scholarly journals Responsiveness to different volume therapies following hemodilution and hemorrhagic shock: a comparative experimental study in rats

2007 ◽  
Vol 22 (5) ◽  
pp. 355-360 ◽  
Author(s):  
Riad Naim Younes ◽  
Fernanda Deutsch ◽  
Mario Itinoshe ◽  
Belchor Fontes ◽  
Renato Poggetti ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Hypertonic Saline ◽  
Hypovolemic Shock ◽  
Isotonic Saline ◽  
High Volume ◽  
Subsequent Treatment ◽  
Volume Replacement ◽  
Trauma Patients

Guidelines for volume replacement for acutely hemorrhaged and hemodiluted trauma patients have not been well established. Purpose: To evaluate the effects of acute hemodilution on mean arterial pressure (MAP), and responsiveness of acutely hemodiluted and subsequently hemorrhaged rats to different volume therapies. Methods: 180 rats were hemodiluted to simulate hemorrhaged trauma patients with persistent bleeding after high volume replacement with isotonic solutions. Thirty hemodiluted [Anemia (ANE) group] animals received no further treatment. The remaining 150 animals were subjected to hypovolemic shock and randomized into five groups, according to the treatment option employed: Control (CTL) animals did not receive subsequent treatment after hemorrhagic hypovolemia, SAL4 animals received isotonic saline 4 mL/kg, SAL32 animals received isotonic saline 32 mL/kg, HS animals received hypertonic saline 4 mL/kg and BLD animals received re-infusion of drawn blood. Results: Highest mean arterial pressure (MAP) was achieved by BLD, followed by SAL32 and HS. MAP after treatment of BLD, HS, SAL32 and ANE were higher than CTL (p=0.036). At 85 and 95 minutes of experiment, SAL4, SAL32 and HS presented the lowest hematocrit levels (p<0.01). At day 3, ANE, CTL and HS had the highest hematocrit. SAL4 and CTL groups presented the highest mortality rates. Conclusion: Hypertonic saline is an effective and safe initial therapy for hemodiluted rats undergoing hemorrhagic shock, with an overall outcome comparable to blood replacement or high volume isotonic saline administration.

Evidence for enhanced uptake of ATP by liver and kidney in hemorrhagic shock

1977 ◽  
Vol 233 (3) ◽  
pp. R83-R88 ◽  
Author(s):  
I. H. Chaudry ◽  
M. M. Sayeed ◽  
A. E. Baue
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Beneficial Effect ◽  
Hemorrhagic Shock ◽  
Kidney Slices ◽  
Atp Levels ◽  
Salutary Effect ◽  
Liver And Kidney ◽  
In Vitro Uptake

It has been shown that infusion of ATP-MgCl2 proved beneficial in the treatment of shock; however, it is not known whether this effect is due to improvement in the microcirculation or direct provision of energy or a combination of the above or other effects. To elucidate the mechanism of the salutary effect of ATP-MgCl2, we have now examined the in vitro uptake of ATP by liver and kidney of animals in shock. Rats were bled to a mean arterial pressure of 40 Torr and so maintained for 2 hrs. After the rats were killed, liver and kidney were removed and slices of tissue (0.3-0.5 mm thick) were incubated for 1 h in 1.0 ml of Krebs-HCO3 buffer containing 10 mM glucose, 5 mM MgCl2, and 5 mM [8-14C]ATP or 5 mM [8-14C]ADP, or 5 mM [8-14C]AMP, or 5 mM [8-14C]adenosine in 95% O2-5% CO2 and then homogenized. Tissue and medium samples were subjected to electrophoresis to separate and measure the various nucleotides. The uptake of [14C]ATP but not that of [14C]ADP or [14C]adenosine by liver and kidney slices from animals in shock was 2.5 times greater than the corresponding uptake by control slices. Thus, the beneficial effect of ATP-MgCl2 in shock could be due to provision of energy directly to tissue in which ATP levels were lowered.

Effect of cortisol on vasopressin response to hypertonic saline in fetal sheep

1989 ◽  
Vol 257 (4) ◽  
pp. R861-R865
Author(s):  
T. L. Bennett ◽  
J. C. Rose
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Partial Pressure ◽  
Hypertonic Saline ◽  
Arginine Vasopressin ◽  
Positive Influence ◽  
Serum Osmolality ◽  
Base Line ◽  
Fetal Sheep ◽  
Cortisol Levels

To determine the effect of cortisol on vasopressin responses to hyperosmolality, we infused hypertonic saline (HS) (12 meq/kg NaCl) into nine chronically cannulated fetal sheep ranging from 110 to 132 days of gestation. The experiment was performed twice on each fetus, once during a continuous cortisol infusion and once during a vehicle infusion. Administration of HS resulted in a prompt increase in serum osmolality from 292.1 +/- 1.8 to 310.4 +/- 2.5 mosmol/kg. Decreases were seen in pH, partial pressure of O2, and hematocrit from 7.37 +/- 0.01 to 7.31 +/- 0.01, from 22.5 +/- 1.6 to 20.0 +/- 2.0 mmHg, and from 35.6 +/- 1.7 to 32.6 +/- 1.6, respectively. Mean arterial pressure increased from 41.3 +/- 1.4 to 48.9 +/- 2.0 mmHg (P less than 0.01). Arginine vasopressin (AVP) rose from base line after HS (P = 0.11 vehicle experiments, P = 0.04 cortisol experiments), and AVP responses were greater in the cortisol experiments than in the vehicle experiments (delta AVP = 21.9 +/- 10.9 vs. 3.1 +/- 0.9 pg/ml, P = 0.05). Also there was a correlation noted between differences in AVP response and cortisol levels (P less than 0.04). We conclude that cortisol exerts a positive influence on the AVP response to HS in fetal sheep.

Effects of V1- and V2-vasopressin (AVP) antagonists on the pressor, AVP and atrial natriuretic peptide responses to a hypertonic saline infusion in conscious anephric rats

1995 ◽  
Vol 133 (1) ◽  
pp. 127-132 ◽  
Author(s):  
Kozo Ota ◽  
Tokihisa Kimura ◽  
Minoru Inoue ◽  
Takeharu Funyu ◽  
Masaru Shoji ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Receptor Antagonist ◽  
Hypertonic Saline ◽  
Natriuretic Peptide ◽  
Plasma Volume ◽  
Control Group ◽  
Antagonist Group

Ota K, Kimura T, Inoue M, Funyu T, Shoji M, Sato K, Ohta M, Yamamoto T, Abe K, Effects of V1- and V2-vasopressin (AVP) antagonists on the pressor, AVP and atrial natriuretic peptide responses to a hypertonic saline infusion in conscious anephric rats. Eur J Endocrinol 1995;133:127–32. ISSN 0804–4643 To examine the role of vasopressin (AVP) receptors in the regulation of the hemodynamics and release of atrial natriuretic peptide (ANP), and the participation of renal nerve inputs in the osmotic AVP release, hypertonic saline (HS) was infused into conscious, bilaterally nephrectomized rats with nonpeptide, selective antagonists for the V1-receptor or V2-receptor of AVP. In the control group, HS alone increased mean arterial pressure, plasma ANP and AVP, plasma volume and plasma osmolality, and decreased the heart rate. In the V1-receptor antagonist group, an increase in the mean arterial pressure and a decrease in heart rate were completely abolished and an increase in plasma ANP was attenuated. In the V2-receptor antagonist group, increases in mean arterial pressure and plasma ANP and a decrease in heart rate were attenuated. However, the ratio of the changes in heart rate to the changes in mean arterial pressure in the V2-receptor antagonist group is significantly higher than that in the control group. In both experimental groups, increases in plasma AVP, plasma volume and plasma osmolality were not different from those in the control group. These results suggest that a HS-induced increase in mean arterial pressure is mediated by the pressor effect of AVP, mainly through V1-receptors, and that the depressor effect of AVP through V2-receptors may not influence tonically HS-induced hypertension. Moreover, HS-induced increase in plasma ANP is mediated mainly by increases in plasma volume and blood pressure, but may not be affected by a direct action of AVP to the heart. Renal afferent nerve inputs may not have effects on the regulation of osmotic AVP release. Kozo Ota, Second Department of Internal Medicine, Tohoku University School of Medicine, 1-1 Seiryo-cho, Aoba-ku, Sendai 980-77, Japan

Systemic inhibition of nitric oxide and prostaglandins in volume-induced natriuresis and hypertension

1998 ◽  
Vol 274 (1) ◽  
pp. R175-R180 ◽  
Author(s):  
James D. Krier ◽  
Juan Carlos Romero
Keyword(s):  
Nitric Oxide ◽  
Mean Arterial Pressure ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Significant Elevation ◽  
Synthesis Inhibition ◽  
Anesthetized Dogs ◽  
Change Map

Nitric oxide (NO) synthesis inhibition with N G-nitro-l-arginine methyl ester (l-NAME) (10 μg ⋅ kg−1 ⋅ min−1iv), cyclooxygenase inhibition with meclofenamate (Meclo; 5 mg/kg iv bolus), and combination of drugs (l-NAME+Meclo) were used to investigate the roles of NO and prostaglandins (PG) in the hemodynamic and natriuretic responses to isotonic saline volume expansion (VE; 5% body wt over 60 min) in anesthetized dogs. Before VE,l-NAME ( n = 6), Meclo ( n = 6), andl-NAME+Meclo ( n = 6) produced significant increments in mean arterial pressure (MAP) of 12 ± 2, 15 ± 3, and 17 ± 3 mmHg, respectively. VE did not change MAP in Meclo-treated dogs, but produced a significant elevation in the control dogs (14 ± 6 mmHg), inl-NAME-treated dogs (17 ± 6 mmHg), and in dogs pretreated withl-NAME+Meclo (12 ± 5 mmHg). VE alone induced marked natriuretic responses in the control (38 ± 9 to 562 ± 86 μmol/min),l-NAME (31 ± 9 to 664 ± 65 μmol/min), and Meclo groups (41 ± 10 to 699 ± 51 μmol/min). However, this natriuretic response was attenuated in dogs pretreated with l-NAME+Meclo (12 ± 4 to 185 ± 52 μmol/min). These results indicate that 1) blockade of both NO and PGs has significant diminishing effects on volume-induced natriuresis, 2) NO blockade alone impairs volume-induced natriuresis in a manner that requires further increases in MAP to restore the natriuresis, and 3) PG blockade alone does not curtail volume-induced natriuresis.

Hypertonic Saline Versus Isotonic Saline Nasal Irrigation: Systematic Review and Meta-analysis

2018 ◽  
Vol 32 (4) ◽  
pp. 269-279 ◽  
Author(s):  
Dichapong Kanjanawasee ◽  
Kachorn Seresirikachorn ◽  
Wirach Chitsuthipakorn ◽  
Kornkiat Snidvongs
Keyword(s):  
Side Effects ◽  
Adverse Effects ◽  
Hypertonic Saline ◽  
Meta Analysis ◽  
Isotonic Saline ◽  
High Volume ◽  
Mean Difference ◽  
Saline Irrigation ◽  
Nasal Irrigation ◽  
Subgroup Analyses

Background Saline nasal lavage is one of the treatments of sinonasal diseases. Evidence from basic research favors hypertonic saline (HS) over isotonic saline (IS) for mucociliary clearance, but evidence from clinical studies is controversial. Conversely, HS may carry greater side effects. Objective To compare the effects of HS and IS nasal irrigation in treating sinonasal diseases. Methods Systematic search with Ovid MEDLINE, Scopus, PubMed, Google Scholar, and Manual additional sources was conducted. Randomized controlled trials comparing HS with IS nasal irrigation in treating any sinonasal diseases, including rhinitis and rhinosinusitis, were included. Data were pooled for meta-analyses. Outcomes were symptom scores, sinonasal outcome test (SNOT), and adverse events. Heterogeneity was explored by subgroup analyses. Results Nine studies (740 patients) were included. HS nasal irrigation brought greater benefits over IS in symptom reduction (standardized mean difference (SMD) −0.58; 95% confidence interval [CI]: −0.76, −0.40); however, no difference was shown in SNOT-20 improvement (mean difference 1.81; 95% CI: −0.68, 4.30). In subgroup analyses, effects favoring HS on symptoms were larger in 4 subgroups. These were (1) patients with rhinitis (SMD −1.09; 95% CI: −1.42, −0.76) compared with rhinosinusitis (SMD −0.37; 95% CI: −0.58, −0.15), P < .01; (2) patients under the age of 18 years (SMD −1.22; 95% CI: −1.53, −0.91) compared with patients over the age of 18 years (SMD −0.26; 95% CI: −0.49, −0.04), P < .01; (3) saline irrigation using high volume (SMD −0.89; 95% CI: −1.18, −0.60) compared with low volume (SMD −0.39; 95% CI: −0.62, −0.16), P < .01; and (4) saline irrigation with hypertonicity of <3% (SMD −1.09; 95% CI: −1.42, −0.76) and hypertonicity of 3%–5% (SMD −1.20; 95% CI: −1.61, −0.78) compared with hypertonicity of >5% (SMD 0.20; 95% CI: −0.15, 0.55), P < .01. Buffered saline and operative status did not have impact. HS brought greater minor adverse effects. No major adverse effects were reported. Conclusion HS improves symptoms over IS nasal irrigation in treating sinonasal diseases. There is no difference in disease-specific quality of life. However, HS brings greater minor side effects than IS.

scholarly journals Prolonged severe hemorrhagic shock at a mean arterial pressure of 40 mmHg does not lead to brain damage in rats

2018 ◽  
Vol 5 (4) ◽  
pp. 350-357 ◽  
Author(s):  
Ryosuke Mihara ◽  
Akira Takasu ◽  
Kentaro Maemura ◽  
Toshiaki Minami
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Brain Damage

Contribution of AV3V region in anephric NaCl-induced hypertension in the rat

1987 ◽  
Vol 252 (3) ◽  
pp. F536-F542 ◽  
Author(s):  
J. R. Haywood ◽  
N. A. Ball ◽  
M. D. Lifschitz ◽  
T. J. Brennan
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Hypertonic Saline ◽  
Third Ventricle ◽  
Isotonic Saline ◽  
The Other ◽  
Pressor Responses ◽  
Dependent Component ◽  
Vasopressin Receptors ◽  
Osmotic Stimulus

The role of the anteroventral third ventricle (AV3V) region in mediating hypertonic sodium chloride-induced pressor responses was investigated in conscious rats. Sham- and AV3V-lesioned rats were prepared with femoral artery and vein catheters and subjected to bilateral nephrectomy under gaseous anesthesia. After recovery, animals were infused intravenously with isotonic (0.5 meq/kg) or hypertonic (10 meq/kg) saline at a rate of 0.0103 ml/min over 2 h. Isotonic saline infusion did not affect arterial pressure or heart rate in either group of rats. Hypertonic saline increased arterial pressure 35 +/- 3 mmHg in sham-lesioned rats and only 10 +/- 4 mmHg in AV3V-lesioned animals (P less than 0.0005). Sham-lesioned rats infused with hypertonic saline had a greater vasopressin-dependent component maintaining arterial pressure than the other groups of rats. Conversely, the sympathetic nervous system-dependent component of blood pressure was suppressed in the hypertonic saline-infused sham-lesioned animals compared with the other animals. However, when the vasopressin receptors were blocked, the neurally mediated portion of blood pressure was similar in all four groups of rats. These results emphasize that circulating vasopressin is important for the rise in arterial pressure accompanying the osmotic stimulus. Furthermore, this study demonstrates that the AV3V region is necessary for vasopressin-dependent pressor responses caused by an osmotic stimulus.

Recombinant Human Hemoglobin with Reduced Nitric Oxide–scavenging Capacity Restores Effectively Pancreatic Microcirculatory Disorders in Hemorrhagic Shock

2004 ◽  
Vol 100 (6) ◽  
pp. 1484-1490 ◽  
Author(s):  
Ernst von Dobschuetz ◽  
Joerg Hutter ◽  
Tomas Hoffmann ◽  
Konrad Messmer
Keyword(s):  
Nitric Oxide ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Hydroxyethyl Starch ◽  
Capillary Density ◽  
Functional Capillary Density ◽  
Human Hemoglobin ◽  
Scavenging Capacity ◽  
Area Functional

Background Scavenging of nitric oxide by hemoglobin-based oxygen carriers could aggravate microcirculatory failure in splanchnic organs after hemorrhagic shock as a consequence of vasoconstrictive side effects. The aim of this study was to compare the effects of two recombinant human hemoglobin solutions, a second-generation product bearing reduced nitric oxide-scavenging properties (rHb2.0) due to site directed mutagenesis of the heme pocket and a first-generation recombinant hemoglobin (rHb1.1) with scavenging capacity similar to native hemoglobin, on the pancreatic microcirculation after hemorrhagic shock. Methods Twenty-eight pentobarbital-anesthetized rats were bled to a mean arterial pressure of 40 mmHg and maintained at this level for 1 h. Using an intravital microscope, the length of erythrocyte-perfused pancreatic capillaries per observation area (functional capillary density) were measured in animals resuscitated by volumes of hydroxyethyl starch, rHb1.1, or rHb2.0 equivalent to the shed blood volume. Animals without shock induction served as control. Results As compared with control (438 +/- 10 cm(-1)), animals treated with hydroxyethyl starch (315 +/- 44 cm(-1)) and rHb1.1 (288 +/- 67 cm(-1)) showed a significant reduction of functional capillary density after 2 h of resuscitation. rHb2.0 was able to restore functional capillary density (410 +/- 42 cm(-1)) and mean arterial pressure to baseline values. Conclusion rHb2.0 was effectively able to restore pancreatic microcirculation after hemorrhagic shock. This may be related to the compound's effective lack of nitric oxide-scavenging properties. This hemoglobin solution or ones similar to it might be uniquely valuable for resuscitation from hemorrhagic shock.

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