PubMed Health⌕ Search

Biomedical subjects

S Lazarov

Publications and source records attributed to S Lazarov.

17 recordsLinked to original sources
PubMed2001

[Pulmonary surfactant system].

The lung surfactant system (LSS) has a complex morphological and biochemical structure. LSS contains two components: cellular and non-cellular. The cellular component comprises three types of alveolar epithelium cells (type I, II, and II pneumocytes), alveolar macrophages (AM) and Clara bronchiolar cells. The non-cellular component consists of alveolar surfactant (AS), hypo(epi)phase and alveolar epithelium cell glycocalix. AS represents phospholipids, proteins and carbohydrates mono-molecular layer. AM lamellar bodies (LB) and tubular myelin (TM) are disposed in the hypophase. LB and TM represent the depot-forms of lung surfactant (LS). Lung surfactant (LS) has a complex biochemical structure and comprise the following components: phospholipids, neutral lipids, glycolipids, surfactant-specific proteins, plasmaproteins, enzymes, carbohydrates and aminoacids. LS is synthesized in type II pneumocytes and Clara cells. LS catabolism is mainly effected by AM. The LSS has a fundamental role in the physiological functions of lungs. Through its antiatelectatic and antioedematic functions, LSS sustains the basic physiological functions of lungs--alveolar ventilation and gas diffusion through the alveolar-capillary wall. Besides this, LSS performs several protecting functions--antioxidant defense, non-specific defense mechanisms, immunodulatory action, cytotoxicity agents metabolism and others. The injury of the structure and functions of LSS is an important pathogenic mechanism in the pathogenesis of different lung diseases. Practically, a pathological process in lungs, which is not related to changes in LSS structure and functions, does not exist. Recently developed surfactant replacement therapy with natural and synthetic surfactants has an important place in the therapy of several lung diseases.

Animals↗
PubMed2001

[Adult respiratory distress syndrome--etiology and pathogenesis].

Adult respiratory distress syndrome (ARDS) is not a specific lung disease. It represents an acute respiratory insufficiency syndrome in patients with non-injured lung as a result of severe multiple lung lesions of different etiology and pathogenesis. ARDS is provoked by a great number of etiologic factors of two main groups: 1) etiologic factors directly injuring the alveolo-capillary wall and 2) etiologic factors indirectly injuring the alveolo-capillary wall. ARDS develops in three phases: phase of exudation, phase of injury of the alveolocapillary wall and phase of proliferation (chronic phase).

Adult↗
PubMed2001

[Interleukins and endocrine function].

Views and experimental data on the role of interleukins in the regulation of the endocrine functions of hypothalamus, pituitary gland, thyroid gland, suprarenal gland and pancreas are presented. The role of interleukin-1 and interleukin-6 in the regulation of normal and pathological processes is examined. Data on cellular and molecular operation mechanisms of some interleukins on functions of the endocrine glands are included in the survey. The clarification of these mechanisms leads to new pharmacotherapeutical approaches to endocrine diseases treatment.

Adrenal Glands↗
PubMed2000

[Adult respiratory distress syndrome].

Adult respiratory distress syndrome (ARDS) represents an excessively dangerous acute respiratory failure, as result of diffuse damage of alveolocapillary membranes in stiff noncompliant lungs. ARDS is a widely disseminated syndrome caused by severe etiologic factors. ARDS usually appears within 12 to 72 hours of an identifiable clinical event and progresses through three phases: 1. exudative phase; 2. alveolar membrane damage and pulmonary surfactant systems; and 3. proliferative phase. Nearly all of the deaths occur within 30 days of the onset of the syndrome. The mortality rate varies according to the causes and the age. ARDS progresses through three clinical phases: 1. basis respiratory failure; 2. progressive respiratory failure; and 3. total respiratory failure. The therapy of ARDS is complex. It consists of: 1. background general therapy of ARDS; 2. background supportive therapy of ARDS; 3. definitive therapy to interrupt mechanisms of inflammation and pulmonary injury; 4. new pharmacologic supportive therapy.

Adult↗
PubMed2000

[Macrolides: pharmacology and clinical use].

Members of macrolides are Erythromycin, Oleandomycin, Spiramycin, Roxithromycin, Josamycin, Midecamycin, Clarithromycin, Azithromycin and Dirithromycin. This review present mechanism of action, pharmacokinetic, adverse drug reactions and main clinical uses of the macrolides.

Anti-Bacterial Agents↗
PubMed2000

[The role of cell adhesion molecules and proinflammatory mediators in the pathogenesis of endotoxin adult respiratory distress syndrome].

The Gram-negative bacterial sepsis that is resistant to therapy results in the development of septic shock and the multiple organ dysfunction syndrome (MODS). It is established that the adult respiratory distress syndrom (ARDS) as a component of MODS is the reason for high mortality in these patients. The basic pathogenetic link between ARDS and the septic shock are the lesions of the alveolo-capillary membrane. They result from the sequestrated neutrophil cells in the lungs. Neutrophil extravasation is manifested by the following steps (stages): 1) weak initial adhesion; 2) rolling; 3) stable adhesion; and 4) extravasation. These processes are mediated by cell adhesion molecules that belong to four classes: selectins, selectin ligands, integrins and immunoglobulin superfamily. Thus cell adhesion molecules mediate the sequestration of neutrophil cells in the lungs and the damage of the pulmonary surfactant system.

Adult↗
PubMed2000

[Contemporary views on the etiology and pathogenesis of atherosclerosis].

Atherosclerosis is caused by a large range of exogenous and endogenous risk factors and does not result simply from the hypercholesterolemia and the accumulation of lipids. Atherogenesis is a dynamic multifactor and multi-stage inflammatory process, where different cells, cytokines and growth factors interacte as results of endothelial cell damage. This process is characterized by a focal subintimal deposition of lipids and lipoproteins in "foam cells" with a further development of chronic focal inflammation and expanditure of fibrosis, stenosis of the arterial lumen and development of further organ complications. The same are found in 50% of the patients, affected by atherosclerosis and are at the root of the death-rate in USA and Europe.

Arteries↗
PubMed2000

[The role of bacterial endotoxins, receptors and cytokines in the pathogenesis of septic (endotoxin) shock].

Sepsis, resistant to therapy, results in the development of septic (endotoxin) shock. The latter is caused by the endotoxins of different Gram-negative bacteria. Endotoxin (bacterial lipopdisacharide--LPS) interacts with cells through specific membrane or plasma soluble endotoxin receptors (sCD14, mlD14, LBP, CD13/CD14, CD16, CD116/CD18, L-selectin, etc.). Endotoxin interaction with the mCD14 receptor of the monocytes, macrophages and the neutrophils results in the production of a number of proinflammatory cytokines--tumor necrosis factor alpha (TNF alpha), interleukines 1 and 6 (IL-1 and IL-6, etc), antiinflammatory cytokines--interleukines 10 and 12 (IL-10 and IL-12), cell adhesion molecules (P-selectin, E-selectin, ICAM-1, VCAM-1, etc.) and inducible enzymes: inducible NO synthase (iNOS), inducible phospholipase A2 (cPL-A2), inducible cyclooxygenase (COX-2). All pathologic processes in the structure and function of human body during endotoxin shock are a result of the disbalance of a number of mediators with a proinflammatory and antiinflammatory effects.

Cell Adhesion Molecules↗
PubMed2000

[Pulmonary repair after adult respiratory distress syndrome].

The adult respiratory distress syndrome (ARDS) represents a particulary dangerous form of acute respiratory failure. The processes of reparation of the lungs start in the course of several hours following the acute pulmonary damage and ARDS. They imply: 1) lysis of intraalveolar fibrin, phagocytosis of the necrotic products and resorption of the edematous fluid from the alveolar lumen and the pulmonary interstitium. 2) reparation of the pneumocytes and the bronchiolar Clara cells. 3) reparation of the pulmonary interstitium (pulmonary fibrosis and sclerosis). These processes of reparation in the lung are modulated by cell adhesion molecules of the integrin group and a number of growth factors (PDGF, AMDGF, EGF, FGF, IGF-I). Apoptosis is the main factor that controls the correct outcome of the processes of pulmonary reparation.

Adult↗
PubMed1999

Metabolic changes in children with severe traumatic injuries.

INTRODUCTION: Combined traumatic injuries are the leading cause for more than half the cases of lethal outcome in childhood. Trauma triggers a series of endocrinic and metabolic changes commonly known as acute metabolic stress. The hypermetabolic and hypercatabolic condition which develops as a result contributes to the high morbidity and mortality rates in children with traumatic injuries. METHODS: Twenty five children (16 boys and 9 girls aged 4-15 years) were recruited from the patients admitted for treatment to the Department of Pediatric Anesthesia and Intensive Care at the Clinic of Pediatric Surgery in the Higher Medical Institute--Plovdiv, between 1994 and 1998. All children had severe combined trauma. Of these 20 (80%) presented with severe craniocerebral trauma; they were comatose with Glasgow Coma Scale Score of 7.3 +/- 4.3 (Sx = 3.59); the children were on mechanical ventilation and total parenteral nutrition. Energy expenditure was measured using computerised metabolic monitor Deltatrac II. VO2, VCO2, RQ, energy expenditure (MEE), oxygen consumption and nitrogen excretion levels were monitored. RESULTS: The mean energy expenditure measured during the first, second and third 24-hour period was 50.04 kcal/kg/d-1, 50.54 kcal/kg/d-1 and 51.38 kcal/kg/d-1, respectively; the respiratory quotient was 0.81 +/- 0.0114 Sd, the oxygen consumption index 7.32 +/- 0.08 Sd ml/min/m2. The energy expenditure calculated by the Fleisch formula was 42.38 +/- 1.24 kcal/kg/d-1, (Sx = 6.19); this value differed statistically significantly from the value we measured (50.63 +/- 1.31, Sx = 6.57, p < 0.0001), the injury correction factor (ICF) was calculated to be 1.22 +/- 0.02 Sd. CONCLUSIONS: Actual energy expenditure in children with severe traumatic injuries is considerably higher than that calculated by formulae. Based on our results we recommend that the energy and substrate intake to be increased above the values calculated by formulae by a coefficient of 1.22 which is the measured correction factor. Thus the increased energy requirements will be met and the patients' prognosis will be improved.

Adolescent↗
PubMed1995

Blood gases, electrolytes and metabolic monitoring in children with acute failure of vital functions.

The priority of direct monitoring of blood gases in Paediatric Intensive Care Units (PICU) increased substantially after introduction of the Deep Picture method and Oxygen Status Algorithm (OSA) (1) into medical practice. We used the advantages of these methods as a prerequisite for a more detailed and deeper analysis of the blood oxygen profile (2, 3). The aims of the present paper were: 1. To illustrate the applicability of the capacity coefficients beta 1.0, beta 2.3, beta 5-4 of the transported oxygen and the "Useful Ratio" (UR) index of the haemoglobin oxygen, previously described by us, and the benefit derived from differentiation of the states of hyperoxia, normoxia and hypoxia; hyperoxaemia, normoxaemia and hypoxaemia on the Blood Oxygen Binding Curve (BOBC) in critically ill newborns, infants and children. 2. To expand the diagnostic capacity of the Blood Gas Map (BGM) used with the OSA in children and to supplement the arterial oxygen diagnostics with new indices that reflect the relationship between oxygen uptake and oxygen transported in the body. 3. To share our experience in PICU related to the acid-base-electrolytes relationship and to the possibility of assessing the reno-hepatic regulation according to the changes of the acid-base status in critically ill children.

Acid-Base Equilibrium↗
PubMed1990

[A modified technic of preoperative acute normovolemic hemodilution--the advantages and economic effect of its use in planned colorectal surgery].

In a prospective and comparative study were included 129 patients undergone planned operation for colorectal cancer. They were divided in two randomized groups: Group A consisted of 65 patients operated under conditions of preoperative acute normovolemic hemodilution (PANHD) by an own modified technique with Ringer-lactate and hemodex. Group B (control) included 64 patients operated with the use of homologous blood substitution. The results in the two groups were compared as to: intra- and postoperative blood transfusions; time (in days) of postoperative treatment; number of postoperative complications. Statistically significant differences (p less than 0.001) referrable to all three compared values were found. The modified PANHD technique in planned colorectal surgery is safer for the patients than the so far suggested techniques and may readily gain acceptance with the use of solutions of domestic produce. It leads to significant decrease in homologous blood transfusion, shortening the postoperative stay in hospital of patients subjected to hemodilution. The number of patients in whom postoperative complications developed was reduced.

Adult↗
PubMed1990

[Continuous thoracic epidural analgesia in surgical interventions on the upper half of the abdomen--the noninvasive monitoring of the early hemodynamic changes].

Operative interventions in the upper half of the abdomen have been performed in 32 surgical patients under thoracic epidural analgesia (TEA) with bupivacain at T4-L2 level, with the use of catheter technique. Before operation the patients were hydrated with 12.5 per cent of the circulating blood volume, calculated by nomogram. By noninvasive approach were monitored: pulse rate (PR), mean arterial pressure (MAP), minute cardiac volume (MCV), peripheral vascular resistance (PVR) and cardiac index (CI) for the following times; T0--basal preoperative value, T1--on the 5. min; T2--on the 10. min; T3--on the 15. min.; T4--on the 20 min.; T5--on the 50. min after application of bupivacain analgesia. The results were compared by variation analysis to T0. PVR was reduced with statistical significance for T2, T3 and T4 (p less than 0.01). MCV, CI and MAP tended to be reduced, while PR showed no significant changes. The results may be summarized, as follows: 1. Noninvasive monitoring of PR, MAP, MCV, CI and PVR in TEA is necessary for early detection and control of their pathologic changes; 2. The hemodynamic changes in TEA with bupivacain at T4-L2 level after premedication with vagolytic and hydration with Ringer-lactate (in amount 12.5 per cent of the circulating blood volume) are not significant and do not require additional treatment; 3, TEA at T4--L2 level allows performance of operative interventions in the upper half of the abdomen with adequate analgesia and relaxation, being particularly indicated for patients at risk.

Abdomen↗
PubMed1989

[Functional disorders of cardiac pacemakers--their diagnosis and treatment].

Implantation of artificial pacemaker has proven invaluable in the treatment of patients with heart block and other arrhythmias. It has been found that, however seldom, this device may function inadequately after implantation. This malfunction is secondary to alteration in the previously assigned rate, to irregular pacing and failure of sensing, impaired capture or depolarization and/or various combinations of these events. The welfare of patients with pacemaker depends on the adequate investigation and interpretation of the malfunction and its proper management. The numerous signs of pacemaker malfunction are associated with changes in the output of impulses and inadequate pacing. It is believed that in the future the developing technology will provide more refined pacemaker device, and the incidence of pacemaker malfunction with fall to a reasonable limit.

Arrhythmias, Cardiac↗
PubMedDate not supplied

[The hemodynamic changes during preoperative acute normovolemic hemodilution (prospective, randomized and comparative research)].

Fifteen patients examined after preoperative acute normovolemic hemodilution (PANH) up to hematocrit value of 0.30 developed a significant increase in cardiac output (CO) and cardiac index (CI) and a decrease in total peripheral resistance (TPR), other hemodynamic parameters remained unchanged. In normal hemodynamics the patient's age is not a contraindication for PANH. Noninvasive monitoring of hemodynamic parameters, CO, CI and TPR in particular, during surgery employing PANH is obligatory for the early diagnosis and correction of impaired circulation.

Adult↗