Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HEMATOCRIT”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1975

Hemodynamic effects of staged hematocrit reduction in patients with stable cor pulmonale and severely elevated hematocrit levels.

Patients with cor pulmonale and high hematocrit levels are often subjected to phlebotomy in the belief that the adverse effects of high viscosity may outweigh the benefit of increased oxygen carrying capacity. To evaluate this, 12 patients with stable cor pulmonale and hematocrit values greater than 55 per cent were studied before and after a series of venesections. Right heart and aortic pressures, cardiac output and blood gases were measured at three mean hematocrit levels, 61 per cent (stage I), 50 per cent (stage II) and 44 per cent (stage III), with blood volume unchanged. From stages I to II, there were significant decreases in both man pulmonary artery pressure and total pulmonary resistance. Oxygen transport fell but not oxygen consumption. Right ventricular end-diastolic pressure and cardiac output did not change. Right ventricular work either fell or was maintained by increased output. Frank-Starling performance (supine exercise) improved. No significant changes occurred with further reduction in hematocrit to normal levels (stage III). The findings of this study support the concept of overcompensating erythrocytosis in cor pulmonale, and the effects of moderate hematocrit reduction should not be overlooked in these severely ill patients.

Adult↗
PubMed1996

Hematocrit values and mortality from ascites in cold-stressed broilers from parents selected by hematocrit.

A hypothesis that the relative hematocrit value of broilers is inherited and can serve as an indicator of partial resistance to the ascites syndrome in cold-stressed broilers was shown to be valid in a field trial. Hematocrits were determined for male and female grandparent breeding stocks. Matings were then made between low (LL), low-medium (LM), medium-high (MH), and high (HH) hematocrit parents: LL x LL, LM x LM, MH x MH, and HH x HH. The progeny of HH parents had higher hematocrit values than the progeny of lower hematocrit parents (P < 0.0001). Exposure of the progeny from all the parental groups to an ascites-predisposing cold environment caused higher losses from ascites in the progeny of the HH parents (P < 0.0001). The progeny of LH parents had an increased mortality from causes other than ascites (P < 0.0001). This work suggests that elimination of birds with HH in broiler breeding programs may be desirable where cold-induced ascites is an important problem.

Age Factors↗
PubMedDate not supplied

Increased whole body hematocrit: venous hematocrit ratio in diabetes mellitus, evidence of microcirculatory hemoconcentration.

Plasma volume and red cell volume were measured in 24 diabetic outpatients. From the blood volume measurements, the whole body hematocrit was derived, and the ratio between whole body hematocrit:venous hematocrit (WBH:VH ratio) was considered to represent an index of the difference in red cell distribution between small and large blood vessels. The WBH:VH ratio was increased in 9 out of 13 males and in 1 out of 11 females, being inversely correlated to the plasma volume (r = -0.51, p less than 0.001). Although the significance of these findings is far from clear, the occurrence of small vessel hemoconcentration in male patients with diabetes mellitus may be relevant to the pathophysiology of vascular complications of diabetes.

Diabetes Mellitus↗
PubMed1978

Rabbit lung plasma and erythrocyte volumes. Lung hematocrit in relation to total body hematocrit.

The total body hematocrit has been reported to be 85--90% of packed cell volume (PCV) in several species. We have found similar values in rabbits. An "extra" plasma volume must exist somewhere in the vascular bed to explain this observation. We have looked for such an extra plasma volume in the pulmonary vasculature. The dynamic hematocrit was estimated in isolated, perfused rabbit lungs from distribution volumes for plasma and erythrocyte tracers. Estimation was also obtained from indicator-dilution curves using bolus-injections of such tracers avoiding their recirculation. It was thus possible to calculate mean transit times for the tracers from their dilution curves directly or applying monoexponential extrapolation from the first part of the downslope of the curves. The dynamic hematocrit of the lung vessels was about 94% of perfusate PCV and there was no difference between the results obtained by the different methods. We concluded that in the rabbit only a very small part of the extra plasma volume is located in the lung vessels. The lung plasma volume is not underestimated by the indicator-dilution technique.

Animals↗
PubMed1987

Hematocrit fluctuations within capillary tubes and estimation of Fåhraeus effect.

Experimental and theoretical approaches were used to study hematocrit fluctuations in blood flowing along a uniform microvessel. In the experimental studies, human blood cell suspensions were passed along glass tubes with inside diameters 9.8 micron to 16.8 micron. A characteristic pattern of hematocrit fluctuation was observed in the neighborhood of white blood cells, the cell being preceded by a 'plasma gap' with reduced hematocrit and followed by a 'train' of increased hematocrit. The passage times of trains and plasma gaps and the hematocrits within the plasma gaps were determined by microphotometry. From these data, train hematocrits were deduced, expressed as equivalent discharge hematocrits. They ranged from the feed hematocrit to a value of more than 0.8 and were found to vary inversely with white cell velocity at a given flow rate. A theoretical model was developed which relates train formation to the Fåhraeus effect. The Fåhraeus effect is the reduction of tube hematocrit (HT) below discharge hematocrit (HD) which occurs in capillary tubes because the mean velocity of the red blood cells (VRBC) is higher than the mean bulk flow velocity (VB). The ratio of these velocities decreased with increasing hematocrit, and it is shown that train hematocrit is sensitive to this hematocrit-dependence. Increased hematocrit in trains behind slowly moving white cells is associated with reduced red cell velocity in the trains. From the dependence of train hematocrit on white cell velocity, the variation of Fåhraeus effect with hematocrit was deduced. The results were shown to be consistent with a model for the Fåhraeus effect in which VRBC/VB varies linearly with discharge hematocrit HD. In addition, the Fåhraeus effect was found to be approximately independent of vessel diameter over the range examined.

Biomechanical Phenomena↗
PubMed2001

Diaspirin crosslinked hemoglobin enables extreme hemodilution beyond the critical hematocrit.

BACKGROUND: Normovolemic hemodilution is an effective strategy to limit perioperative homologous blood transfusions. The reduction of hematocrit related to hemodilution results in reduced arterial oxygen content, which initially is compensated for by an increase in cardiac output and oxygen extraction ratio. To increase the efficacy of hemodilution, a low hematocrit should be aimed for; however, this implies the risk of myocardial ischemia and tissue hypoxia. OBJECTIVE: To assess whether hemodilution can be extended to lower hematocrit values by the use of a hemoglobin-based artificial oxygen carrier solution. DESIGN: Prospective, randomized, controlled. SETTING: Animal laboratory of a university hospital. SUBJECTS: Twelve anesthetized, mechanically ventilated pigs. INTERVENTIONS: Isovolemic hemodilution was performed with either 10% diaspirin crosslinked hemoglobin (DCLHb Baxter Healthcare, Boulder, CO; n = 6) or 8% human albumin solution (HSA, oncotically matched to DCLHb, Baxter Healthcare; n = 6) to a hematocrit of 15%, 8%, 4%, 2%, and 1%. MEASUREMENTS AND MAIN RESULTS: In both groups, measurements were performed at baseline at the previously mentioned preset hematocrit values and at the onset of myocardial ischemia characterized by critical hematocrit (significant ST-segment depression >0.1 mV and/or arrhythmia). To determine peripheral tissue oxygenation and myocardial perfusion and function, the following variables were evaluated: total body oxygen transport variables, tissue oxygen partial pressure (tPo2, MDO-Electrode, Eschweiler Kiel, Germany) on the surface of the skeletal muscle, coronary perfusion pressure, left ventricular (LV) end-diastolic pressure, global and regional myocardial contractility (maximal change in pressure over time, LV segmental shortening, microsonometry method), LV myocardial blood flow (fluorescent microsphere technique), LV oxygen delivery, and the ratio between LV subendocardial and subepicardial myocardial perfusion. In the HSA group, critical hematocrit was found at 6.1 (1.8)% (hemoglobin, 2 g x dL(-1)), whereas all DCLHb-treated animals survived hemodilution until hematocrit 1.2 (0.2)% (hemoglobin, 4.7 g x dL(-1)) was achieved without signs of hemodynamic instability. Although arterial oxygen content was higher in the DCLHb group at 1.2% hematocrit than in the HSA group at critical hematocrit (i.e., hematocrit, 6.1%; hemoglobin, 2 g.dL-1) neither oxygen delivery and oxygen uptake nor median tPo2 and hypoxic tPo2 values on the skeletal muscle were different between groups. In contrast, subendocardial ischemia was absent in DCLHb-diluted animals until 1.2% hematocrit was achieved. This was attributable to a higher coronary perfusion pressure (65 (22) mm Hg vs. 19 (8) mm Hg; p <.05), higher subendocardial perfusion (4.1 (2.6) mL.min-1.g-1 vs. 1.2 (0.4) mL x min(-1) x g(-1)), and subendocardial oxygen delivery (5.7 (2) mL x min(-1) x g(-1), p <.05) in DCLHb-diluted animals, resulting in superior myocardial contractility reflected by maximal change in pressure over time (3829 (1914) vs. 1678 (730); p <.05) and higher regional myocardial contractility (11 (8)% vs. 6 (2)%; p <.05). An increased LV end-diastolic pressure reflected LV myocardial pump failure in HSA-diluted animals but was unchanged in DCLHb-diluted animals. In the DCLHb group, systemic vascular resistance index remained at baseline values throughout the protocol, whereas coronary vascular resistance decreased. In contrast, both variables decreased in HSA-diluted animals. CONCLUSION: DCLHb as a diluent allowed for hemodilution beyond the hematocrit value, determined "critical" after hemodilution with HSA (6.1% (1.8)%). Even at 1.2% hematocrit (hemoglobin, 4.7 g x dL(-1)) myocardial perfusion and function were maintained, although at the expense of peripheral tissue oxygenation. This discrepancy in regional oxygenation might be caused by a redistribution of blood flow favoring the heart, which is related to a disproportionate decrease of coronary vascular resistance index during hemodilution with DCLHb.

Animals↗