CARDIOVASCULAR CHANGES DURING LACTATION IN THE RAT

1969 ◽  
Vol 44 (2) ◽  
pp. 247-254 ◽  
Author(s):  
A. L. CHATWIN ◽  
J. L. LINZELL ◽  
B. P. SETCHELL

SUMMARY The effect of lactation on cardiac output, measured by Fegler's thermodilution technique, and on organ blood flow, measured by Sapirstein's indicator fractionation technique, has been investigated by studying three groups of rats: (1) on day 1 of lactation; (2) on day 12 of lactation, suckling a large litter; (3) on day 12, the young having been removed on day 1. Lactation was accompanied by a significant increase in the weight of the mammary glands, the liver and the small and large intestines and a decrease in the weight of the female reproductive tract and of the skin. Cardiac output in 12-day lactating animals was significantly higher than in non-lactating and in rats on day 1. The proportion of the cardiac output taken by the mammary glands, liver, gastrointestinal tract and their blood flow/g. tissue, increased. Skin blood flow increased, but not that of brain, heart or kidney.

PEDIATRICS ◽  
1985 ◽  
Vol 76 (6) ◽  
pp. 918-921
Author(s):  
Frans J. Walther ◽  
Paul Y. K. Wu ◽  
Bijan Siassi

Phototherapy is known to increase peripheral blood flow in neonates, but information on the associated cardiovascular effects is not available. Using pulsed Doppler echocardiography we evaluated cardiac output and stroke volume in 12 preterm and 13 term neonates during and after phototherapy. We concomitantly measured arterial limb blood flow by strain gauge plethysmography and skin blood flow by photoplethysmography. Cardiac output decreased by 6% due to reduced stroke volume during phototherapy, whereas total limb blood flow and skin blood flow increased by 38% and 41%, respectively. Peripheral blood flow increments tended to be higher in the preterm than in the term infants. The reduced stroke volume during phototherapy may be an expression of reduced activity of the newborn during phototherapy. For healthy neonates the reduction in cardiac output is minimal, but for sick infants with reduced cardiac output, this reduction may further aggravate the decrease in tissue perfusion.


1999 ◽  
Vol 277 (3) ◽  
pp. H1036-H1044 ◽  
Author(s):  
Shaolong Yang ◽  
Mian Zhou ◽  
Douglas J. Koo ◽  
Irshad H. Chaudry ◽  
Ping Wang

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.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Stig Müller ◽  
Ole-Jakob How ◽  
Stig E Hermansen ◽  
Truls Myrmel

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.


1981 ◽  
Vol 59 (2) ◽  
pp. 204-208 ◽  
Author(s):  
R. Keeler ◽  
Anamaria Barrientos ◽  
K. Lee

A study was made of the effects of acute (4 h) or chronic (4 days) infusion of Escherichia coli endotoxin on cardiovascular function in rats. Rats with acute endotoxemia had a reduced cardiac output but maintained their arterial blood pressure. Fractional distribution of the cardiac output was increased to the liver and reduced to the gastrointestinal tract and skin. No changes in fractional distribution to the kidneys, lungs, or heart were observed although absolute blood flow to these areas was reduced.Rats with chronic endotoxemia had a reduced cardiac output and hypotension with no change in peripheral resistance. Other changes resembled those seen in acute endotoxemia apart from a low renal fraction of the cardiac output. Calculation and interpretation of blood flow changes in these animals was difficult because of a large fall in hematocrit and changes in organ weight.


1987 ◽  
Vol 117 (8) ◽  
pp. 1469-1474 ◽  
Author(s):  
Tammy M. Sakanashi ◽  
Heather E. Brigham ◽  
Kathleen M. Rasmussen

1963 ◽  
Vol 204 (2) ◽  
pp. 301-303 ◽  
Author(s):  
L. Takács ◽  
V. Vajda

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.


1968 ◽  
Vol 46 (4) ◽  
pp. 653-659 ◽  
Author(s):  
L. Jansky ◽  
J. S. Hart

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.


1983 ◽  
Vol 64 (5) ◽  
pp. 471-474 ◽  
Author(s):  
R. A. Banks ◽  
L. J. Beilin ◽  
J. Soltys

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.


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