Role of postural status in the nocturnal hemodynamic patterns of nonhuman primates

1993 ◽  
Vol 74 (4) ◽  
pp. 1684-1688 ◽  
Author(s):  
B. T. Engel ◽  
M. I. Talan ◽  
P. H. Chew

We compared the nocturnal hemodynamic patterns of seven tethered monkeys (Macaca mulatta) with those of seven chaired animals to determine whether the overnight changes are comparable in the two conditions. In both groups, we found a consistent hemodynamic pattern characterized by an overnight fall in cardiac output and central venous pressure and a rise in total peripheral resistance that maintained blood pressure homeostasis. The pattern of overnight change occurred despite major differences in response levels: cardiac output and central venous pressure were significantly elevated, and total peripheral resistance was significantly reduced at all times (from 1800 to 1200 h the following day) in the chaired animals relative to the tethered animals. This difference was probably due to an expanded plasma volume in the chaired animals, because stroke volume was also significantly elevated. Because the nocturnal hemodynamic pattern occurred under both conditions, it is likely that it is a stable biologic effect, which is probably related to an overnight loss in fluid volume that is not replaced in animals that sleep throughout the night.

1978 ◽  
Vol 06 (03) ◽  
pp. 253-259
Author(s):  
DONALD H. CLIFFORD ◽  
DO CHIL LEE ◽  
CHONG YUL KIM ◽  
MYUNG O. LEE

An electromagnetic flowmeter probe was chronically implanted around the ascending aorta in a group of dogs. Subsequently, ten dogs were lightly anesthetized with halothane (0.75%), and a third (aqueous) extract of ginseng (40 mg/kg) was administered intravenously. Five dogs were anesthesized without the administration of ginseng. Eleven cardiovascular variables including cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure, total peripheral resistance, pH, PaCO2, PaO2, and base deficit were compared. The cardiac output, stroke volume, and central venous pressure were decreased significantly, while total peripheral resistance was increased significantly following ginseng.


1983 ◽  
Vol 244 (2) ◽  
pp. R292-R298
Author(s):  
B. L. Langille

Central venous pressure of ducks rose from resting values of 0.31 +/- 0.16 (SE) to 1.75 +/- 0.20 kPa during forced head immersion. Because a similar increase in mean circulatory pressure (Pmc) was also observed (0.71 +/- 0.16 to 2.15 +/- 0.20 kPa) the rise in central venous pressure was attributed to a venoconstrictor mechanism. When this venoconstrictor-induced rise in central venous pressure was prevented by graded withdrawal of venous blood, then immersion bradycardia was inhibited, and the reduced cardiac output associated with head immersion was largely the result of reduced stroke volume. When compared with normal dives, this intervention resulted in greater myocardial energy requirements, as assessed by the pressure-rate product. It is concluded that venoconstriction increases central venous pressure during head immersion. The increase in central venous pressure alters cardiac function through the Frank-Starling mechanism such that myocardial energy requirements are minimized during this period of low oxygen availability.


1988 ◽  
Vol 65 (2) ◽  
pp. 625-632 ◽  
Author(s):  
Y. M. Evans ◽  
J. N. Funk ◽  
J. B. Charles ◽  
D. C. Randall ◽  
C. F. Knapp

The effects of endurance training on vascular responsiveness to an alpha 1-agonist and the associated changes in baroreflex modulation of heart rate and vascular resistance were studied. Graded dosages of phenylephrine were given to eight treadmill-trained dogs and to eight untrained dogs; both groups were chronically instrumented and were sedated and resting when tested. These dosages were repeated after ganglionic blockade. Aortic pressure, cardiac output, central venous pressure, peripheral resistance, and heart rate were each averaged over 30 s before injection and 90 s after injection. The slope of the peripheral resistance-dose relationship was significantly increased in trained compared with untrained dogs in both the unblocked and blocked cases [unblocked: trained 0.89, untrained 0.47; blocked: trained 4.30, untrained 2.05 (mmHg.l-1.min)/(microgram.kg-1)]. The unblocked resistance slopes were reduced with respect to the blocked slopes by 77 (untrained) and 79% (trained). The slope of the heart rate-aortic pressure response was reduced, but not significantly, by endurance training. We conclude that 6 wk of endurance training in dogs resulted in a doubling of the vascular responsiveness to an alpha 1-agonist, with no significant change in the baroreflex regulation of resistance or heart rate.


1992 ◽  
Vol 72 (5) ◽  
pp. 1798-1802 ◽  
Author(s):  
B. T. Engel ◽  
M. I. Talan ◽  
P. H. Chew

Heart rate (HR), stroke volume (SV), intra-arterial blood pressure, and central venous pressure were recorded on a beat-to-beat basis, 18 h/day (1800–1200 h the following day), for approximately 2 mo in four monkeys (Macaca mulatta). Cardiac output, left ventricular work, and total peripheral resistance were derived from these primary measurements. During the 1st mo we measured these parameters under control conditions, and during the 2nd mo the animals were studied while HR was paced by atrial demand pacing sufficient to prevent the normal nocturnal fall in HR (approximately 10 beats/min above the fastest hourly average rate recorded during the control condition). The main hypothesis of this study was that when HR is prevented from falling, SV, which normally does not fall overnight, would fall; this hypothesis was confirmed. In addition, we observed that, during the period of pacing, relative to the control period, SV was approximately 14% greater during the early evening and 4% lower during the early morning; total peripheral resistance was similar during the early evening but was 13% higher by morning. Throughout the night, systolic pressure was approximately 4% greater, diastolic pressure was 17% higher, central venous pressure was 43% greater, and left ventricular work was 27% higher. These findings show that when HR is prevented from falling overnight by atrial demand pacing, even to a relatively modest degree, there can be very significant sustained changes in cardiovascular function.


1991 ◽  
Vol 260 (1) ◽  
pp. H254-H259
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe

We tested the hypothesis that the blood volumes of the spleen and liver of cats are reflexly controlled by the carotid sinus (CS) baroreceptors. In pentobarbital-anesthetized cats the CS area was isolated and perfused so that intracarotid pressure (Pcs) could be controlled while maintaining a normal brain blood perfusion. The volume changes of the liver and spleen were estimated by measuring their thickness using ultrasonic techniques. Cardiac output, systemic arterial blood pressure (Psa), central venous pressure, central blood volume, total peripheral resistance, and heart rate were also measured. In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (-67.8%), cardiac output (-26.6%), total peripheral resistance (-49.5%), and heart rate (-15%) and significantly increased spleen volume (9.7%, corresponding to a 2.1 +/- 0.5 mm increase in thickness). The liver volume decreased, but only by 1.6% (0.6 +/- 0.2 mm decrease in thickness), a change opposite that observed in the spleen. The changes in cardiovascular variables and in spleen volume suggest that the animals had functioning reflexes. These results indicate that in pentobarbital-anesthetized cats the carotid baroreceptors affect the volume of the spleen but not the liver and suggest that, although the spleen has an active role in the control of arterial blood pressure in the cat, the liver does not.


1959 ◽  
Vol 197 (5) ◽  
pp. 1005-1007 ◽  
Author(s):  
Calvin Hanna ◽  
Patricia B. McHugo ◽  
William H. MacMillan

The cardiovascular actions of intravenous histamine, in doses from 2.5 to 20 µg/kg of the free base, were studied in the pentobarbitalized dog using the dye dilution method. With the small dose there was a consistent but small initial increase in cardiac output and with the larger doses there was a biphasic change in output. Cardiac rate, central venous pressure, central blood volume, hematocrit and the mean circulation time were essentially unchanged. Infusions of histamine and of potassium chloride at the rate of 1 µg and 1 mg/kg/min., respectively, moderately increased the cardiac output. Potassium chloride had no effect on the arterial blood pressure, cardiac rate and central venous pressure. Both the infusion of potassium chloride and injection of histamine produced a comparable elevation of the plasma potassium. It is possible that the actions of histamine to increase the plasma potassium contribute to the cardiovascular actions of this amine, especially on the cardiac output.


1987 ◽  
Vol 252 (5) ◽  
pp. H894-H899 ◽  
Author(s):  
Y. W. Chien ◽  
E. D. Frohlich ◽  
N. C. Trippodo

To examine mechanisms by which administration of atrial natriuretic peptide (ANP) decreases venous return, we compared the hemodynamic effects of ANP (0.5 microgram X min-1 X kg-1), furosemide (FU, 10 micrograms X min-1 X kg-1), and hexamethonium (HEX, 0.5 mg X min-1 X kg-1) with those of vehicle (VE) in anesthetized rats. Compared with VE, ANP reduced mean arterial pressure (106 +/- 4 vs. 92 +/- 3 mmHg; P less than 0.05), central venous pressure (0.3 +/- 0.3 vs. -0.7 +/- 0.2 mmHg; P less than 0.01), and cardiac index (215 +/- 12 vs. 174 +/- 10 ml X min-1 X kg-1; P less than 0.05) and increased calculated resistance to venous return (32 +/- 3 vs. 42 +/- 2 mmHg X ml-1 X min X g; P less than 0.01). Mean circulatory filling pressure, distribution of blood flow between splanchnic organs and skeletal muscles, and total peripheral resistance remained unchanged. FU increased urine output similar to that of ANP, yet produced no hemodynamic changes, dissociating diuresis, and decreased cardiac output. HEX lowered arterial pressure through a reduction in total peripheral resistance without altering cardiac output or resistance to venous return. The results confirm previous findings that ANP decreases cardiac output through a reduction in venous return and suggest that this results partly from increased resistance to venous return and not from venodilation or redistribution of blood flow.


2004 ◽  
Vol 187 (3) ◽  
pp. 398-402 ◽  
Author(s):  
Vassilios Smyrniotis ◽  
Georgia Kostopanagiotou ◽  
Kassiani Theodoraki ◽  
Dimitrios Tsantoulas ◽  
John C Contis

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