Effect of Hemorrhagic Shock on Tissue Adenine Nucleotides in Conscious Rats

1974 ◽  
Vol 52 (2) ◽  
pp. 131-137 ◽  
Author(s):  
Irshad H. Chaudry ◽  
Mohammed M. Sayeed ◽  
Arthur E. Baue
Keyword(s):  
Skeletal Muscle ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Subclavian Artery ◽  
Adenine Nucleotides ◽  
Creatine Phosphate ◽  
Atp Content ◽  
Conscious Rats ◽  
Liver And Kidney

Hemorrhagic shock was produced in conscious rats by cannulating the subclavian artery and bleeding the animals to a mean arterial pressure of 40 mm Hg which was maintained for 1 (early shock) or 2 h (late shock). Analysis of tissues showed that there was a significant decrease in ATP and ADP levels in liver and kidney in early and late shock. Associated with the decrease in ATP and ADP levels were increases in AMP and P1 levels. In contrast to the above organs, adenine nucleotides and creatine phosphate levels of skeletal muscle did not decrease in early shock but a significant reduction of these compounds was observed in late shock. The decrease in ATP content was greater in liver and kidney than in skeletal muscle. The present experiments indicate that there is a decrease in the energy available to tissues during severe hemorrhagic shock. This could be due to decreased biosynthesis, to continuing or increased utilization of the nucleotides, or to both.

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.

Is postexercise hypotension related to excess postexercise oxygen consumption through changes in leg blood flow?

2005 ◽  
Vol 98 (4) ◽  
pp. 1463-1468 ◽  
Author(s):  
Jay T. Williams ◽  
Mollie P. Pricher ◽  
John R. Halliwill
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Causal Link ◽  
Skeletal Muscle Blood Flow ◽  
Leg Blood Flow ◽  
Postexercise Hypotension

After a single bout of aerobic exercise, oxygen consumption remains elevated above preexercise levels [excess postexercise oxygen consumption (EPOC)]. Similarly, skeletal muscle blood flow remains elevated for an extended period of time. This results in a postexercise hypotension. The purpose of this study was to explore the possibility of a causal link between EPOC, postexercise hypotension, and postexercise elevations in skeletal muscle blood flow by comparing the magnitude and duration of these postexercise phenomena. Sixteen healthy, normotensive, moderately active subjects (7 men and 9 woman, age 20–31 yr) were studied before and through 135 min after a 60-min bout of upright cycling at 60% of peak oxygen consumption. Resting and recovery V̇o2 were measured with a custom-built dilution hood and mass spectrometer-based metabolic system. Mean arterial pressure was measured via an automated blood pressure cuff, and femoral blood flow was measured using ultrasound. During the first hour postexercise, V̇o2 was increased by 11 ± 2%, leg blood flow was increased by 51 ± 18%, leg vascular conductance was increased by 56 ± 19%, and mean arterial pressure was decreased by 2.2 ± 1.0 mmHg (all P < 0.05 vs. preexercise). At the end of the protocol, V̇o2 remained elevated by 4 ± 2% ( P < 0.05), whereas leg blood flow, leg vascular conductance, and mean arterial pressure returned to preexercise levels (all P > 0.7 vs. preexercise). Taken together, these data demonstrate that EPOC and the elevations in skeletal muscle blood flow underlying postexercise hypotension do not share a common time course. This suggests that there is no causal link between these two postexercise phenomena.

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.

Participation of alpha 2-adrenergic receptors in neural vascular tone of canine skeletal muscle

1992 ◽  
Vol 262 (6) ◽  
pp. H1705-H1710 ◽  
Author(s):  
P. Kubes ◽  
M. Melinyshyn ◽  
K. Nesbitt ◽  
S. M. Cain ◽  
C. K. Chapler
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Sciatic Nerve ◽  
Arterial Pressure ◽  
Adrenergic Receptors ◽  
Receptor Agonist ◽  
Vascular Tone ◽  
Adrenergic Blockade ◽  
Adrenergic Blockers

Studies were carried out in anesthetized, paralyzed, and ventilated dogs to determine whether postsynaptic alpha 2-adrenergic receptors participated in neurally mediated vascular tone in skeletal muscle. Hindlimb skeletal muscle resistance (RL) and blood flow (QL) were determined before, during, and after reversible cold block of the sciatic nerve. This sequence of observations was repeated 30 min after blockade of alpha 1-adrenergic receptors with prazosin. Then the alpha 2-adrenergic receptors were blocked with yohimbine, and the nerve cold block was repeated. When the sciatic nerve was cold blocked before alpha 1-adrenergic blockade, RL decreased approximately 50% and QL increased 75% (P less than 0.05) and then returned to control when the nerve was rewarmed. After alpha 1-block 76% of neural tone remained as assessed by nerve cooling (P less than 0.05). This phenomenon occurred despite effective alpha 1-adrenergic blockade as assessed by the alpha 1-receptor agonist methoxamine. With alpha 1- plus alpha 2-block no change in RL or QL was seen with nerve cold block. The same protocol was repeated in a second series of animals, but mean arterial pressure, which fell after alpha 1-block in the group above, was maintained by dextran infusion at normotensive levels. In these animals, 40% of neural tone remained after alpha 1-block. Both alpha 1- and alpha 2-adrenergic blockers were again needed to abolish the QL and RL response to nerve cold block. In another series of animals, yohimbine was administered before prazosin. In this series, alpha 2-adrenergic blockade greatly reduced neural tone as assessed by nerve cooling.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular responses to intrathecal vasopressin in conscious and anesthesized rats

1989 ◽  
Vol 256 (1) ◽  
pp. R193-R200 ◽  
Author(s):  
A. Martinez-Arizala ◽  
J. W. Holaday ◽  
J. B. Long
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Intrathecal Administration ◽  
Motor Dysfunction ◽  
Sprague Dawley ◽  
Cardiovascular Changes ◽  
Conscious Rats

Increases in mean arterial pressure and heart rate have been documented after the intrathecal administration of [Arg8]vasopressin (AVP) in rats. Prior studies in our laboratories with conscious rats indicated that these cardiovascular changes were associated with a marked hindlimb sensorimotor dysfunction. In this study, which represents the first systematic comparison of the effects of intrathecal AVP in conscious and anesthesized rats, we demonstrate that in conscious male Sprague-Dawley rats 1) the motor dysfunction induced by intrathecal AVP is accompanied by a rise in mean arterial pressure that is significantly greater than that produced by an equal intravenous dose of AVP, and 2) both paralytic and pressor effects of intrathecal but not intravenous AVP are blocked by the intrathecal administration of the V1-receptor antagonist d(CH2)5[Tyr(Me)2]AVP (V1-ANT) but are not blocked by intravenous phenoxybenzamine, hexamethonium, or [Sar1, Thr8]angiotensin II, an angiotensin II antagonist. In contrast, in anesthesized rats the arterial pressor response to intrathecal AVP was blocked by intrathecal V1-ANT, intravenous hexamethonium, and intravenous phenoxybenzamine. Furthermore, conscious but not anesthesized rats exhibited a tachyphylaxis to intrathecal AVP. These results indicate that intrathecal AVP produces both the cardiovascular changes and the sensorimotor deficits through interactions with centrally located V1-receptors. In addition, sympathetic catecholaminergic mechanisms mediate the rise in mean arterial pressure produced by intrathecal AVP in anesthesized rats, but they do not in conscious rats.

Sustained hyperinsulinemia increases arterial pressure in conscious rats

1991 ◽  
Vol 260 (4) ◽  
pp. R764-R768 ◽  
Author(s):  
M. W. Brands ◽  
D. A. Hildebrandt ◽  
H. L. Mizelle ◽  
J. E. Hall
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Insulin ◽  
Large Body ◽  
Experimental Period ◽  
Underlying Mechanism ◽  
Urinary Sodium Excretion ◽  
Plasma Insulin Concentration ◽  
Conscious Rats

A large body of correlational evidence relating plasma insulin levels and arterial pressure in obese hypertensives suggests that hyperinsulinemia may play a causal role in the development of hypertension in these subjects. However, experimental evidence supporting the ability of increased plasma insulin per se to increase blood pressure is lacking. The goal of this study was to determine the effect of hyperinsulinemia on mean arterial pressure and renal electrolyte excretion in eight conscious rats. Arterial pressure was determined by sampling the signal from an abdominal aortic catheter once per minute, 19 h/day by computer. A 5-day intravenous insulin and glucose infusion that increased plasma insulin concentration 43% significantly increased mean arterial pressure from 93 +/- 1 mmHg to an average of 101 +/- 2 mmHg for the 5-day experimental period. Heart rate increased from 369 +/- 8 to 406 +/- 3 beats/min. Urinary sodium excretion transiently decreased on day 1 of insulin, but no significant sodium retention was measured after 5 days of insulin infusion, suggesting that the blood pressure increase was not volume mediated. There were no changes in any of these variables in eight vehicle-infused rats. These results suggest that hyperinsulinemia can increase mean arterial pressure in conscious rats, but the underlying mechanism remains to be elucidated.

Effect of insulin on regional vascular resistances in conscious rats

1996 ◽  
Vol 270 (2) ◽  
pp. R450-R455
Author(s):  
E. Qadir ◽  
J. P. Porter
Keyword(s):  
Skeletal Muscle ◽  
Arterial Pressure ◽  
Low Dose ◽  
Chronic Administration ◽  
High Dose ◽  
Ganglionic Blockade ◽  
Conscious Rats ◽  
Before And After ◽  
Vascular Beds ◽  
Renal Vascular

In the rat, but not in humans and other mammals, chronic administration of insulin produces hypertension. The present aim was to determine the effect of acute insulin infusion on regional vascular resistances and to determine the neurogenic contribution to the response. Conscious rats were infused with insulin (2 or 6 mU/min) before and after ganglionic blockade with chlorisondamine (5 mg/kg). The low dose of insulin produced an increase in arterial pressure and hindquarter vascular resistance; the high dose produced a gradual decrease in arterial pressure and renal resistance. After ganglionic blockade, the hindquarter vasoconstriction produced by the low dose was abolished. The high dose of insulin produced both hindquarter and renal vasodilation. Thus the low dose of insulin had a selective neurogenic vasoconstrictor effect in rat skeletal muscle vascular beds. With higher doses, direct vasodilatory effects in both skeletal muscle and renal vascular beds appeared. This greater sensitivity of the sympathoexcitatory effects of insulin in rats may explain the ability of chronic insulin infusions to increase blood pressure in this species.

Rapid vasoregulatory mechanisms in exercising human skeletal muscle: dynamic response to repeated changes in contraction intensity

2006 ◽  
Vol 291 (3) ◽  
pp. H1065-H1073 ◽  
Author(s):  
Anna M. Rogers ◽  
Natasha R. Saunders ◽  
Kyra E. Pyke ◽  
Michael E. Tschakovsky
Keyword(s):  
Skeletal Muscle ◽  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Exercise Intensity ◽  
Time Course ◽  
Human Skeletal Muscle ◽  
Muscle Blood Flow ◽  
Relaxation Phase

We tested the hypothesis that vasoregulatory mechanisms exist in humans that can rapidly adjust muscle blood flow to repeated increases and decreases in exercise intensity. Six men and seven women (age, 24.4 ± 1.3 yr) performed continuous dynamic forearm handgrip contractions (1- to 2-s contraction-to-relaxation duty cycle) during repeated step increases and decreases in contraction intensity. Three step change oscillation protocols were examined: Slow (7 contractions per contraction intensity × 10 steps); Fast (2 contractions per contraction intensity × 15 steps); and Very Fast (1 contraction per contraction intensity × 15 steps). Forearm blood flow (FBF; Doppler and echo ultrasonography), heart rate (ECG), and mean arterial pressure (arterial tonometry) were examined for the equivalent of a cardiac cycle during each relaxation phase (FBFrelax). Mean arterial pressure and heart rate did not change during repeated step changes ( P = 0.352 and P = 0.190). For both Slow and Fast conditions, relaxation phase FBFrelax adjusted immediately and repeatedly to both increases and decreases in contraction intensity, and the magnitude and time course of FBFrelax changes were virtually identical. For the Very Fast condition, FBFrelax increased with the first contraction and thereafter slowly increased over the course of repeated contraction intensity oscillations. We conclude that vasoregulatory mechanisms exist in human skeletal muscle that are capable of rapidly and repeatedly adjusting muscle blood flow with ongoing step changes in contraction intensity. Importantly, they demonstrate symmetry in response magnitude and time course with increasing versus decreasing contraction intensity but cannot adjust to very fast exercise intensity oscillations.

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

Defense reaction alters the response to blood loss in the conscious rabbit

2001 ◽  
Vol 280 (4) ◽  
pp. R985-R993 ◽  
Author(s):  
James C. Schadt ◽  
Eileen M. Hasser
Keyword(s):  
Skeletal Muscle ◽  
Mean Arterial Pressure ◽  
Blood Loss ◽  
Arterial Pressure ◽  
Cardiovascular Response ◽  
Muscle Blood Flow ◽  
Venous Blood ◽  
Defense Reaction ◽  
Simultaneous Exposure ◽  
Air Jet

The interaction of sensory stressors with the cardiovascular response to blood loss has not been studied. The cardiovascular response to a stressor (i.e., the defense reaction) includes increased skeletal muscle blood flow and perhaps a reduction in arterial baroreflex function. Arterial pressure maintenance during blood loss requires baroreflex-mediated skeletal muscle vasoconstriction. Therefore, we hypothesized that the defense reaction would limit arterial pressure maintenance during blood loss. Male, New Zealand White rabbits were chronically prepared with arterial and venous catheters and Doppler flow probes. We removed venous blood in conscious rabbits until mean arterial pressure decreased to <40 mmHg. We repeated the experiment with (air) and without (sham) simultaneous exposure to an air jet stressor. Air resulted in a defense reaction (e.g., mean arterial pressure = 94 ± 1 and 67 ± 1 mmHg for air and sham, respectively). Contrary to our hypothesis, air increased the blood loss necessary to produce hypotension (19.3 ± 0.2 vs. 16.9 ± 0.2 ml/kg for sham). Air did not reduce skeletal muscle vasoconstriction during normotensive hemorrhage. However, air did enhance renal vasoconstriction (97 ± 3 and 59 ± 3% of baseline for sham and air, respectively) during the normotensive phase. Thus the defense reaction did not limit but rather extended defense of arterial pressure during hemorrhage.

Sign in / Sign up

Export Citation Format

Share Document