples were scored on a scale from 0 (normal) to 4 (most severe) in a blind fashion by a pathologist. Mortality 72 hours after CLP was 14.3% in HTS and 76.9% in LR treated animals (p < 0.002). At 24 hours after CLP, 44% of HTS, but 77% of LR treated animals had > 1,000 colony forming units/mL of blood. Positive liver cultures (> 100,000 colony forming units/g) also showed the same trend (HTS = 30%, LR = 60%). Autopsies revealed a better containment of the infection (abscess formation) in the HTS group. At 2 hours, lung scores were 1.2 +/- 0.25 and 2.6 +/- 0.31 for HTS and LR, respectively (p < 0.002). At 24 hours, HTS treated animals showed marked improvement of lung injury, while the scores in the LR group remained high. A significant difference was also observed regarding liver injury. At 2 hours, scores were 0.4 +/- 0.22 and 2.3 +/- 0.16 for HTS and LR, respectively (p < 0.002). At 24 hours, HTS treated animals showed normal hepatic architecture, although mild injury was still observed in the LR group. HTS resuscitation leads to increased survival after hemorrhage and CLP. Marked improvements were observed in lung and liver injury compared with isotonic resuscitation. The better containment of the infection observed with HTS resuscitation corresponds to a marked decreased in bacteremia. HTS resuscitation stands as an alternative resuscitation regimen with immunomodulatory potential.

Initial small-volume hypertonic resuscitation of shock and brain injury: short- and long-term effects.

Initial small-volume hypertonic saline resuscitation of a combined hemorrhagic shock and head injury model was studied. Twenty-three sheep underwent hemorrhage (20 mL/kg) and parietal freeze injury followed by initial bolus resuscitation with lactated Ringer's solution (40 mL/kg) or 7.5% hypertonic saline (HS) (4 mL/kg). Cardiac index was maintained with lactated Ringer's solution for either 2 or 24 hours. Parietal lobe water content, blood volume, and blood flow were determined. Intracranial pressure (millimeters of mercury) was followed. Overall fluid requirements (milliliters per kilogram) were less at 2 and 24 hours with HS resuscitation. Early intracranial pressure was less with HS resuscitation. Brain water contents were similar between groups. Blood flow in injured and blood volume in uninjured parietal lobe were less for HS at 2 hours, although not different at 24 hours. Less fluid was needed in the short- and long-term with HS resuscitation. Early intracranial pressure was higher with lactated Ringer's solution resuscitation, possibly in part owing to increased blood volume.

6 Hypertonic saline resuscitation: a new concept

Early treatment of haemorrhagic shock offers few theoretical, but many practical problems. Ideal or minimum volume replacement, and O 2 carrying capacity, are essential but logistics of pre-hospital management impose severe restrictions on what may, or may not, be done. Scoop-and-run, withheld fluid replacement and small volume resuscitation are alternative strategies under discussion at present. This review covers historical aspects of the introduction of small volume resuscitation, general properties required for its application, toxicological studies, available clinical and experimental data, physical, pharmacological and immune effects, mechanisms of action, prospects for clinical use. The controversial case of its interaction with uncontrolled bleeding is covered. It is concluded that the multiple physical, physiological and immune effects of hypertonic saline resuscitation, many of which require further research suggest potential clinical applications, in the primary treatment of hypovolemic shock, in cardiac surgery with cardiopulmonary bypass and in myocardial infarct. The interaction of hypertonic solutions with pro-inflammatory mediators has barely been scratched, and may induce a critical review of many concepts.

Hypertonic Saline Activates Protein Tyrosine Kinases and Mitogen-activated Protein Kinase p38 in T-cells

In previous in vitro studies, we have found that hypertonic saline (HTS) can augment T-cell proliferation and restore the function of suppressed T-cells. Our animal models have shown that HTS resuscitation reverses immunosuppression after hemorrhage and reduces mortality from sepsis. In the present study, we investigated if and how HTS may influence T-cell signaling and function on a subcellular level. Human peripheral blood mononuclear cells (PBMC) were used to determine the effect of HTS on T-cell interleukin 2 (IL-2) production and proliferation. Human Jurkat T-cells were used to study the effects of HTS on T-cell signal transduction, IL-2 mRNA transcription, and IL-2 expression. The effect of HTS on T-cell proliferation and IL-2 production was measured with PBMC and Jurkat T-cells. IL-2 mRNA transcription in HTS-treated Jurkat cells was measured by reverse transcriptase polymerase chain reaction. HTS-induced protein tyrosine phosphorylation in Jurkat T-cells was determined by immunoblotting with anti-phosphotyrosine antibodies. Expression in Jurkat cells of the mitogen-activated protein kinase p38 (MAPK p38), a signal transduction protein that is activated by osmotic stress, was determined by immunoblotting with anti-MAPK p38 antibodies. HTS-induced MAPK p38 activation in Jurkat cells was measured with an immune-complex kinase assay using ATF-2 as a substrate. Proliferation of activated human PBMC increased significantly upon addition of HTS to the culture medium. This effect of HTS was paralleled by enhanced IL-2 production of activated PBMC and Jurkat cells and IL-2 mRNA transcription of Jurkat cells. HTS exposure of Jurkat cells caused tyrosine phosphorylation of a number of cellular proteins. We found that Jurkat T-cells expressed MAPK p38 and that it was activated in the presence of HTS. All these effects of HTS on T-cell signaling and function were observed at NaCl concentrations that were within physiologically relevant levels (20-100 mmol/L hypertonicity). In T-cells, HTS triggers a signaling pathway that includes increased tyrosine phosphorylation of several cellular proteins and activation of MAPK p38. HTS alone does not result in IL-2 mRNA transcription, IL-2 expression, or T-cell proliferation. However, in combination with other stimuli, HTS augments T-cell IL-2 expression and proliferation. We speculate that HTS could "resuscitate" suppressed T-cells in trauma patients by circumvention of, or substituting for, blocked signaling pathways.

Hypertonic Saline Resuscitation Restores Hemorrhage-Induced Immunosuppression by Decreasing Prostaglandin E2and Interleukin-4 Production

It was previously shown that hypertonic saline (HTS) enhancesin vivoandin vitrocellular immune function of normal mice and reversesin vitroprostaglandin E2(PGE2)-induced immunosuppression of normal peripheral blood mononuclear cells. Hemorrhage induces immunosuppression despite adequate isotonic fluid resuscitation. The effects of HTS resuscitation on immunosuppression following hemorrhage were studied. A mouse model of hemorrhagic shock was used. Bleeding was performed through a catheter placed in the femoral artery. Phytohemagglutinin-induced splenocyte proliferation and interleukin (IL)-1, IL-2, IL-4, IL-6, IL-10, transforming growth factor β, and PGE2plasma levels were measured 2 and 24 hr following hemorrhage and resuscitation with lactated Ringer's and HTS.In vivocellular immune function was measured using a contact hypersensitivity test. Suppression of splenocyte proliferation (40%) 24 hr following hemorrhage occurred after lactated Ringer's resuscitation. HTS prevented immunosuppression.In vivocell-mediated immune function 24 hr after hemorrhage was improved by HTS. HTS-resuscitated animals showed significantly lower levels of IL-4 and PGE2, and slightly elevated levels of proinflammatory cytokines (IL-1, IL-2, and IL-6). HTS reverses hemorrhage-induced T-cell suppression by reducing the production and/or release of IL-4 and PGE2.

Hypertonic saline improves brain resuscitation in a pediatric model of head injury and hemorrhagic shock

Introduction: Brain injury accompanied by hypovolemic shock is a frequent cause of death in multiply injured children. Hypertonic saline (HTS) has been shown to return hemodynamics to normal in adult models, without increasing intracranial pressure (ICP) as seen with crystalloids. To assess fluid resuscitation, the authors evaluated HTS versus lactated Ringer's solution (LR) with respect to hemodynamics and cerebrovascular hemoglobin oxygen saturation (Sco 2 in anesthetized, head-injured, 1-month-old piglets. Methods: Group 1 (n =6) was studied for 3.5 hours after a cryogenic brain injury and no shock. Groups 2 and 3 had cryogenic brain injury followed by hemorrhagic shock, in which mean arterial pressure (MAP) was reduced to 40 to 50 mm Hg and maintained for 30 minutes. Group 2 (n = 5) was then resuscitated with 1 mL of 7.5% HTS per 1 mL of blood loss. Group 3 (n = 6) was resuscitated with 3 mL of LR per 1 mL of blood loss. Sco 2 was determined by near-infrared spectroscopy in the injured region of the brain. All data were analyzed using analysis of variance with repeated measures. Results: MAP, ICP, temperature, serum sodium, and cardiac output (CO) were similar in all groups during baseline and between groups 2 and 3 during shock. After resuscitation, MAP, CO, and core temperature were similar in all three groups, and serum sodium was increased in the HTS group (by 29%). Sco 2 increased transiently after cryogenic injury in all groups, then gradually decreased to below baseline. After shock, Sco 2 decreased precipitously in groups 2 and 3. After resuscitation, Sco 2 was different in the two resuscitation groups, increasing in the HTS group, above baseline values, but remaining below baseline values in the LR group ( P < .002). ICP was lowered by HTS resuscitation and increased by LR resuscitation ( P < .002). Conclusion: In our model of head injury and shock, resuscitation with either HTS or LR restored MAP and CO to control levels. However, during shock, the injured brain was severely deoxygenated, and administration of HTS restored cerebral oxygenation whereas LR did not, reflecting improved cerebral resuscitation by HTS without elevating ICP. The data suggest that HTS is a better resuscitation fluid than LR in head-injured children with hemorrhagic shock.

The role of the adrenal medulla in cardiovascular responses to hypertonic saline in haemorrhaged conscious rats: Acta Physiol Scand 1994; 151/4: 429–439

The aim of this study was to determine if the adrenal medulla plays a role in mediating haemodynamic effects of hypertonic saline (HTS) resuscitation during haemorrhagic hypotension in conscious rats. Wistar-Kyoto rats were either adrenomedullectomized (ADMX, n = 11) or sham-operated (SHAM, n = 10) and implanted with intravascular catheters. Pre-haemorrhage resting mean arterial pressure (MAP) was lower in the ADMX than in the SHAM group. Haemorrhage was performed by withdrawal of blood through the venous catheter, and a MAP of 50 mmHg was maintained for 1 h by further withdrawal when necessary. Both groups responded to haemorrhage with marked bradycardia. Plasma adrenaline (A) rose 10-fold in response to hypotension in the SHAM group, while remaining at pre-haemorrhage levels in the ADMX group, indicating successful adrenal demedullation. Infusion of 2.0 ml kg-1 HTS (NaCl 8.0 mg ml-1 i.v.) produced an immediate increase in MAP and heart rate (HR) in both groups, to pre-haemorrhage values or higher. Plasma noradrenaline (NA) increased in both groups after HTS, while the high levels of A in the SHAM group slowly returned toward baseline. Plasma glucose and rate of haemodilution was higher in the SHAM group during and after hypotension. The maintenance of MAP above 60 mmHg was less effective in the SHAM group during the first 2 h after HTS, but after 24 h, prehaemorrhage MAP was established in both groups. In conclusion, the adrenal medulla does not play a major role in the response to HTS resuscitation.

Effects of acid-base correction on hemodynamics, oxygen dynamics, and resuscitability in severe canine hemorrhagic shock

To compare the effects of hypertonic saline, sodium bicarbonate, and Carbicarb resuscitation on acid-base balance, hemodynamics, and oxygen dynamics in a reperfused, canine hemorrhagic shock model. Prospective, randomized trial. Laboratory at a university medical center. Thirty-five anesthetized, mongrel dogs. After the administration of anesthesia, the dogs were intubated and mechanically ventilated. Vascular catheters were inserted into each femoral artery, for continuous blood pressure monitoring, intermittent blood sampling, and for establishing controlled hemorrhage. A pulmonary artery catheter was inserted via the right jugular vein. Inhaled and exhaled gases were continuously analyzed using a metabolic gas monitor. The animals were subjected to 90 mins of controlled hemorrhagic shock. They were then randomly given a 2.5-mL/kg equimolar injection of 8.4% sodium bicarbonate, Carbicarb, or 5.84% hypertonic saline. The sodium load per kilogram of body weight was identical in all three groups. Thirty minutes later, the animals were retransfused with the shed blood over 15 mins and further observed for 120 mins. Carbicarb and sodium bicarbonate both significantly increased bicarbonate concentrations compared with saline. Arterial and venous blood pH increased more with Carbicarb than with bicarbonate but this increase was not statistically significant. After shock but before retransfusion, all three treatments moderately increased blood pressure, cardiac index, oxygen delivery index, and oxygen consumption index to a similar extent. After retransfusion, blood pressure, cardiac index, and oxygen dynamics temporarily improved in all groups, without significant improvement in the bicarbonate and Carbicarb-treated animals, despite their excellent acid-base status. In severe canine hemorrhagic shock, Carbicarb, bicarbonate, and hypertonic saline appear to possess similar hemodynamic properties despite the buffering properties of bicarbonate and Carbicarb. The similar responses may be due to their identical sodium content. Arterial pH correction does not appear to further improve the responses to blood retransfusion.

The role of the adrenal medulla in cardiovascular responses to hypertonic saline in haemorrhaged conscious rats

The aim of this study was to determine if the adrenal medulla plays a role in mediating haemodynamic effects of hypertonic saline (HTS) resuscitation during haemorrhagic hypotension in conscious rats. Wistar-Kyoto rats were either adrenomedullectomized (ADMX, n = 11) or sham-operated (SHAM, n = 10) and implanted with intravascular catheters. Pre-haemorrhage resting mean arterial pressure (MAP) was lower in the ADMX than in the SHAM group. Haemorrhage was performed by withdrawal of blood through the venous catheter, and a MAP of 50 mmHg was maintained for 1 h by further withdrawal when necessary. Both groups responded to haemorrhage with marked bradycardia. Plasma adrenaline (A) rose 10-fold in response to hypotension in the SHAM group, while remaining at pre-haemorrhage levels in the ADMX group, indicating successful adrenal demedullation. Infusion of 2.0 ml kg-1 HTS (NaCl 8.0 mg ml-1 i.v.) produced an immediate increase in MAP and heart rate (HR) in both groups, to pre-haemorrhage values or higher. Plasma noradrenaline (NA) increased in both groups after HTS, while the high levels of A in the SHAM group slowly returned toward baseline. Plasma glucose and rate of haemodilution was higher in the SHAM group during and after hypotension. The maintenance of MAP above 60 mmHg was less effective in the SHAM group during the first 2 h after HTS, but after 24 h, prehaemorrhage MAP was established in both groups. In conclusion, the adrenal medulla does not play a major role in the response to HTS resuscitation.

Hypertonic saline resuscitation: Efficacy in a community-based burn unit: Griswold J, Anglin B, Love R, Scott-Connor C. South Med J. 1991;84:692-6

Hypertonic saline resuscitation: Efficacy in a community-based burn unit: Griswold J, Anglin B, Love R, Scott-Connor C. South Med J. 1991;84:692-6

Combined Hemorrhagic Shock and Head Injury:

Hypertonic saline resuscitation was compared to isotonic fluid resuscitation in a large animal model combining hemorrhagic shock with head injury. Sheep were subjected to a freeze injury of one cerebral hemisphere as well as 2 hours of hypotension at a mean arterial pressure (MAP) of 40 mm Hg. Resuscitation was then carried out (MAP = 80 mm Hg) for 1 hour with either lactated Ringer's (LR, n = 6) or 7.5% hypertonic saline (HS, n = 6). Hemodynamic parameters and intracranial pressure (ICP) were followed. At the end of resuscitation brain water content was determined in injured and uninjured hemispheres. No differences were detected in cardiovascular parameters; however, ICPs were lower in animals resuscitated with HS (4.2 +/- 1.5 mm Hg) compared to LR (15.2 +/- 2.2 mm Hg, p less than 0.05). Additionally, brain water content (ml H2O/gm dry weight) in uninjured brain hemispheres was lower after HS resuscitation (HS = 3.3 +/- 0.1; LR = 4.0 +/- 0.1; p less than 0.05). No differences were detected in the injured hemispheres. We conclude that hypertonic saline abolishes increases in ICP seen during resuscitation in a model combining hemorrhagic shock with brain injury by dehydrating areas where the blood-brain barrier is still intact. Hypertonic saline may prove useful in the early management of multiple trauma patients.

Metabolic acidosis associated with hypertonic saline resuscitation in an intracranial mass, hemorrhagic shock model: Is plasma lactate elevation the cause?

Metabolic acidosis associated with hypertonic saline resuscitation in an intracranial mass, hemorrhagic shock model: Is plasma lactate elevation the cause?

Is Hypertonic Saline Resuscitation Safe in 'Uncontrolled' Hemorrhagic Shock?

Departments of Anesthesiology, Urology, and Surgery B and the Laboratory of Surgical Research, Hadassah University Hospital, Jerusalem, Israel

Hypertonic Saline Resuscitation of Head Injury

Ideal resuscitation would simultaneously replete intravascular volume and minimize cerebral edema. We assessed the effects of hypertonic saline (HS) shock resuscitation on cerebral edema after head injury. Rats were subjected to hemorrhagic shock (40 mm Hg for 1 hour) in the presence or absence of mechanical brain injury, followed by 1 hour of resuscitation with either hypertonic saline (6.5%) or lactated Ringer's (LR). After resuscitation, animals were sacrificed and brain water contents determined. Less HS than LR was needed for resuscitation both in animals without brain injury (7 +/- 2 ml/kg vs. 97 +/- 16 ml/kg; p less than 0.0003) and with brain injury (10 +/- 1 ml/kg vs. 68 +/- 6 ml/kg; p less than 0.0001). Brain water content (ml H2O/gm dry wt) after HS resuscitation was decreased compared to LR resuscitation in animals without brain injury (3.36 +/- 0.12 vs. 3.74 +/- 0.08; p less than 0.025) and in the uninjured hemisphere of head-injured animals (3.29 +/- 0.11 vs. 3.78 +/- 0.09; p less than 0.025). Brain water content was increased in injured brain in both resuscitation groups, but the increase was the same (HS 4.10 +/- 0.13; LR 4.25 +/- 0.17; p greater than 0.05). HS resuscitation of hemorrhagic shock decreases brain water content in uninjured but not injured brain. HS may be useful in resuscitation of combined hemorrhagic shock and head injury.

Is hypertonic saline resuscitation safe in uncontrolled hemorrhagic shock?: Gross D, Landau EH, Assalia A, Krausz MM. J Trauma 1988;28:751-6

Is hypertonic saline resuscitation safe in uncontrolled hemorrhagic shock?: Gross D, Landau EH, Assalia A, Krausz MM. J Trauma 1988;28:751-6

Is hypertonic saline resuscitation safe in 'uncontrolled' hemorrhagic shock?

Hypertonic saline treatment of hemorrhagic shock (HS) results in increased systemic blood pressure, cardiac output, and splanchnic blood flow. To determine whether this elevation in blood pressure and flow would augment blood loss from injured intra-abdominal vessels and thus enhance mortality rate, "controlled" HS was induced by bleeding of 20 ml/kg from an arterial cannula that was immediately occluded after hemorrhage, and "uncontrolled" HS was induced by incision of three major radicals of the ileocolic artery leading to continuous intra-abdominal blood loss. Seventy rats were divided into eight groups: Group I (n = 5) underwent carotid artery and jugular vein cannulation and was observed for 3 hr; in Group II (n = 10) "controlled" HS was induced by arterial hemorrhage of 20 ml/kg; in Group III (n = 7) "controlled" HS was treated by 5 ml/kg NaCl 0.9%; in Group IV (n = 8) "controlled" HS was treated by 5 ml/kg NaCl 7.5%; in Group V (n = 4) midline laparotomy and identification of the ileocolic artery was performed; in Group VI (n = 9) "uncontrolled" HS was induced by incision of three major branches of the ileocolic artery; in Group VII (n = 9) "uncontrolled" HS was treated by 5 ml/kg NaCl 0.9%, and in Group VIII (n = 18) "uncontrolled" HS was treated by 5 ml/kg NaCl 7.5%. In untreated "controlled" HS (Group II), mean arterial pressure (MAP) fell to 35 torr followed by a spontaneous rise to 62 torr (p less than 0.001) after 3 hr with a survival of 80% of the animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Alterations of the Intracranial Pressure After Normal Saline, 3% Saline and Dextran-40

Resuscitation from hemorrhagic shock by infusion of isotonic (normal) saline (NS) is accompanied by a transient elevation in intracranial pressure (ICP), although cerebral edema, as measured by brain weights at 24 hours, is prevented by adequate volume resuscitation. The transient increase in ICP is not observed during hypertonic saline (HS) resuscitation. The effect of colloid resuscitation on ICP is unknown. Beagles were anesthetized, intubated, and ventilated, maintaining pCO2 between 30-45 torr. Femoral artery, pulmonary artery, and urethral catheters were positioned. ICP was measured with a subarachnoid bolt. Forty per cent of the dog's blood volume was shed and the shock state maintained for 1 hour. Resuscitation was done with shed blood and a volume of either NS (n = 5), 3% HS (n = 5), or 10% dextran-40 (D-40, n = 5) equal to the amount of shed blood. Intravascular volume was then maintained with NS. ICP fell from baseline values (4.7 +/- 3.13 mmHg) during the shock state and increased greatly during initial fluid resuscitation in NS and D-40 groups, to 16.0 +/- 5.83 mmHg and 16.2 +/- 2.68 mmHg, respectively. ICP returned to baseline values of 3.0 +/- 1.73 mmHg in the HS group with initial resuscitation and remained at baseline values throughout resuscitation. NS and D-40 ICP were greater than HS ICP at 1 hour (p less than .001) and 2 hours (p less than .05) after resuscitation. These results demonstrate that NS or colloid resuscitation from hemorrhagic shock elevates ICP and that HS prevents elevated ICP.

Resuscitation with hypertonic lactate saline in thermal injury

Four groups of animals were resuscitated by various methods after a scald burn over 40 per cent of the body. All animals receiving intravenous fluids responded equally well when evaluated by selected indexes. Hypertonic saline resuscitation produced natriuresis and no gain in weight. Animals receiving half-Brooke formula resuscitation had the smallest net gain of sodium. These two types of resuscitation may be of advantage clinically in patients with limited cardiopulmonary reserve.

Carotid sinus reflex in response to hemorrhage.

ARTICLESCarotid sinus reflex in response to hemorrhageM Kumada, RM Schmidt, K Sagawa, and KS TanM Kumada, RM Schmidt, K Sagawa, and KS TanPublished Online:01 Nov 1970https://doi.org/10.1152/ajplegacy.1970.219.5.1373MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByPhysiology of Human Hemorrhage and Compensation12 February 2021A regulated multiscale closed-loop cardiovascular model, with applications to hemorrhage and hypertension19 April 2018 | International Journal for Numerical Methods in Biomedical Engineering, Vol. 34, No. 6On the integration of the baroreflex control mechanism in a heterogeneous model of the cardiovascular system2 November 2011 | International Journal for Numerical Methods in Biomedical Engineering, Vol. 28, No. 4Ballistics reviews: mechanisms of bullet wound trauma31 July 2009 | Forensic Science, Medicine, and Pathology, Vol. 5, No. 3AFFERENT PATHWAYS INVOLVED IN CARDIOVASCULAR ADJUSTMENTS INDUCED BY HYPERTONIC SALINE RESUSCITATION IN RATS SUBMITTED TO HEMORRHAGIC SHOCKShock, Vol. 32, No. 2Effect of carotid or aortic baroreceptor denervation on arterial pressure during hemorrhage in conscious dogsTerry N. Thrasher, and Cassandra Shifflett1 June 2001 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 280, No. 6A mathematical model of the carotid baroregulation in pulsating conditionsIEEE Transactions on Biomedical Engineering, Vol. 46, No. 4Interaction between carotid baroregulation and the pulsating heart: a mathematical modelMauro Ursino1 November 1998 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 275, No. 5The role of pressure pulsatility in the carotid baroreflex control: A computer simulation studyComputers in Biology and Medicine, Vol. 26, No. 4Cardiovascular MechanoreceptorsHaemodynamic information encoded in the aortic baroreceptor discharge during haemorrhageActa Physiologica Scandinavica, Vol. 140, No. 2Expert system reasoning about dynamic systems by semi-quantitative simulationComputer Methods and Programs in Biomedicine, Vol. 29, No. 2New Insights into the Influence of Pulsatile Pressure on the Arterial Baroreceptor Reflex3 July 2009 | Clinical and Experimental Hypertension. Part A: Theory and Practice, Vol. 10, No. sup1Baroreflex Control of Systemic Arterial Pressure and Vascular Bed1 January 2011Further studies on beta-adrenergic control of transcapillary fluid absorption from skeletal muscle to blood during hemorrhageActa Physiologica Scandinavica, Vol. 112, No. 3The role of arterial baroreceptors in the regulation of arterial pressure in conscious dogs.Circulation Research, Vol. 39, No. 5Aspects of Overall Circulatory Regulation: CommentaryIFAC Proceedings Volumes, Vol. 6, No. 4Studies on the Arterial Baroreceptor Reflex SystemIFAC Proceedings Volumes, Vol. 6, No. 4Comparative Models of Overall Circulatory MechanicsStudies of Blood-pressure Regulation IV. The Effects of Impulse Train Stimulation of the Carotid-sinus NervesActa Physiologica Scandinavica, Vol. 85, No. 3The Use of Control Theory and Systems Analysis in Cardiovascular DynamicsInfluence of initial resistance on gain of short-term systemic autoregulation More from this issue > Volume 219Issue 5November 1970Pages 1373-1379 Copyright & PermissionsCopyright © 1970 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1970.219.5.1373PubMed5473121History Published online 1 November 1970 Published in print 1 November 1970 Metrics