Hemodynamic functions and blood viscosity in surface hypothermia

1978 ◽  
Vol 235 (2) ◽  
pp. H136-H143 ◽  
Author(s):  
R. Y. Chen ◽  
S. Chien
Keyword(s):  
Body Temperature ◽  
Blood Viscosity ◽  
Flow Resistance ◽  
Plasma Viscosity ◽  
Low Flow ◽  
Flow State ◽  
Surface Cooling ◽  
Plasma Loss ◽  
Pulmonary Flow ◽  
Anesthetized Dogs

Hemodynamic functions and blood viscosity changes in hypothermia (core approximately 25 degrees C) were studied in 14 pentobarbital-anesthetized dogs subjected to surface cooling. The viscosity of blood (eta B) increased progressively to 173% of that at 37 degrees C when body temperature was lowered to 25 degrees C. The increase in blood viscosity was caused by: a) the direct effect of low temperature on plasma viscosity, b) hemoconcentration as a result of plasma loss, and c) the low-flow (low-shear) state induced by hypothermia. A larger portion of the increased viscosity was caused by the low-flow state in hypothermia. The systemic flow resistance (SFR) increased to 271% of control, and this was attributable about equally to the increases in blood viscosity and systemic vascular hindrance (SFR/eta B). Similarly, the viscosity of blood contributed significantly to raising the pulmonary flow resistance. The relative constancy of mixed venous O2 saturation suggests that the cardiac output at low body temperature is generally adequate to meet the metabolic needs

Correlation of blood rheology with vascular resistance in critically ill patients

1975 ◽  
Vol 39 (6) ◽  
pp. 1008-1011 ◽  
Author(s):  
P. M. Scholz ◽  
J. H. Karis ◽  
F. E. Gump ◽  
J. M. Kinney ◽  
S. Chien
Keyword(s):  
Critically Ill ◽  
Blood Viscosity ◽  
Critically Ill Patients ◽  
Peripheral Resistance ◽  
Plasma Viscosity ◽  
Low Flow ◽  
Red Cell Deformability ◽  
Group I ◽  
Group Ii

Blood rheologic measurements together with peripheral resistance determinations in vivo were made in 27 critically ill patients. Eighteen of these patients (group I) suffered from violent trauma or operative injury and the other 9 (group II) were patients with generalized sepsis. As a result of fluid therapy all patients underwent hemodilution, resulting in a decrease in blood viscosity. This drop in blood viscosity was counteracted to some extent by an increased plasma viscosity due to elevated fibrinogen levels and a decreased red cell deformability associated with massive transfusions of stored blood. The correlation of vivo hemodynamics with blood rheological data made it possible to separate the relative roles of vascular dimensions and blood viscosity in affecting the total peripheral resistance. This approach permitted us to distinguish varying degrees of vasoconstriction in nonseptic patients in low flow states (group I) and varying degrees of vasodilation in septic patients (group II). This type of analysis serves to elucidate the pathophysiology of hemodynamic alterations in disease and provides a rational basis for devising an effective therapeutic program.

scholarly journals Postischemic Canine Cerebral Blood Flow is Coupled to Cerebral Metabolic Rate

1991 ◽  
Vol 11 (4) ◽  
pp. 611-616 ◽  
Author(s):  
John D. Michenfelder ◽  
James H. Milde ◽  
Zvonimir S. Katušić
Keyword(s):  
Brain Temperature ◽  
Energy State ◽  
Reactive Hyperemia ◽  
Low Flow ◽  
Global Cerebral Ischemia ◽  
Flow State ◽  
Arterial Blood ◽  
Cerebral Ischemia And Reperfusion ◽  
Anesthetized Dogs ◽  
The Brain

Following complete global cerebral ischemia and reperfusion, a brief period of reactive hyperemia is followed by a prolonged period of low flow commonly referred to as the delayed postischemic hypoperfusion state. It is generally assumed that this low-flow state may be injurious because of inadequate substrate delivery, thus implying that flow is no longer coupled to metabolic needs. This relationship of CBF to CMRO2 was examined in six anesthetized dogs that were subjected to 12 min of complete ischemia induced either by CSF compression or aortic occlusion. Following reperfusion and onset of the low-flow state, which stabilized at 45 min postischemia, control normothermic (37°C) measurements of CBF and CMRO2 were determined. Thereafter, femoral arterial blood was circulated through a heat exchanger (42.5°C), and brain temperature was increased to 40°C and measurements were repeated. The brain was then cooled back to 37°C for a final set of normothermic measurements. Thereafter, brain biopsies were taken to determine the energy state of the brain. CMRO2 changed ∼6%/°C. CBF paralleled the change in CMRO2. Accordingly, the ratio of CBF to CMRO2 remained constant throughout at a value of 8 to 9, demonstrating maintained coupling. The brain energy state was normal at the end of the study. The authors conclude that postischemic CBF is modulated by the brain's metabolic needs.

The Effects of KBT-3022, a New Anti-platelet Agent, on Hemorheological Properties in Guinea Pigs

1995 ◽  
Vol 73 (01) ◽  
pp. 118-121 ◽  
Author(s):  
Noriko Yamamoto ◽  
Koichi Yokota ◽  
Akira Yamashita ◽  
Minoru Oda
Keyword(s):  
Shear Stress ◽  
Blood Viscosity ◽  
Guinea Pigs ◽  
Direct Action ◽  
Plasma Viscosity ◽  
Fibrinogen Concentration ◽  
Anti Platelet Agent ◽  
Blood Filterability ◽  
2,3 Dpg ◽  
Rbc Deformability

SummaryUsing guinea pigs, a study was conducted on the effects of KBT-3022, a new anti-platelet agent, on hemorheological properties in various tests including blood filterability, blood viscosity, shear stress-induced red blood cell (RBC) deformability and contents of ATP and 2,3-diphosphoglycerate (2,3-DPG). Oral administration of KBT-3022 at 1 and 10 mg/kg significantly increased blood filterability, and significantly reduced blood viscosity at 10 mg/kg without changing the hematocrit, plasma fibrinogen concentration or plasma viscosity. KBT-3022 (10 mg/kg, p.o.) improved RBC deformability in response to shear stress, which was evoked by passing the blood through a thin tube. This dose of KBT-3022 also increased the contents of ATP and 2,3-DPG in RBC. These findings indicate that KBT-3022 may reduce blood viscosity as a sequel to improvement of RBC deformability through direct action on RBC. The increase in the intracellular levels of ATP and 2,3-DPG was considered to be involved in this improvement of hemorheological properties. These hemorheological effects of KBT-3022 appear to be promising for the treatment of patients with ischemic vascular disease.

Viscosity and Red Cell Deformity in Arterial Disease

1979 ◽  
Author(s):  
G Cella ◽  
H de Haas ◽  
M Rampling ◽  
V Kakkar
Keyword(s):  
Vascular Disease ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Arterial Disease ◽  
Plasma Viscosity ◽  
Control Group ◽  
Fibrinogen Concentration ◽  
Red Cell ◽  
Whole Blood Viscosity ◽  
Significant Difference

Haemorrheological factors have been shown to be affected in many kings of vascular disease. The present study was undertaken to correlate these factors in normal subjects and patients suffering from peripheral arterial disease. Twenty-two patients were investigated; they had moderate or severe intermittent claudication, extent of disease being confirmed by aorto-arteriography and ankle-systolic pressure studies. Twenty-five controls with no symptoms or signs of arterial disease were selected with comparable age and sex distribution. Whole blood viscosity was measured at shear rates of 230 secs-1 and 23 secs-lat 37°c using a Wells Brookfield cone plate microvisco meter. Plasma viscosity was also measured in an identical manner. Erythrocyte flexibility was measured by centrifuge technique and fibrinogen concentration as well as haematocrit by standard techniques. The fibrinogen concentration appeared to be the only significant parameter; the mean concentration in patients with peripheral vascular disease of 463 ± 73mg/l00ml in the control group ( < 0.05). Although whole blood viscosity was high in patients, when corrected to a common haematocrit, there was no significant difference between patients and controls. The same megative correlation was found for plasma viscosity. The red cell flexibility was found to be increased in patients as compared to the control group, but this effect appeared to be simply proportional to the fibrinogen concentration.

Abnormal Haemostasis and Blood Viscosity in Malignant Hypertension

1984 ◽  
Vol 52 (03) ◽  
pp. 253-255 ◽  
Author(s):  
C Isles ◽  
G D O Lowe ◽  
B M Rankin ◽  
C D Forbes ◽  
N Lucie ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Viscosity ◽  
Renal Damage ◽  
Antithrombin Iii ◽  
Plasma Viscosity ◽  
Malignant Hypertension ◽  
Fibrin Deposition ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

SummaryWe have previously shown abnormalities of haemostasis suggestive of intravascular coagulation in patients with malignant hypertension, a condition associated with retinopathy and renal fibrin deposition. To determine whether such abnormalities are specific to malignant hypertension, we have measured several haemostatic and haemorheological variables in 18 patients with malignant hypertension (Group 1), 18 matched healthy controls (Group 2), and 18 patients with non-malignant hypertension (Group 3) matched for renal pathology, blood pressure and serum creatinine with Group 1. Both Groups 1 and 3 had increased mean levels of fibrinogen, factor VIIIc, beta-thrombo- globulin, plasma viscosity and blood viscosity (corrected for haematocrit); and decreased mean levels of haematocrit, antithrombin III and platelet count. Mean levels of fast antiplasmin and alpha2-macroglobulin were elevated in Group 1 but not in Group 3. We conclude that most blood abnormalities are not specific to malignant hypertension; are also present in patients with non-malignant hypertension who have similar levels of blood pressure and renal damage; and might result from renal damage as well as promoting further renal damage by enhancing fibrin deposition. However increased levels of fibrinolytic inhibitors in malignant hypertension merit further investigation in relation to removal of renal fibrin.

Control of breathing in anesthetized dogs by a left-heart baroreflex

1986 ◽  
Vol 61 (6) ◽  
pp. 2095-2101 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Pulmonary Veins ◽  
Vagal Afferents ◽  
Low Flow ◽  
Base Line ◽  
Left Heart ◽  
Breathing Frequency ◽  
Autonomic Ganglion ◽  
Anesthetized Dogs ◽  
The Right ◽  
Vagal Cooling

Anesthetized open-chest dogs on cardiopulmonary bypass were used to test the hypothesis that breathing reflexly responds to distension of the left-heart chambers. Bypass perfusion withdrew systemic flow from the right atrium and returned it to the aorta after gas exchange. Ventricles were fibrillated. The left heart was isolated by tying all pulmonary veins, and it was perfused separately at low flow admitted through one pulmonary vein and withdrawn from the ventricle. Left-heart pressure was intermittently raised abruptly from a nominal base line of 0 by partial occlusion of outflow. Pressures from approximately 10 to 50 cmH2O caused proportional increases in breathing frequency and decreases in expiratory and inspiratory times. Changes occurred immediately, reached a plateau within approximately 20 s, and were sustained for periods of observation as long as 3 min. Recovery to base line followed stimulus removal. Vagal cooling to 8 degrees C prevented responses, but autonomic ganglion blockade with hexamethonium had no effect. I conclude that breathing may be stimulated by left-heart distension and that this is mediated by large myelinated vagal afferents.

High Prevalence of Severe Aortic Stenosis in Low-Flow State Associated With Atrial Fibrillation

2021 ◽  
Author(s):  
Said Alsidawi ◽  
Sana Khan ◽  
Sorin V. Pislaru ◽  
Jeremy J. Thaden ◽  
Edward A. El-Am ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Aortic Valve ◽  
Aortic Stenosis ◽  
Left Ventricular ◽  
Hazard Ratio ◽  
Low Flow ◽  
Left Ventricular Ejection ◽  
Aortic Valve Area ◽  
Flow State ◽  
Ventricular Ejection Fraction

Background: Atrial fibrillation (AF) is a low-flow state and may underestimate aortic stenosis (AS) severity. Single-high Doppler signals (HS) consistent with severe AS (peak velocity ≥4 m/s or mean gradient ≥40 mm Hg) are averaged down in current practice. The objective for the study was to determine the significance of HS in AF low-gradient AS (LGAS). Methods: One thousand five hundred forty-one patients with aortic valve area ≤1 cm 2 and left ventricular ejection fraction ≥50% were identified and classified as high-gradient AS (HGAS) (≥40 mm Hg) and LGAS (<40 mm Hg), and AF versus sinus rhythm (SR). Available computed tomography aortic valve calcium scores (AVCS) were retrieved from the medical record. Outcomes were assessed. Results: Mean age was 76±11 years, female 47%. Mean gradient was 51±12 in SR-HGAS, 48±10 in AF-HGAS, 31±5 in SR-LGAS, and 29±7 mm Hg in AF-LGAS, all P ≤0.001 versus SR-HGAS; HS were present in 33% of AF-LGAS. AVCS were available in 34%. Compared with SR-HGAS (2409 arbitrary units; interquartile range, 1581–3462) AVCS were higher in AF-HGAS (2991 arbitrary units; IQR1978–4229, P =0.001), not different in AF-LGAS (2399 arbitrary units; IQR1817–2810, P =0.47), and lower in SR-LGAS (1593 arbitrary units; IQR945–1832, P <0.001); AVCS in AF-LGAS were higher when HS were present ( P =0.048). Compared with SR-HGAS, the age-, sex-, comorbidity index-, and time-dependent aortic valve replacement-adjusted mortality risk was higher in AF-HGAS (hazard ratio=1.82 [1.40–2.36], P <0.001) and AF-LGAS with HS (hazard ratio=1.54 [1.04–2.26], P =0.03) but not different in AF-LGAS without HS or SR-LGAS (both P =not significant). Conclusions: Severe AS was common in AF-LGAS. AVCS in AF-LGAS were not different from SR-HGAS. AVCS were higher and mortality worse in AF-LGAS when HS were present.

Alteration of the erythrocyte ultrastructure and blood viscosity by morphine

1978 ◽  
Vol 56 (2) ◽  
pp. 245-251 ◽  
Author(s):  
E. B. Vadas ◽  
E. A. Hosein
Keyword(s):  
Cell Volume ◽  
Blood Viscosity ◽  
Whole Blood ◽  
Plasma Viscosity ◽  
Cell Geometry ◽  
Flow Properties ◽  
Mean Cell Volume ◽  
Morphine Administration ◽  
The Mean ◽  
Volume Cell

The effects of acute morphine administration on intact erythrocytes and on their flow properties were studied by measuring the mean cell volume, cell geometry, and whole blood and plasma viscosities. Morphine caused a small (2–7%) increase in mean cell volume. Changes in cell geometry were found to be time dependent and most pronounced in concave portions of the red cells. Whole blood viscosity was found to decrease upon morphine treatment; this may be due in part to a concurrent decrease in plasma viscosity.

Intestinaler ”low flow state” unter Monitoring von Mukosa- und Serosa-Kalium-Aktivität, Elektromyographie und Schockmediatorprofilen

1994 ◽  
pp. 271-275 ◽  
Author(s):  
H. W. Ch. Töns ◽  
M. Polivoda ◽  
M. Anurov ◽  
Ch. Klein ◽  
A. Öttinger ◽  
...  
Keyword(s):  
Low Flow ◽  
Flow State
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