L-ARGININE INDUCES AN INCREASE IN ARTERIAL BLOOD PRESSURE FOLLOWING HYPERTONIC SALINE INFUSION IN CONTROLLED HEMORRHAGIC SHOCK

Corticosteroids administered in amounts more than 100 times those required to sustain a fully adrenalectomized animal were highly effective in increasing survival following hemorrhagic shock. In rats with intact adrenal glands, hemorrhagic shock was produced by maintaining arterial blood pressure at 35 mm Hg for 240 min. Glucocorticoids and aldosterone were administered only after blood was reinfused. The therapeutic benefit is due to a pharmacological action of the adrenocortical hormone. Aldosterone had a lesser and relatively narrow dosage range of effectiveness.

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Humoral factor depletion and reticuloendothelial depression during hemorrhagic shock

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1977.232.3.h283 ◽

1977 ◽

Vol 232 (3) ◽

pp. H283-H287

Author(s):

D. J. Loegering

Keyword(s):

Blood Pressure ◽

Hemorrhagic Shock ◽

Arterial Blood Pressure ◽

Liver Slice ◽

Phagocytic Index ◽

Phagocytic Function ◽

Opsonic Activity ◽

Shed Blood ◽

Arterial Blood

Circulating opsonic activity and reticuloendothelial system (RES) phagocytic function were determined in anesthetized rats subjected to hemorrhagic shock. Animals were hemorrhaged to and maintained at 40 mmHg arterial blood pressure until they spontaneously took back 5% or 40% of the maximum bled volume. The phagocytic index, as determined by colloid clearance kinetics, was decreased in both groups following reinfusion of the shed blood. The reduction in phagocytic index was associated with decreased liver, unchanged spleen, and increased lung test colloid localization. Plasma opsonic activity, as determined by liver slice bioassay, was decreased 50-60% at 5% and 40% uptake of the maximum shed volume, decreased further 15 min after reinfusion in both groups, and tended to recover 1 h after reinfusion in the 5% uptake group. In vitro hepatic phagocytic activity of liver slices from shocked animals in the presence of normal rat plasma was decreased only in the 40% uptake animals after reinfusion when the arterial blood pressure had decreased to 50 mmHg. These data indicate that the depression of RES phagocytic function during hemorrhagic shock is associated with and may be mediated, in part, by decreased circulating opsonic activity.

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Effect of intravenous infusion of adrenaline on the cardiovascular responses to distal body subatmospheric pressure in man

Clinical Science ◽

10.1042/cs0750389 ◽

1988 ◽

Vol 75 (4) ◽

pp. 389-394 ◽

Cited By ~ 7

Author(s):

I. W. Fellows ◽

I. A. MacDonald ◽

T. Bennett ◽

D. P. O'Donoghue

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Blood Flow ◽

Arterial Blood Pressure ◽

Forearm Blood Flow ◽

Cardiovascular Responses ◽

Saline Infusion ◽

Subatmospheric Pressure ◽

Arterial Blood ◽

Adrenaline Infusion

1. On two separate occasions, at least 1 week apart, seven young healthy male subjects received intravenous infusions of either adrenaline [0.27 nmol (50 ng) min−1 kg−1] or saline (154 mmol/l NaCl), plus ascorbic acid (5.68 mmol/l), over 30 min. 2. On each occasion, the subjects were exposed to distal body subatmospheric pressure (DBSP), 0 to 50 mmHg (0 to 6.65 kPa) in 10 mmHg (1.33 kPa) steps, before infusion, during the final 15 min of the infusion, and at 15 min and 30 min after the cessation of the infusion. 3. Venous adrenaline concentrations of 2.85 ±0.22 nmol/l were achieved during the adrenaline infusion, compared with 0.49 ± 0.07 nmol/l during the saline infusion (P < 0.001). At 15 min and at 30 min after cessation of the adrenaline infusion, venous adrenaline concentrations had fallen to levels similar to those achieved after the cessation of the saline infusion. 4. Heart rate rose significantly from 58 ±4 beats/min to 67 ±4 beats/min during the adrenaline infusion (P < 0.05), but there was no further significant change in response to 50 mmHg (6.65 kPa) DBSP. At 30 min after the cessation of the adrenaline infusion, heart rate rose from 60 ± 4 beats/min to 78 ± 7 beats/min in response to 50 mmHg DBSP. This increase was significantly greater than that observed before the adrenaline infusion [58 ± 4 beats/min to 69 ±7 beats/min during 50 mmHg (6.65 kPa) DBSP; P < 0.01]. 5. During the infusion of adrenaline, systolic arterial blood pressure rose and diastolic arterial blood pressure fell, but the blood pressure responses to DBSP were unaffected. 6. Forearm blood flow increased significantly during adrenaline infusion but there was no significant difference in the fall in forearm blood flow during DBSP compared with the values before infusion. At 15 min after the cessation of the adrenaline infusion, forearm vascular resistance rose proportionately more in response to DBSP than it had before the adrenaline infusion (P < 0.05). 7. These results are consistent with adrenaline-mediated facilitation of sympathetic neuronal release of noradrenaline in the heart and in the forearm vascular bed.

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Hypertonic saline infusion in hemorrhagic shock treated by military antishock trousers (MAST) in awake sheep

Critical Care Medicine ◽

10.1097/00003246-199310000-00026 ◽

1993 ◽

Vol 21 (10) ◽

pp. 1554-1562 ◽

Cited By ~ 8

Author(s):

EZEKIEL H. LANDAU ◽

DITZA GROSS ◽

AHMED ASSALIA ◽

ELAD FEIGIN ◽

MICHAEL M. KRAUSZ

Keyword(s):

Hemorrhagic Shock ◽

Hypertonic Saline ◽

Saline Infusion ◽

Hypertonic Saline Infusion

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Time course of synergistic interaction between DOCA and salt on blood pressure: roles of vasopressin and hepatic osmoreceptors

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00068.2006 ◽

2006 ◽

Vol 291 (6) ◽

pp. R1825-R1834 ◽

Cited By ~ 12

Author(s):

Virginia L. Brooks ◽

Korrina L. Freeman ◽

Yue Qi

Keyword(s):

Blood Pressure ◽

Hypertonic Saline ◽

Time Course ◽

Synergistic Interaction ◽

Saline Infusion ◽

Second Phase ◽

Dark Phase ◽

Developmental Phase ◽

Pressure Transducers ◽

Hypertonic Saline Infusion

In DOCA-salt rats, the time course of the synergistic interaction between osmolality and DOCA to produce hypertension is unknown. Therefore, in rats 2 wk after implantation of subcutaneous silicone pellets containing DOCA (65 mg) or no drug (sham), we determined blood pressure (BP) and heart rate (HR) responses, using telemetric pressure transducers, during 2 wk of excess salt ingestion (1% NaCl in drinking water). BP was unaltered in sham rats after increased salt, but in DOCA rats BP increased within 4 h. The initial hypertension of 30–35 mmHg stabilized within 2 days, followed ∼5 days later by a further increment of ∼30 mmHg. HR first decreased during the dark phase; the second phase was linked to an abrupt increase in HR and BP variability and decreased HR variability. Pressor responses to acute intravenous hypertonic saline infusion were doubled in DOCA-treated rats via vasopressin and nonvasopressin mechanisms. Only in DOCA-treated rats, portal vein hypertonic saline infusion increased BP, which was prevented by V1 vasopressin blockade. After 2 wk of DOCA-salt, oral ingestion of water rapidly decreased BP. Intraportal infusion of water did not lower BP in DOCA-salt rats, suggesting that hepatic osmoreceptors were not involved. In summary, the hypertension of DOCA-treated rats consuming excess salt exhibits multiple phases and can be rapidly reversed. Hypertonicity-induced vasopressin and nonvasopressin pressor mechanisms that are augmented by DOCA, and hepatic osmoreceptors may contribute to the initial developmental phase. With time, combined DOCA-salt induces marked changes in the regulation of the autonomic nervous system, which may favor hypertension development.

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Sympathetic innervation of the splanchnic region mediates the beneficial hemodynamic effects of 8-OH-DPAT in hemorrhagic shock

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00689.2011 ◽

2012 ◽

Vol 303 (5) ◽

pp. R527-R538 ◽

Cited By ~ 4

Author(s):

Ruslan Tiniakov ◽

Kalipada Pahan ◽

Karie E. Scrogin

Keyword(s):

Blood Pressure ◽

Hemorrhagic Shock ◽

Arterial Blood Pressure ◽

Sympathetic Innervation ◽

Hypovolemic Shock ◽

Pressor Effect ◽

Venous Tone ◽

Blood Withdrawal ◽

Arterial Blood ◽

Splanchnic Nerves

Administration of the 5-HT1A receptor agonist, 8-OH-DPAT, improves cardiovascular hemodynamics and tissue oxygenation in conscious rats subjected to hypovolemic shock. This effect is mediated by sympathetic-dependent increases in venous tone. To determine the role of splanchnic nerves in this response, effects of 8-OH-DPAT (30 nmol/kg iv) were measured following fixed-arterial blood pressure hemorrhagic shock (i.e., maintenance of 50 mmHg arterial pressure for 25 min) in rats subjected to bilateral splanchnic nerve denervation (SD). Splanchnic denervation decreased baseline venous tone as measured by mean circulatory filling pressure (MCFP) and accelerated the onset of hypotension during blood loss. Splanchnic denervation did not affect the immediate pressor effect of 8-OH-DPAT but did reverse the drug's lasting pressor effect, as well as its ability to increase MCFP and improve metabolic acidosis. Like SD, adrenal demedullation (ADMX) lowered baseline MCFP and accelerated the hypotensive response to blood withdrawal but also reduced the volume of blood withdrawal required to maintain arterial blood pressure at 50 mmHg. 8-OH-DPAT raised MCFP early after administration in ADMX rats, but the response did not persist throughout the posthemorrhage period. In a fixed-volume hemorrhage model, 8-OH-DPAT continued to raise blood pressure in ADMX rats. However, it produced only a transient and variable rise in MCFP compared with sham-operated animals. The data indicate that 8-OH-DPAT increases venoconstriction and improves acid-base balance in hypovolemic rats through activation of splanchnic nerves. This effect is due, in part, to activation of the adrenal medulla.

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Effect of Varying the Hematocrit Ratio on the Susceptibility to Hemorrhagic Shock

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1957.192.1.171 ◽

1957 ◽

Vol 192 (1) ◽

pp. 171-174 ◽

Cited By ~ 20

Author(s):

Jack W. Crowell ◽

Sara H. Bounds ◽

W. W. Johnson

Keyword(s):

Blood Pressure ◽

Hemorrhagic Shock ◽

Arterial Blood Pressure ◽

Natural Variation ◽

Time Lapse ◽

Arterial Blood ◽

Time Required

By the use of a) acetyl phenylhydrazine, b) hemorrhage, c) transfusion, and d) natural variation, 67 dogs with hematocrit ratios varying from 12 to 56 were obtained. These dogs were subjected to hemorrhagic shock by lowering their arterial blood pressure to 30 mm Hg, and the time lapse between the initial production of hypotension and the beginning deterioration of the animal determined. This time lapse is a measure of the resistance of the animal to the development of irreversible shock. A graph of initial hematocrit versus the time required for the development of irreversible shock shows that an increase in the hematocrit ratio from 12 to 35 increases the resistance of the animals by a factor of approximately 5; however, increasing the hematocrit ratio above 35 decreases the resistance of the animal to the development of irreversible shock.

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Renovascular reactivity measured by near-infrared spectroscopy

Journal of Applied Physiology ◽

10.1152/japplphysiol.00024.2012 ◽

2012 ◽

Vol 113 (2) ◽

pp. 307-314 ◽

Cited By ~ 36

Author(s):

Christopher J. Rhee ◽

Kathleen K. Kibler ◽

R. Blaine Easley ◽

Dean B. Andropoulos ◽

Marek Czosnyka ◽

...

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Infrared Spectroscopy ◽

Hemorrhagic Shock ◽

Renal Blood Flow ◽

Arterial Blood Pressure ◽

Near Infrared Spectroscopy ◽

Near Infrared ◽

Laser Doppler ◽

Arterial Blood

Hypotension and shock are risk factors for death, renal insufficiency, and stroke in preterm neonates. Goal-directed neonatal hemodynamic management lacks end-organ monitoring strategies to assess the adequacy of perfusion. Our aim is to develop a clinically viable, continuous metric of renovascular reactivity to gauge renal perfusion during shock. We present the renovascular reactivity index (RVx), which quantifies passivity of renal blood volume to spontaneous changes in arterial blood pressure. We tested the ability of the RVx to detect reductions in renal blood flow. Hemorrhagic shock was induced in 10 piglets. The RVx was monitored as a correlation between slow waves of arterial blood pressure and relative total hemoglobin (rTHb) obtained with reflectance near-infrared spectroscopy (NIRS) over the kidney. The RVx was compared with laser-Doppler measurements of red blood cell flux, and renal laser-Doppler measurements were compared with cerebral laser-Doppler measurements. Renal blood flow decreased to 75%, 50%, and 25% of baseline at perfusion pressures of 60, 45, and 40 mmHg, respectively, whereas in the brain these decrements occurred at pressures of 30, 25, and 15 mmHg, respectively. The RVx compared favorably to the renal laser-Doppler data. Areas under the receiver operator characteristic curves using renal blood flow thresholds of 50% and 25% of baseline were 0.85 (95% CI, 0.83–0.87) and 0.90 (95% CI, 0.88–0.92). Renovascular autoregulation can be monitored and is impaired in advance of cerebrovascular autoregulation during hemorrhagic shock.

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