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.

Effects of nonanticoagulant heparin on cardiovascular and hepatocellular function after hemorrhagic shock

1996 ◽  
Vol 270 (4) ◽  
pp. H1294-H1302 ◽  
Author(s):  
P. Wang ◽  
Z. F. Ba ◽  
S. S. Reich ◽  
M. Zhou ◽  
K. R. Holme ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Anticoagulant Activity ◽  
Cecal Ligation ◽  
Cardiovascular Responses ◽  
Microvascular Blood Flow ◽  
Organ Function ◽  
Ringer Lactate ◽  
Shed Blood ◽  
Beneficial Effects

Although heparinization of animals before hemorrhage improves cell and organ function, the potent anticoagulant activity of conventional heparin sodium precludes its potential clinical use. To determine whether a novel nonanticoagulant heparin, GM1892, would have any beneficial effects on cardiovascular and hapatocellular functions and would decrease susceptibility to sepsis after hemorrhage, laparotomy was performed on rats (i.e., trauma induced), after which they were bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of maximal bleedout volume was returned in the form of Ringer lactate solution (RL). The rats were then resuscitated with three times the volume of shed blood with RL over 45 min, followed by infusion of two times RL plus GM1892 (7 mg/kg body wt; approximately 2% the anticoagulant activity of regular heparin) of saline over 60 min. At 2 and 4 h after the completion of resuscitation, cardiac output, hepatocellular function, and microvascular blood flow were determined. The results indicated that cardiac output, hepatocellular function, and microvascular blood flow in the liver, spleen, and small intestine decreased significantly after hemorrhage and resuscitation. Administration of GM1892, however, restored these parameters. The morphological abnormality observed after hemorrhage in the liver, kidney, and small gut was also attenuated with GM1892 treatment. Moreover, GM1892 normalized the elevated plasma prostaglandin E2 levels. Sepsis was induced in additional rats by cecal ligation and puncture (CLP) 20 h after hemorrhage, and the necrotic cecum was excised 10 h thereafter. GM1892 treatment significantly decreased mortality after CLP and cecal excision. Thus GM1892 appears to be a useful adjunct to fluid resuscitation, since it restores the depressed cardiovascular responses and decreases susceptibility to sepsis after trauma and hemorrhage.

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 Dietary Restriction during Lactation on Cardiac Output, Organ Blood Flow and Organ Weights of Rats

1987 ◽  
Vol 117 (8) ◽  
pp. 1469-1474 ◽  
Author(s):  
Tammy M. Sakanashi ◽  
Heather E. Brigham ◽  
Kathleen M. Rasmussen
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Dietary Restriction ◽  
Organ Blood Flow ◽  
Organ Weights

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.

Cardiac output and organ blood flow in warm- and cold-acclimated rats exposed to cold

1968 ◽  
Vol 46 (4) ◽  
pp. 653-659 ◽  
Author(s):  
L. Jansky ◽  
J. S. Hart
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Skeletal Muscles ◽  
Organ Blood Flow ◽  
Internal Organs ◽  
Exposure To Cold ◽  
Brown Adipose ◽  
Production Increase ◽  
Distribution Of Cardiac Output ◽  
Fractional Distribution

Cold acclimation increased the cardiac output of unanesthetized rats when measured at 30 °C. After exposure to 9 °C for 70 min cardiac output further increased by 46% in both warm- and cold-acclimated rats. From the changes in the fractional distribution of cardiac output after cold exposure it was shown that the blood flow increased significantly in muscular organs (heart, diaphragm, skeletal muscles) and in the adrenals of warm-acclimated rats. In cold-acclimated rats the blood flow to the brown and white adipose tissues, pancreas, kidney, intestine, liver, and other internal organs was also increased in a cold environment, and accounted for 65% of the increase in blood flow during exposure to cold compared with only 36% in warm-acclimated rats. It is estimated that the extramuscular thermogenesis can account for a greater proportion of the total nonshivering thermogenesis in cold-acclimated rats. The contribution of brown adipose tissue is estimated not to exceed about 6% of the total heat production increase in cold-acclimated rats during exposure to cold.

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.

scholarly journals Effects of Asphyxia on Cardiac Output and Organ Blood Flow in the Newborn Piglet

1978 ◽  
Vol 12 (8) ◽  
pp. 824-827 ◽  
Author(s):  
Charles T Alward ◽  
Jerry B Hook ◽  
Thomas A Helmrath ◽  
Joan C Mattson ◽  
Michael D Bailie
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Newborn Piglet ◽  
Organ Blood Flow
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