Trauma-hemorrhage and resuscitation in the mouse: effects on cardiac output and organ blood flow

1993 ◽  
Vol 264 (4) ◽  
pp. H1166-H1173 ◽  
Author(s):  
P. Wang ◽  
Z. F. Ba ◽  
J. Burkhardt ◽  
I. H. Chaudry
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Reliable Method ◽  
Sham Operation ◽  
Organ Blood Flow ◽  
Radioactive Microspheres ◽  
Ringer Lactate ◽  
Late Mortality ◽  
The Brain

Although mice are widely used for the study of immune consequences of hemorrhage, the changes of cardiac output (CO) and blood flow (BF) in response to trauma and hemorrhage in this species have not been well defined. To study this, nonheparinized C3H/HeN mice (n = 6 per group) underwent laparotomy (i.e., trauma induced), were bled to a mean arterial pressure of 35 mmHg, and maintained for 90 min by withdrawing more blood or returning Ringer lactate. The animals were then resuscitated with four times the volume of maximal bleedout in the form of Ringer lactate over 60 min. Sham-operated mice underwent the same procedure but were neither bled nor resuscitated. At the end of hemorrhage, 60 min postresuscitation, or corresponding time after sham operation, CO and BF were determined by radioactive microspheres. Results indicate that CO and BF decreased significantly at the end of hemorrhage. Resuscitation, however, restored CO and BF in various organs except the brain and skeletal muscle. Despite this, 9 of 16 mice died within 6 days postresuscitation, whereas none of sham mice died (n = 16 per group in this additional study). Therefore, we have developed a nonheparinized model of trauma-hemorrhage and resuscitation in mice that is associated with late mortality. Furthermore, the microsphere technique provides a reliable method for assessing CO and BF in mice. Thus it may be possible to study the correlation between cardiovascular and immunologic alterations under such conditions.

Abstract 67: Vasopressin impairs Brain, Heart and Kidney Perfusion in Acute Heart Failure

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Stig Müller ◽  
Ole-Jakob How ◽  
Stig E Hermansen ◽  
Truls Myrmel
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Heart Function ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Arterial Blood Flow ◽  
Organ Blood Flow ◽  
Arterial Blood ◽  
Time Flow ◽  
The Brain

Arginin Vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in various circulatory shock states including cardiogenic shock. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. Aim: We hypothesized that restoring MAP by AVP improves vital organ blood flow in experimental acute cardiac failure. Methods: Cardiac output (CO) and arterial blood flow to the brain, heart, kidney and liver were measured in nine pigs by transit-time flow probes. Heart function and contractility were measured using left ventricular Pressure-Volume catheters. Catheters in central arteries and veins were used for pressure recordings and blood sampling. Left ventricular dysfunction was induced by intermittent coronary occlusions, inducing an 18 % reduction in cardiac output and a drop in MAP from 87 ± 3 to 67 ± 4 mmHg. Results: A low-dose therapeutic infusion of AVP (0.005 u/kg/min) restored MAP but further impaired systemic perfusion (CO and blood flow to the brain, heart and kidney reduced by 29, 18, 23 and 34 %, respectively). The reduced blood flow was due to a 2.0, 2.2, 1.9 and 2.1 fold increase in systemic, brain, heart and kidney specific vascular resistances, respectively. Contractility remained unaffected by AVP. The hypoperfusion induced by AVP was most likely responsible for observed elevated plasma lactate levels and an increased systemic oxygen extraction. Oxygen saturation in blood drawn from the great cardiac vein fell from 31 ± 1 to 22 ± 3 % dropping as low as 10 % in one pig. Finally, these effects were reversed forty minutes after weaning the pigs form the drug. Conclusion: The pronounced reduction in coronary blood flow point to a potentially deleterious effect in postoperative cardiac surgical patients and in patients with coronary heart disease. Also, this is the first study to report a reduced cerebral perfusion by AVP.

Effect of serotonin on cardiac output and organ blood flow of rats

1963 ◽  
Vol 204 (2) ◽  
pp. 301-303 ◽  
Author(s):  
L. Takács ◽  
V. Vajda
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Intravenous Infusion ◽  
Organ Distribution ◽  
Organ Blood Flow ◽  
Cutaneous Blood Flow ◽  
Pulmonary Parenchyma ◽  
Cutaneous Blood

The effects of intraperitoneal and intravenous administration of serotonin on cardiac output, blood pressure, and organ distribution of blood flow (Rb86) were studied in the rat. Fifteen to thirty minutes after intraperitoneal injection (10 mg/kg) cardiac output was unchanged, while blood pressure was significantly reduced. Increase in blood flow was noted in the myocardium, pulmonary parenchyma and "carcass" (skeletal muscle, bone, CNS), with decrease in the kidney and the skin. Splanchnic blood flow was unchanged. Conversely, intravenous infusion of serotonin produced an increase of cardiac output, blood pressure, and cutaneous blood flow.

Dose-Dependent Effects of Meclofenamate on Peripheral Vasculature of Conscious Rabbits

1983 ◽  
Vol 64 (5) ◽  
pp. 471-474 ◽  
Author(s):  
R. A. Banks ◽  
L. J. Beilin ◽  
J. Soltys
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Organ Blood Flow ◽  
Hepatic Circulation ◽  
Peripheral Vasculature ◽  
Conscious Rabbits ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
The Brain ◽  
Intravenous Sodium

1. Changes in systemic haemodynamics and organ blood flow were measured in conscious rabbits after various doses of intravenous sodium meclofenamate, an inhibitor of prostaglandin cyclo-oxygenase. 2. Meclofenamate had no effect on arterial pressure or cardiac output but caused a dose-dependent fall in renal blood flow. 3. Meclofenamate also reduced adrenal perfusion but, in contrast, caused a dose-dependent increase in blood flow to the brain, bronchial and hepatic circulation and to the testis. No effect was demonstrated on other organs studied. 4. The effect on the cerebral circulation was observed at the lowest dose of meclofenamate (0.75 mg/kg). Higher total doses were necessary for an effect on the renal and bronchial (3 mg/kg) and testicular and hepatic arteries (6 mg/kg). 5. The results suggest a variety of local vasomotor influences of renal and non-renal prostaglandins in conscious rabbits.

Changes in distribution of cardiac output by surface-induced deep hypothermia in dogs

1976 ◽  
Vol 40 (6) ◽  
pp. 876-882 ◽  
Author(s):  
Y. Kawashima ◽  
K. Okada ◽  
I. Kosugi ◽  
H. In-Nami ◽  
Y. Yamaguchi
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Deep Hypothermia ◽  
Total Output ◽  
Organ Blood Flow ◽  
Relative Distribution ◽  
Low Cardiac Output ◽  
Vascular Beds ◽  
The Brain ◽  
Distribution Of Cardiac Output

The effects of surface-induced deep hypothermia on organ blood flow and on the distribution of cardiac output were investigated in the anesthetized dog. Organ flows were determined by the radioactive microsphere technique. Phenoxybenzamine (POB) was administered prior to hypothermia to minimize vasoconstriction and hence facilitate cooling. Measurements were made before POB, on stabilization after POB, and during hypothermia. Cardiac output was reduced by POB as was blood flow to the pancreas, small intestine, and skeletal muscle. Hypothermia, following POB, produced a further fall in Q and during this maneuver blood flow fell in all organs and vascular beds studied. The relative distribution of Q during hypothermia was essentially the same as in the control except the brain, kidneys, and pancreas received a smaller fraction of the total output. The relatively normal distribution of a reduced cardiac output during hypothermia was in marked contrast to distribution of comparable low cardiac output induced by hemorrhage. In the latter condition, the fraction of the cardiac output perfusing the brain, kidneys, adrenals, and hepatic artery was increased.

Blood flow to respiratory, cardiac, and limb muscles in dogs during graded exercise

1976 ◽  
Vol 231 (5) ◽  
pp. 1515-1519 ◽  
Author(s):  
DE Fixler ◽  
JM Atkins ◽  
JH Mitchell ◽  
LD Horwitz
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Gastrocnemius Muscle ◽  
Submaximal Exercise ◽  
Moderate Exercise ◽  
Radioactive Microspheres ◽  
Graded Exercise ◽  
Limb Muscles ◽  
The Brain ◽  
Distribution Of Cardiac Output

The distribution of cardiac output was analyzed in six dogs, with the animals at rest and running on a level treadmill for 3 min at 3-4 mph (mild exercise) and 3 min at 6-8 mph (moderate exercise). Organ flows were measured using 25-mug-diam radioactive microspheres. Cardiac output averaged 2.5, 4.6, and 5.7 liters/min, for rest, mild exercise, and moderate exercise, respectively. The greatest change was in diaphragmatic flow which increased by 275% with mild exercise and 500% with moderate exercise. Flow to intercostal muscles increased by 160 and 186%, to the exercising gastrocnemius muscle by 153 and 224%, and to cardiac muscle by 57 and 109% during mild and moderate exercise, respectively. Renal and cerebral flows did not change significantly. Significant decreases in flow occurred in the small and large intestines during moderate exercise. It is concluded that the increase in cardiac output during submaximal exercise was redistributed in a manner which limited flow to the brain, intestines, and kidneys and increased flow flow to the diaphragm, heart, and limb muscles.

Control of Blood Pressure and the Distribution of Blood Flow

1991 ◽  
Vol 7 (S1) ◽  
pp. 79-84 ◽  
Author(s):  
Hans T. Versmold
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Systemic Blood Pressure ◽  
Adrenergic Innervation ◽  
Systemic Blood ◽  
Low Cardiac Output ◽  
Neurohumoral Control ◽  
The Brain

Systemic blood pressure (BP) is the product of cardiac output and total peripheral resistance. Cardiac output is controlled by the heart rate, myocardial contractility, preload, and afterload. Vascular resistance (vascular hindrance × viscosity) is under local autoregulation and general neurohumoral control through sympathetic adrenergic innervation and circulating catecholamines. Sympathetic innovation predominates in organs receivingflowin excess of their metabolic demands (skin, splanchnic organs, kidney), while innervation is poor and autoregulation predominates in the brain and heart. The distribution of blood flow depends on the relative resistances of the organ circulations. During stress (hypoxia, low cardiac output), a raise in adrenergic tone and in circulating catecholamines leads to preferential vasoconstriction in highly innervated organs, so that blood flow is directed to the brain and heart. Catecholamines also control the levels of the vasoconstrictors renin, angiotensin II, and vasopressin. These general principles also apply to the neonate.

Time course of hemodynamic changes in rats with healed severe myocardial infarction

1989 ◽  
Vol 257 (1) ◽  
pp. H289-H296 ◽  
Author(s):  
A. DeFelice ◽  
R. Frering ◽  
P. Horan
Keyword(s):  
Myocardial Infarction ◽  
Blood Flow ◽  
Cardiac Output ◽  
Diastolic Pressure ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Male Rats ◽  
Coronary Artery Ligation ◽  
Sham Operation ◽  
Functional Changes

Male rats were monitored for 8 mo after severe myocardial infarction (MI) to chronicle hemodynamic and left ventricular (LV) functional changes. Blood pressure (BP), heart rate (HR), cardiac output index (CO), regional blood flow, and systemic vascular resistance (SVR) were measured with catheters and radiolabeled microspheres at 4, 7, 10, 20, and 35 wk after coronary artery ligation (n = 10–16/group) or sham operation (control; n = 9–14/group). At 4 wk, 43 +/- 1% of the LV circumference was scarred, peak LV BP, LV dP/dtmax, mean BP, SVR, and HR were 11–38% less than control (P less than 0.05), and LV end-diastolic pressure (LVEDP) was increased by 313% (P less than 0.05). Mean BP, LVEDP, LVBP, and LV dP/dtmax did not further deviate after 4 wk. However, CO and SVR changed progressively and were 67 and 33%, respectively, of control by 35 wk (P less than 0.05) when blood flow to stomach, small intestine, and kidney was 55, 38, and 27% of control. Lung and heart weights were significantly increased by 148 and 22% at 4 wk, and remained elevated, and lung dry weight-to-wet weight ratio was reduced at 7 and 10 wk. Thus the trajectory of rats with healed severe MI reflects progressive cardiac decompensation, cardiac output redistribution, and terminal heart failure.

scholarly journals Pentoxifylline prevents the transition from the hyperdynamic to hypodynamic response during sepsis

1999 ◽  
Vol 277 (3) ◽  
pp. H1036-H1044 ◽  
Author(s):  
Shaolong Yang ◽  
Mian Zhou ◽  
Douglas J. Koo ◽  
Irshad H. Chaudry ◽  
Ping Wang
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Cecal Ligation ◽  
Organ Blood Flow ◽  
Adult Rats ◽  
Male Adult ◽  
Morphological Alterations ◽  
Beneficial Effects ◽  
Renal Oxygen

The cardiovascular response to sepsis includes an early, hyperdynamic phase followed by a late, hypodynamic phase. Although administration of pentoxifylline (PTX) produces beneficial effects in sepsis, it remains unknown whether this agent prevents the transition from the hyperdynamic to the hypodynamic response during the progression of sepsis. To study this, male adult rats were subjected to polymicrobial sepsis by cecal ligation and puncture (CLP). At 1 h after CLP, PTX (50 mg/kg body wt) or vehicle was infused intravenously over 30 min. At 20 h after CLP (i.e., the late stage of sepsis), cardiac output and organ blood flow were measured by radioactive microspheres. Systemic and regional (i.e., hepatic, intestinal, and renal) oxygen delivery (Do 2) and oxygen consumption (V˙o 2) were determined. Moreover, plasma levels of lactate and alanine aminotransferase (ALT) were measured, and histological examinations were performed. In additional animals, the necrotic cecum was excised at 20 h after CLP, and mortality was monitored for 10 days thereafter. The results indicate that cardiac output, organ blood flow, and systemic and regional Do 2decreased by 36–65% ( P < 0.05) at 20 h after CLP. Administration of PTX early after the onset of sepsis, however, prevented reduction in measured hemodynamic parameters and increased systemic and regional Do 2 andV˙o 2 by 50–264% ( P < 0.05). The elevated levels of lactate (by 173%, P < 0.05) and ALT (by 718%, P < 0.05), as well as the morphological alterations in the liver, small intestine, and kidneys during sepsis were attenuated by PTX treatment. In addition, PTX treatment decreased the mortality rate from 50 to 0% ( P < 0.05) after CLP and cecal excision. Because PTX prevents the occurrence of hypodynamic sepsis, this agent appears to be a useful adjunct for maintaining hemodynamic stability and preventing lethality from sepsis.

Microsphere Determination of Cochlear Blood Flow in Chickens

1987 ◽  
Vol 96 (4) ◽  
pp. 341-348 ◽  
Author(s):  
Daniel Zaluzec ◽  
Joseph Ramzy ◽  
Robert Wotring ◽  
Lincoln Gray
Keyword(s):  
Blood Flow ◽  
Inverse Relationship ◽  
External Auditory Meatus ◽  
Blood Gas ◽  
Radioactive Microspheres ◽  
Cochlear Blood Flow ◽  
Camera Lucida ◽  
Micron Diameter ◽  
The Brain

Chickens were injected with 9-micron-diameter radioactive microspheres. Cochleas were removed through the external auditory meatus, and the positions of all embedded microspheres were drawn under camera-lucida. Constant measurements of arterial pressures and postinjection blood-gas determinations confirmed that injections were made into normal circulatory systems. The averaged estimate of cochlear blood flow in chickens is 0.75 μl/min. Variability in these data from chickens is similar to that reported from mammals. A potentially important but puzzling observation is an inverse relationship between blood flow to the cochlea and to the brain. The ease of cochlear extraction makes chickens ideal models for study of cochlear blood flow.

Respiratory muscle and organ blood flow with inspiratory elastic loading and shock

1985 ◽  
Vol 58 (4) ◽  
pp. 1148-1156 ◽  
Author(s):  
S. Magder ◽  
D. Lockhat ◽  
B. J. Luo ◽  
C. Roussos
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Respiratory Muscle ◽  
Respiratory Muscles ◽  
Organ Blood Flow ◽  
Normal Blood Pressure ◽  
Elastic Load ◽  
Severe Hypotension ◽  
Elastic Loading ◽  
The Brain

Since respiratory muscles fail when blood flow is inadequate, we asked whether their blood flow would be maintained in severe hypotensive states at the expense of other vital organs (brain, heart, kidney, gut, spleen). We measured blood flow (radiolabeled microspheres) to respiratory muscles and vital organs in 11 dogs breathing against an inspiratory elastic load, first with normal blood pressure (BP) and then hypotension produced by cardiac tamponade. With the elastic load alone, there was no change in BP or cardiac output; diaphragmatic blood flow (Qdi) increased from 12.8 +/- 7.0 to 34.1 +/- 15.6 ml/100 g, and total respiratory muscle flow (QTR) increased from 56.5 +/- 19.1 to 97.4 +/- 36.5 ml/100 g, but except for the brain, there was no change in blood flow to other organs. With tamponade (mean BP = 79 +/- 16 mmHg), flow decreased to all organs, whereas Qdi (39.0 +/- 19.4) did not change. QTR decreased, but not significantly, to 88.6 +/- 49.5. With more tamponade (mean BP = 53 +/- 13 mmHg), flow to all vital organs decreased as well as QTR (57.9 +/- 47.18), but Qdi did not significantly decrease and had the same relationship to respiratory force as with normal BP. Thus, with severe inspiratory elastic loading and severe hypotension, the diaphragm and external intercostal muscles did most of the respiratory work, and their flow was maintained at the expense of other vital organs.

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