Search

This study evaluated the effect of different washing and centrifuge rates of the Cell Saver 5 on the quality of processed autologous blood. Autologous blood was washed with 1000 ml of sterile normal saline at centrifuge speed of 5650 revolutions per minute (rpm) (group I) or 4350 rpm (group II) with different washing pump speeds--500, 800 and 1000 ml/min. Hemoglobin, free hemoglobin, hematocrit, erythrocytes, leukocytes, platelets, and protein were measured before and after processing. The highest values of hemoglobin, hematocrit and erythrocytes were achieved using 800 and 1000 ml/min pump speeds in group I and 500 ml/min speed in group II. Red blood cells concentration was higher in group I. There were no significant changes of free hemoglobin removal within group I. In group II the lowest free hemoglobin was achieved when 1000 ml/min rate was used. Platelets and protein did not depend on wash pump speeds in both groups. Platelet recovery in group I was higher than in group II at all washing pump speeds. Leukocytes were not adequately removed at all pump speeds. The Cell Saver 5 produces optimum results when the high wash pump speeds (800 and 1000 ml/min) and standard centrifuge speed are used.

The aim of the investigation was to study effectiveness of washing autoblood by Cell Saver 5 (Haemonetics ) device in using different rates of washing and centrifuging. Autoblood was washed with 1000 ml 0.9% NaCl with different rates (500, 800 and 1000 ml/min) at different rates of centrifuge (5650 r/min and 4350 r/min). It was shown that Haemonetics Cell Saver 5 secured the optimum composition of the end product when using high rates of washing (800 and 1000 ml/min) and standard rate of the centrifuge rotation (5650 r/min).

Central hemodynamic parameters were retrospectively studied in 284 patients. After aortic declamping, sinus rhythm spontaneously restored in 179 patients (Group 1), ventricular fibrillation occurred in 105 (Group 2). The preoperative parameters were similar in both groups. The number of grafts and the time of aortic clamping and cardiopulmonary bypass (CPB) were higher in Group 1. In the groups, the volume of cardioplegic solution and the average dose of phenylephrine and nitroglycerin per perfusion did not differ. After CPB, the values of cardiac output (CO) and cardiac index (CI) were significantly higher in Group 1 than in Group 2. At the end of an operation and 3 hours after its termination, there were no differences between two groups. Twelve hours after surgery, cardiac output and systolic blood pressure were significantly higher in Group 1. Following 24 hours of surgery, heart rate was significantly greater in Group 1 than in Group 2 After surgery, all hemodynamic parameters were within normal physiological values. The mean duration and the degree of inotropic support did not differ in the groups. The incidence of atrial fibrillation, perioperative myocardial infarction, and low cardiac output syndrome were comparable in both groups. Thus, various modes of cardiac performance recovery affect perioperative hemodynamics; however, this impact is insignificant and does not make management policy be changed in such patients. After aortic declamping, ventricular fibrillation requiring for defibrillation is not a clinical sensitive factor that negatively affects the intra- and postoperative period.

It was shown that in spite of using different methods of saving the autologous patient's blood, cell saver included, in elderly patients operated upon under conditions of extracorporeal circulation the frequency and volume of allogenic transfusions was higher as compared with the younger patients, in elderly women the allogenic transfusions being necessary more frequently.

A blind prospective randomized investigation included 109 patients with ischemic heart disease undergoing operations of coronary shunting under conditions of extracorporeal circulation. It was shown that aprotinin in the dose of 3 ppm KIU in operations of coronary shunting under conditions of reserving autoblood, extracorporeal circulation and using cell saver facilitates reducing postoperative blood loss, but does not lead to less frequent allogenic transfusions.

Seventy-three patients with ischemic heart disease (IHD), who underwent coronary artery bypass grafting with artificial circulation (AC), were examined within a prospective randomized study. The patients were randomized between three groups. The group-1 patients were administered trasilol (T) according to the below scheme: 1 mln KIU from patient's admission to the surgery room to the time the skin incision is made plus 2 mln KIU from the moment the surgical approach is preformed to the beginning of AC. KIU was added to the artificial circulation apparatus (ACA) when it was initially filled (total T dose of 6 min KIU). T was administered in the group-2 patients similarly to the scheme used in group 1; however, it was not added to the ACA (total T dose of 3 mln KIU). And T was not used at all in the group-3 patients. The dose of mezatone administered at the AC stage was reliably higher in groups 3 and 4 versus group 1 (p < 0.05 and p < 0.1, respectively). Doses of mezatone that were used for the vasopressin management did not differ significantly between the groups after surgery. A statistically more significant increase of stroke index (deltaSI) and a decrease of general peripheral vascular resistance (GPVR--deltaGPVR) were registered in 12 hours after surgery in group 3 versus group 1, p < 0.05 and p < 0.01, respectively. The negative deltaGPRV was also more pronounced versus the parameters observed in group 1 and 2 (p < 0.01 and p < 0.02, respectively). Therefore, T, when used at 6 mln KIU in AC, provides for a smaller-scope vasopressin management in AC. And, when it is used before AC at 3 mln KIU, T dose not diminish the dose of vasopressin management in AC. The intraoperative use of T (6 or 3 mln KIU) arrests a pronounced decreased postoperative deltaGPRVR and an increased postoperative CI irrespective of a dose.

The prospective randomized investigation was carried out in 61 patients with ischemic heart disease who were subjected to planned operations of coronary shunting under conditions of extracorporeal circulation. In the first group of patients autoblood as much as 24% of the calculated circulating blood volume (CBV) was reserved at the stage of isolation of the mammary artery, before systemic heparinization. The volume of the reserved blood of the patients of the second group was about 12% of CBV. It was shown that the reserving and reinfusion of massive (about 24% of CBV) volumes of autoblood in surgical treatment of ischemic heart disease under conditions of extracorporeal circulation failed to cause a substantial change of indices of central hemodynamics as compared to the reserving and reinfusion of autoblood in volume of about 12% of CBV.

The effects of water deprivation and hydration on plasma corticosterone concentration and the activity of tryptophan hydroxylase (TPH), the rate-limiting enzyme in serotonin (5-HT) biosynthesis, in the hypothalamus of vasopressin- (AVP-) deficient homozygous Brattleboro and normal Wistar rats were studied. In the Wistar rats, water deprivation caused an increase in the TPH activity in the anterior and middle (infundibular) parts of the hypothalamus, while hydration did not affect the activity of the enzyme in the anterior hypothalamus but produced an increase in its middle part. In contrast, in the Brattleboro rats, water deprivation had no effect on TPH activity in the anterior and middle parts of the hypothalamus but hydration produced a decrease in TPH activity in the anterior hypothalamus. After 48 h of water deprivation, the plasma corticosterone concentration significantly increased in water-deprived and decreased in hydrated Wistar rats. Under water deprivation, the rise in corticosterone concentration in the homozygous Brattleboro rats was significantly greater than that in the Wistar rats. The data provide evidence that the CRH-like activity of AVP is not necessary for activation of the hypothalamic-pituitary-adrenal system induced by water deprivation. The observations show that AVP is involved in the activation of TPH induced by water deprivation. This suggests that AVP modulates the metabolism of 5-HT and the response of the 5-HT-ergic system to water deprivation.

Serotonin 5-HT(1A)receptor agonist 8-OH DPAT suppressed drinking behavior in Brattleboro and Wistar rats. 5-HT(1B)agonist CGS-12066A and 5-HT(2A)antagonist ketanserin did not affect drinking behavior in Brattleboro rats; 5-HT(3)antagonist ondansetron suppressed water consumption and 5-HT(1A)agonist stimulated salt appetite in Brattleboro, but not in Wistar rats. Presumably, vasopressin regulates thirst and salt appetite by modulating sensitivity/density of various types of 5-HT receptors.

The effects of two-day water deprivation and hyperhydration (provision of 4% sucrose solution for 48 h) on levels of serotonin and its major metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the midbrain and hypothalamus were studied in Wistar rats. The rates of diuresis (0.05 +/- 0.01 and 0.84 +/- 0.12 ml/h/100 g in water deprivation and hyperhydration respectively) and urine osmolality (1896 +/- 182 and 50 +/- 13 mOsm/kg) reflected increases and decreases in blood vasopressin levels. Water deprivation was associated with a significant increase in 5-HIAA levels in the midbrain and hypothalamus, along with a decrease in serotonin levels and a three-fold increase in serotonin catabolism (the 5-HIAA:serotonin concentration ratio). Hyperhydration induced moderate increases in serotonin and 5-HIAA levels in the hypothalamus with no changes in the midbrain. The blood corticosterone level doubled in water deprivation and decreased in hyperhydration. It is suggested that activation of the serotoninergic system induces a complex adaptive reaction in water deprivation. including mechanisms specific for the regulation of water-electrolyte homeostasis and non-specific stress mechanisms (vasopressin and corticoliberin secretion).

The 5-HT1A agonist 8-OH-DPAT was shown to diminish the water and 1.8% NaCl solution consumption, whereas its antagonist pMPPI--to enhance the water intake in rats. Another agonist: CGS-12066A enhanced water intake or exerted no effect on drinking behaviour and diminished salt intake. Other substances under study exerted various effects. The data obtained suggest that the 5-HT receptors are involved in regulation of water and salt intake, even though the mechanisms of the effects are different. Apparently 5-HT1B and 5-HT2A receptors play an activating role in regulation of water intake, whereas 5-HT1A, 5-HT2C and 5-HT3 receptors act as inhibitory ones. Only three of the receptors under study seem to regulate salt intake by inhibiting the salt appetite.

Water deprivation (WD) decreased the serotonin (5-HT) level and significantly increased the 5-hydroxyindoleacetic acid (5-HIAA) in the rat midbrain and hypothalamus, the catabolic 5-HIAA/5-HT ratio increasing three-fold. Hydration (H) produced a moderate increase in the 5-HT and 5-HIAA levels in the hypothalamus with no changes in the 5-HIAA/5-HT ratio. Hydration exerted no significant effect upon the 5-HT level and metabolism in the midbrain. A two-fold increase of corticosterone concentration in water deprivation and its decrease in hydration were shown to occur in peripheral blood plasma.

Effects of 5-HT2 receptor blockade on the amplitude of startle reflex, induced by an unexpected sound, and on its prepulse inhibition (PPI) were studied on mice of CBA strain and rats of Wistar and the genetically predisposed to catalepsy (GC) strains. The effect was dependent on type and dose of 5-HT2 antagonist used: 5-HT2A antagonist ketanserin increased startle amplitude at the dose of 0.5 mg/kg and decreased it at the dose of 2 mg/kg. Mixed 5-HT2A/2C antagonist ritanserin (0.1 and 0.2 mg/kg) markedly increased startle in mice. Ketanserin and cyproheptadine produced opposite effects on startle reflex in rats with inherited neuropathology and in rats with normal genotype: marked decrease in GC rats and increase in Wistar rats was shown. Ketanserin and cyproheptadine produced a pronounced potentiation of PPI in mice and rats of both strains, ritanserin was ineffective. Results suggest 5-HT2 receptors implication in both startle and PPI regulation with 5-HT2C receptors in startle response and 5-HT2A in PPI predominant involvement.