Changes in circulating blood volume following isoflurane or sevoflurane anesthesia

1993 ◽  
Vol 7 (3) ◽  
pp. 316-324 ◽  
Author(s):  
Hiroshi Hamada ◽  
Masuhiko Takaori ◽  
Ken’ichi Kimura ◽  
Akira Fukui ◽  
Yoshihisa Fujita
Keyword(s):  
Blood Volume ◽  
Sevoflurane Anesthesia ◽  
Circulating Blood Volume

Is oxygen supply a limiting factor for survival during rewarming from profound hypothermia?

2006 ◽  
Vol 291 (1) ◽  
pp. H441-H450 ◽  
Author(s):  
Timofei V. Kondratiev ◽  
Kristina Flemming ◽  
Eivind S. P. Myhre ◽  
Mikhail A. Sovershaev ◽  
Torkjel Tveita
Keyword(s):  
Blood Volume ◽  
Tissue Oxygenation ◽  
Limiting Factor ◽  
Myocardial Tissue ◽  
Circulating Blood Volume ◽  
Profound Hypothermia ◽  
Group 3 ◽  
Vascular Beds ◽  
Group 2 ◽  
Group 1

It has been postulated that unsuccessful resuscitation of victims of accidental hypothermia is caused by insufficient tissue oxygenation. The aim of this study was to test whether inadequate O2supply and/or malfunctioning O2extraction occur during rewarming from deep/profound hypothermia of different duration. Three groups of rats ( n = 7 each) were used: group 1 served as normothermic control for 5 h; groups 2 and 3 were core cooled to 15°C, kept at 15°C for 1 and 5 h, respectively, and then rewarmed. In both hypothermic groups, cardiac output (CO) decreased spontaneously by >50% in response to cooling. O2consumption fell to less than one-third during cooling but recovered completely in both groups during rewarming. During hypothermia, circulating blood volume in both groups was reduced to approximately one-third of baseline, indicating that some vascular beds were critically perfused during hypothermia. CO recovered completely in animals rewarmed after 1 h ( group 2) but recovered to only 60% in those rewarmed after 5 h ( group 3), whereas blood volume increased to approximately three-fourths of baseline in both groups. Metabolic acidosis was observed only after 5 h of hypothermia (15°C). A significant increase in myocardial tissue heat shock protein 70 after rewarming in group 3, but not in group 2, indicates an association with the duration of hypothermia. Thus mechanisms facilitating O2extraction function well during deep/profound hypothermia, and, despite low CO, O2supply was not a limiting factor for survival in the present experiments.

Prompt recovery of plasma arginine vasopressin in diabetic coma after intravenous infusion of a small dose of insulin and a large amount of fluid

1990 ◽  
Vol 122 (4) ◽  
pp. 455-461 ◽  
Author(s):  
San-e Ishikawa ◽  
Toshikazu Saito ◽  
Koji Okada ◽  
Shoichiro Nagasaka ◽  
Takeshi Kuzuya
Keyword(s):  
Blood Volume ◽  
Serum Protein ◽  
Arginine Vasopressin ◽  
Small Dose ◽  
Plasma Osmolality ◽  
Diabetic Coma ◽  
Diabetic Patients ◽  
Volume Depletion ◽  
Circulating Blood Volume ◽  
Plasma Arginine

Abstract. We studied the changes in plasma arginine vasopressin in 5 patients with diabetic ketoacidosis and one patient with non-ketotic hyperosmolar coma who had marked hyperglycemia (36.6 ± 4.6 mmol/l, mean ± sem) and dehydration. Plasma osmolality (Posm) was 342.2 ± 11.4 mOsm/kg H2O, and hematocrit, serum protein, and blood urea nitrogen were also elevated at hospitalization. Circulating blood volume was decreased by approximately 21% as compared with that on day 7. Plasma AVP level was increased to 8.5 ± 1.6 pmol/l at hospitalization. When hyperglycemia was improved by iv infusion of a small dose of insulin plus fluid administration, plasma AVP level promptly decreased to 2.4 ± 0.4 pmol/l within six hours. When plasma AVP level had normalized, Posm was still as high as 305 mOsm/kg H2O, but the loss of circulating blood volume was only 4.2% of the control state. Plasma AVP level was positively correlated with change in hematocrit (plasma AVP = 3.58 + 0.45 · hematocrit, r = 0.468, p < 0.01), serum protein (r = 0.487, p < 0.01), Posm (r = 0.388, p < 0.01), and blood glucose (r = 0.582, p < 0.01). Plasma AVP level was negatively correlated with the change in circulating blood volume (plasma AVP = 3.6 – 0.14 · change in circulating blood volume, r = −0.469, p <0.01). These results indicate that both non-osmotic and osmotic stimuli are involved in the mechanism for AVP release in patients with diabetic coma, and that the non-osmotic control of AVP may contribute to circulating homeostasis, protecting against severe blood volume depletion in diabetic patients suffering from hyperglycemia and dehydration.

Cardiac output, GFR, and renal excretion rates during maintained volume load in rats

1978 ◽  
Vol 235 (6) ◽  
pp. H670-H676 ◽  
Author(s):  
U. Ackermann
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Renal Excretion ◽  
Venous Pressure ◽  
Circulating Blood Volume ◽  
Reservoir Volume ◽  
Volume Load ◽  
Blood Volume Expansion ◽  
Highly Correlated ◽  
Excretion Rates

The correlation among cardiac output (CO), glomerular filtration rate (GFR), fractional tubular sodium rejection (TFRNa), and renal excretion rates of water and salt was investigated during ischemic blood volume expansion in rats. Initially circulating blood volume was equilibrated isovolemically with a reservoir volume of 6% albumin solution equal to one-third the estimated blood volume. Later the equilibrated reservoir contents were infused intravenously. CO was measured by thermodilution, GFR by inulin clearance. Significant linear correlations existed between GFR and the rates of urine flow (r = 0.90), sodium excretion (r = 0.75) and potassium excretion (r = 0.76) that prevailed 5--10 min after a given GFR change. The increased GFR was highly correlated with CO (r = 0.94), probably correlated with mean central venous pressure (r = 0.45), but not correlated with mean abdominal aortic blood pressure. The correlation between CO and time-delayed (5--10 min) TRFNa was also highly significant (r = 0.98). The saluresis appears to have been caused initially by increased tubular load and subsequently by decreased absolute tubular reabsorption.

scholarly journals Evaluation of circulating blood volume and vascular permeability in long-term hemodialysis patients

2011 ◽  
Vol 44 (5) ◽  
pp. 435-440 ◽  
Author(s):  
Susumu Ookawara ◽  
Masayuki Suzuki ◽  
Sachiko Fukase ◽  
Kaoru Tabei
Keyword(s):  
Vascular Permeability ◽  
Blood Volume ◽  
Hemodialysis Patients ◽  
Circulating Blood Volume

Effect of induced respiratory acidosis on the circulating blood volume in normal dogs

1968 ◽  
Vol 115 (5) ◽  
pp. 594-598 ◽  
Author(s):  
Fuad J. Dagher ◽  
Alex Panossian ◽  
Farid J.D. Fuleihan
Keyword(s):  
Blood Volume ◽  
Respiratory Acidosis ◽  
Circulating Blood Volume

Detecting Relative Changes in Circulating Blood Volume using Ultrasound and Simulation

2019 ◽  
Author(s):  
Javad Rahimipour Anaraki ◽  
Saeed Samet ◽  
Mohamed S. Shehata ◽  
Kris Aubrey-Bassler ◽  
Ebrahim Karami ◽  
...  
Keyword(s):  
Blood Volume ◽  
Circulating Blood Volume

SIADH: A Case Review

2001 ◽  
Vol 20 (1) ◽  
pp. 29-33 ◽  
Author(s):  
Lee Shirland
Keyword(s):  
Antidiuretic Hormone ◽  
Blood Volume ◽  
Clinical Course ◽  
Case Review ◽  
Long Term Outcomes ◽  
Circulating Blood Volume ◽  
Neurologic Sequelae ◽  
Effective Circulating Blood Volume

Because the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) can cause neurologic sequelae with the potential to affect long-term outcomes, its prompt recognition and treatment are essential. Normally, antidiuretic hormone (ADH) is secreted when effective circulating blood volume is decreased. SIADH is marked by secretion of ADH in the presence of effective or normal circulating blood volume. This causes plasma hyponatremia simultaneously with plasma hypo-osmolality and inappropriate hyperosmolality of the urine. This article explains the pathophysiology of the syndrome; describes its diagnosis, clinical course, and treatment; and exemplifies the syndrome with a case study.

Actively circulating blood volume in endotoxin shock measured by indicator dilution

1979 ◽  
Vol 236 (2) ◽  
pp. H291-H300 ◽  
Author(s):  
C. F. Rothe ◽  
R. H. Murray ◽  
T. D. Bennett
Keyword(s):  
Blood Cell ◽  
Blood Volume ◽  
Red Blood Cell ◽  
Mixing Time ◽  
Volume Of Distribution ◽  
Endotoxin Shock ◽  
Circulating Blood Volume ◽  
Arterial Blood ◽  
Concentration Changes ◽  
Volumes Of Distribution

To estimate the size of the actively circulating blood volume of splenectomized dogs during control conditions and after endotoxin infusion, the pattern of concentration changes of 51Cr-labeled erythrocytes and 125I-labeled albumin was monitored. A dual exponential equation was fitted to the data. The total red blood cell and albumin volumes of distribution were determined from the slow exponential disappearance curves. The active red blood cell and albumin volumes were 89.8 +/- 5.3% and 92.0 +/- 2.0% of the total volumes, respectively. After endotoxin shock (mean arterial blood pressure 49.1 +/- 17.8 mmHg) the active volumes fell to only 60.0 +/- 10.3% and 56.2 +/- 20.0% of the total volumes, respectively. The fast-mixing time constants were similar (3.1 +/- 1.4 min and 2.5 +/- 2.7 min, respectively) and did not change significantly during the endotoxin shock, indicating that the albumin tag mixed into its larger volume of distribution as rapidly as the cells mixed into their indicated volume. We conclude that 1) an active blood volume can be distinguished, 2) it decreases for both red blood cells and albumin in endotoxin shock, and 3) a major part of the "extravascular plasma volume," as estimated by albumin dilution, is in the actively circulating circulation.

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