Control circulatory values of morphinepentobarbitalized dogs

1960 ◽  
Vol 199 (5) ◽  
pp. 797-799 ◽  
Author(s):  
S. Deavers ◽  
E. L. Smith ◽  
R. A. Huggins

Mean control data on a series of 100 dogs are presented. Cell volume, measured with Cr51-tagged red cells and plasma volume determined simultaneously by T-1824 dye was 33.5 ± 0.74 cc/kg and 50.2 ± 1.11 cc/kg, respectively. The venous hematocrit was 45.2% and the circulatory/venous hematocrit ratio was 0.89 ± 0.01 for the group. The plasma protein concentration of these animals was 6.25 ± 0.07 gm/100 cc. No difference in blood volume per unit of body weight was found between large (12.6 kg) and small (5.8 kg) dogs. The femoral mean systolic pressure was 139.0 ± 2.53 mm Hg, the diastolic pressure 65.6 ± 1.46 mm Hg and the heart rate 85.9 ± 2.86/min.

1990 ◽  
Vol 259 (5) ◽  
pp. H1317-H1324
Author(s):  
R. D. Manning

Studies were performed in 14 conscious, anephric dogs to clarify the role of blood volume in the genesis of hypertension. The dogs were splenectomized and had plasma protein concentration (PPC) reduced to 2.7 g/dl by daily plasmapheresis for 9 days. This hypoproteinemia resulted in a 20% decrease in both blood volume and mean arterial pressure. On the 10th day the dogs were nephrectomized. On the 11th day after a 3-h control period with plasmapheresis, lactated Ringer equivalent to 10 or 20% of body weight was intravenously infused. By 25 h postinfusion blood volume had not increased, and the dogs were still hypotensive. At 25 h plasma protein mass was returned to normal by intravenous infusion of autologous plasma, the average blood volume of the three low PPC groups increased approximately 50%, and the arterial pressure increased greater than 60%. The decrease in PPC shifted the regression of blood volume on sodium space down the blood volume axis. In conclusion, the dependence of arterial pressure on blood volume was demonstrated by the decrease in both blood volume and arterial pressure after PPC reduction, the constancy of blood volume and pressure during Ringer infusion, and the increase in both volume and pressure after plasma infusion.


1999 ◽  
Vol 86 (6) ◽  
pp. 1852-1857 ◽  
Author(s):  
Janice M. Fritsch-Yelle ◽  
Victor A. Convertino ◽  
Todd T. Schlegel

The effects of changes in blood volume on arterial pressure patterns during the Valsalva maneuver are incompletely understood. In the present study we measured beat-to-beat arterial pressure and heart rate responses to supine Valsalva maneuvers during normovolemia, hypovolemia induced with intravenous furosemide, and hypervolemia induced with ingestion of isotonic saline. Valsalva responses were analyzed according to the four phases as previously described (W. F. Hamilton, R. A. Woodbury, and H. T. Harper, Jr. JAMA 107: 853–856, 1936; W. F. Hamilton, R. A. Woodbury, and H. T. Harper, Jr. Am. J. Physiol. 141: 42–50, 1944). Phase I is the initial onset of straining, which elicits a rise in arterial pressure; phase II is the period of straining, during which venous return is impeded and pressure falls (early) and then partially recovers (late); phase III is the initial release of straining; and phase IV consists of a rapid “overshoot” of arterial pressure after the release. During hypervolemia, early phase II arterial pressure decreases were significantly less than those during hypovolemia, thus making the response more “square.” Systolic pressure hypervolemic vs. hypovolemic falls were −7.4 ± 2.1 vs. −30.7 ± 7 mmHg ( P = 0.005). Diastolic pressure hypervolemic vs. hypovolemic falls were −2.4 ± 1.6 vs. −15.2 ± 2.6 mmHg ( P = 0.05). A significant direct correlation was found between plasma volume and phase II systolic pressure falls, and a significant inverse correlation was found between plasma volume and phase III-IV systolic pressure overshoots. Heart rate responses to systolic pressure falls during phase II were significantly less during hypovolemia than during hypervolemia (0.7 ± 0.2 vs. 2.82 ± 0.2 beats ⋅ min−1 ⋅ mmHg−1; P = 0.05) but were not different during phase III-IV overshoots. We conclude that acute changes in intravascular volume from hypovolemia to hypervolemia affect cardiovascular responses, particularly arterial pressure changes, to the Valsalva maneuver and should be considered in both clinical and research applications of this maneuver.


Blood ◽  
1954 ◽  
Vol 9 (12) ◽  
pp. 1205-1207 ◽  
Author(s):  
G. R. WADSWORTH

Abstract Measurements of red cell volume and plasma volume in eight normal women confirm that, in relation to body weight, red cell volume is distinctly lower in women than in men and plasma volume only slightly lower. The relationship between body hematocrit and venous hematocrit (0.90) was found not to be significantly different from that of men.


1958 ◽  
Vol 196 (1) ◽  
pp. 188-192 ◽  
Author(s):  
Louise Wang

A method is described for the catheterization of the carotid of the rat which permits blood volume determinations to be made on unanesthetized animals. The cell volume (P32) and plasma volume (T-1824) were measured simultaneously on the day after catheterization. The average Fcells factor was 0.739 (S.D., 0.053) in 11 normal rats and 0.726 (S.D., 0.041) in 10 splenectomized rats. In 50 unanesthetized normal rats the plasma volume averaged 3.90 ml/100 gm body weight. The blood and cell volumes calculated by using the Fcells factor of 0.74 and the separately determined plasma trapping' factor of 0.95 averaged 5.93 ml/ 100 gm and 2.14 ml/100 gm, respectively. These values agree closely with those determined from the simultaneous measurement of cell and plasma volumes and also with the values obtained on 27 normal rats under ether.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Mary Gheller ◽  
Erica Bender ◽  
Anna Thalacker-Mercer

Abstract Objectives Histidine is an essential amino acid found in the diet through protein-rich foods. Previous research demonstrated benefits of histidine due to anti-inflammatory, anti-oxidant, and glucoregulatory properties. To date, histidine requirement for adults has not be established; current expert opinion for histidine is 8 and 12 mg/(kg body weight × day), an estimate that was extrapolated from the infant requirement for histidine. Further, the clinical safety of histidine supplementation above the average dietary intake has not been determined. Objective: To determine the safety of graded-doses of histidine in a healthy adult population. Methods Our preliminary study includes 30 adults (n = 12 males and n = 18 females, aged 21–50 y). Following the completion and review of a health history questionnaire, vitals, and a biochemical panel, participants were deemed healthy and able to participate. After baseline measures were obtained, participants consumed encapsulated histidine pills daily for four weeks followed by a three-week washout period between each dose. Participants consumed one of three doses (4 g, 8 g, and 12 g) of histidine during each of the four-week supplement periods. A complete biochemical panel was run at baseline, week 2 and 4 of supplement, as well as washout. Anthropometric, body composition, sleep patterns, dietary intake, and urine samples were also collected throughout the study (analyses underway). Results Baseline descriptive statistics are as follows for females [males]: body weight 65 ± 0.55 kg [62.91 ± 3.17 kg], systolic pressure 113 ± .54 mmHg [125 ± 2.93 mmHg], diastolic pressure 70 ±.48 mmHg [74 ± 3.22 mmHg], and heart rate 74 ± 0.56 bpm [63 ±3.17 bpm]. There were no observed differences between baseline and measurements taken at any of the three doses for body weight, systolic blood pressure, diastolic blood pressure, and heart rate. There was no effect of histidine dose on the biochemical measures of aspartarte amino transferase (U/L, P = 0.096), alanine amino transferase (U/L, P = 0.47), creatinine (mg/dL, P = 0.79), glucose (mg/dL, P = 0.06), insulin (μIU/ml, P = 0.48), or c-reactive protein (mg/L, P = 0.19). Conclusions In our current analyses, we observe no deleterious effects of taking up to 12 grams of histidine in healthy young adults. Funding Sources International Council on Amino Acid Science.


1983 ◽  
Vol 245 (2) ◽  
pp. H284-H293 ◽  
Author(s):  
R. D. Manning ◽  
A. C. Guyton

The effects of both moderate and large decreases in plasma protein concentration on arterial pressure and fluid volumes were studied in 23 conscious dogs. In experiment 1, plasma protein concentration decreased 33% during a 5-day plasmapheresis period. During this time sodium space increased 11%, mean arterial pressure decreased slightly, and neither blood volume nor plasma volume decreased. Experiment 2 was performed to see if blockade of the alpha-sympathetic and angiotensin systems could prevent the blood volume homeostasis during moderate hypoproteinemia. Sodium space increased; however, blood volume was unchanged. During experiment 3 plasma protein concentration decreased 68% over a 12-day plasmapheresis period. By the last day of plasmapheresis, plasma protein concentration was 2.4 g/100 ml, mean arterial pressure had decreased 26 mmHg, sodium space had increased 12%, plasma renin activity had increased 11-fold, and blood volume and plasma volume were 63.9 +/- 4.0 and 66.9 +/- 2.5% of control, respectively. We conclude that the maintenance of a normal blood volume during moderate hypoproteinemia does not require active participation of the renin-angiotensin and alpha-sympathetic systems and large decreases in plasma protein concentration are accompanied by marked hypovolemia, hypotension, and hyperreninemia.


1964 ◽  
Vol 19 (5) ◽  
pp. 829-832 ◽  
Author(s):  
Per-Olof Åstrand ◽  
Bengt Saltin

On six subjects plasma volume (Evans blue space) was determined before and 1 hr after an 85-km race in cross-country skiing. The total water loss during the 5- to 9.5-hr competition was estimated to be 5.9 liters, and at the time of measuring the reduction in body weight was 3.9 kg or 5.5% of the weight. The plasma volume was increased 0.41 or 11% (0.01 > P > 0.001). A similar study was undertaken with measurements of red cell volume (Cr51) on five subjects. The decrease in red cell volume was 0.081 or 3.2%. These findings are discussed in light of the small reduction in aerobic work capacity in combination with a marked decrease in total work output after the race. In five workers in a steel mill (three at a hot bank and two at a smelting furnace) the total water loss during an 8-hr shift in a hot environment was 3.9 liters and the reduction in body weight was 1.1 kg or 1.9% of the weight. The blood volume (I131) was increased by 0.23 liters or 3.5%. dehydration; blood volume Submitted on October 16, 1963


1985 ◽  
Vol 14 (6) ◽  
pp. 345-356
Author(s):  
Michael G. Garner ◽  
Andrew F. Phippard ◽  
John S. Horvath ◽  
Geoffrey G. Duggin ◽  
David J. Tiller

1997 ◽  
Vol 83 (3) ◽  
pp. 695-699 ◽  
Author(s):  
Lars Bo Johansen ◽  
Thomas Ulrik Skram Jensen ◽  
Bettina Pump ◽  
Peter Norsk

Johansen, Lars Bo, Thomas Ulrik Skram Jensen, Bettina Pump, and Peter Norsk. Contribution of abdomen and legs to central blood volume expansion in humans during immersion. J. Appl. Physiol. 83(3): 695–699, 1997.—The hypothesis was tested that the abdominal area constitutes an important reservoir for central blood volume expansion (CBVE) during water immersion in humans. Six men underwent 1) water immersion for 30 min (WI), 2) water immersion for 30 min with thigh cuff inflation (250 mmHg) during initial 15 min to exclude legs from contributing to CBVE (WI+Occl), and 3) a seated nonimmersed control with 15 min of thigh cuff inflation (Occl). Plasma protein concentration and hematocrit decreased from 68 ± 1 to 64 ± 1 g/l and from 46.7 ± 0.3 to 45.5 ± 0.4% ( P < 0.05), respectively, during WI but were unchanged during WI+Occl. Left atrial diameter increased from 27 ± 2 to 36 ± 1 mm ( P < 0.05) during WI and increased similarly during WI+Occl from 27 ± 2 to 35 ± 1 mm ( P < 0.05). Central venous pressure increased from −3.7 ± 1.0 to 10.4 ± 0.8 mmHg during WI ( P < 0.05) but only increased to 7.0 ± 0.8 mmHg during WI+Occl ( P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from the legs, whereas the CBVE is caused mainly by blood from the abdomen.


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