Pulmonary microcirculatory bed and alveolar tissue in the postresuscitation period

Structural changes in alveolar lung tissue microcirculatory bed and circulatory disturbances (edema, hemorrhage, thrombosis) were studied in postresuscitation period after experimental clinical death following acute hemorrhage and mechanical asphyxia. Circulatory disturbances proved essential in the pathogenesis of postresuscitation respiratory insufficiency, follow a stepwise pattern and in early postresuscitation (up to 7 days) are pathogenetically associated with coagulopathic changes. There are periods of primary, marked and delayed disturbances, and the period of reparative changes which may cover up to 30 days since resuscitation. It is emphasized that the pattern and the degree of lung tissue damage in the postresuscitation are largely determined by circulatory disturbances.     

The blood and lymph electrolyte composition in the postresuscitation period

The electrolyte composition (Na+, K+, Ca2+, Mg2+) of blood serum and lymph was studied in experiments on 17 mongrel dogs in the postresuscitation period after clinical death. The concentration of these electrolytes reduced in the postresuscitation period. Comparison of data obtained in study of blood and lymph showed the revealed changes to be of one trend. The above-said is evidence of the expediency of including in the complex of postresuscitation therapeutic and preventive measures means for normalizing the electrolyte composition of not only the blood but also the lymph.     

ECG spectral analysis in quick death, during clinical death, and in the early postresuscitation period

The article deals with the results of ECG amplitude-frequency analysis conducted in 17 experiments on dogs in the process of quick death, clinical death, and early postresuscitation period. In group 1 (8 animals) circulatory arrest occurred after ventricular fibrillation, in group 2 (9 animals) clinical death was induced by acute blood loss. The ECG was recorded in 3 orthogonal leads after Frank. The spectral analysis was conducted on a Cb-1-ts-02 spectrobiograph. The spectral form coefficient was calculated to study the relationship of the high- and low- frequency components of the spectrum. The total power of the spectrum was evaluated according to the sum value of maximum frequency peaks in 4 fixed ranges. Analysis of changes of the spectral components of the ECG signal showed them to occur in phases in the process of dying and in restoration of vital functions. The use of the method provides for a new quantitative and qualitative evaluation of the ECG.     

Acid-base balance of the cerebrospinal fluid in the postresuscitation period

In experiments on dogs whose circulation was stopped for 10 min by electric shock the acid-base balance of the cerebrospinal fluid (CSF) and blood was studied in the postresuscitation period. Although uncompensated systemic acidosis continued for 1 h of the postresuscitation period, acidosis of the CSF was compensated much sooner and was maintained for 6 h at the initial level. Despite the high lactate concentration for 3 h of the postresuscitation period, the bicarbonate concentration during this period remained close to its initial value.Laboratory of Experimental Physiology of Resuscitation, Academy of Medical Sciences of the USSR. (Presented by Academician of the Academy of Medical Sciences of the USSR V. A. Negovskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 82, No. 11, pp. 1303–1305, November, 1976.     

Development of postresuscitation morphological changes of hippocampal and cerebellar neurons: common regularities and specific features

A comparative morphometric study of postresuscitation changes in the neuronal populations of the pyramidal cells from hyppocampal sector CA1 and Purkinje cells of the lateral cerebellar region in the course of postresuscitation period after 12-minute cardiac arrest in rats has shown that the changes differ in severity and pattern. In the pyramidal cells there were reversible dystrophic alterations of the neurons. Purkinje cells showed death of some neurons, this process progressed in the course of postresuscitation period. A positive effect of the peptide kyotorphin on the brain condition after resuscitation was found but its efficacy in different neuronal populations varied.     

Effects of presensitization and clinical death in the history on the dynamics of morphofunctional parallels of retinal and cerebral circulation]

A negative effect of preliminary sensibilization with a normal serum and clinical death (restoring to life according to V. A. Negovsky et al.) on cerebral blood supply and eye retina within 5 weeks of postresuscitation period was studied on dogs. Microcirculation disorders in the groups of sensibilized dogs were more prominent as compared to intact animals. The diameter changes of pial and retinal microvessels did not correlate, but qualitative alterations in retinal and cerebral microvessels were of the same type.     

Ca<Superscript>2+</Superscript> Transport into Sarcoplasmic Reticulum and Immediate-Early Response Proteins in the Myocardium of Rats Resuscitated after Systemic Circulatory Arrest

Activity of antioxidant defense enzymes and content of stress protein HSP70 in the heart increased in passive and, to a lesser extent, in active rats on day 7 of the postresuscitation period after systemic circulatory arrest. The resistance of membrane structures in the heart to endogenous damaging factors in passive rats was lower than in active animals. The degree of compensation in active rats was much higher than in passive animals at these terms of the postresuscitation period. __________ Translated from Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 140, No. 7, pp. 52–56, July, 2005     

Pathogenesis of the low cardiac output syndrome in postresuscitation states

Acute hypervolemia induced in experiments on dogs by infusion of dextran, did not produce decompensation of the circulation in animals whose cardiac output was sharply depressed in the postresuscitation period after circulatory arrest lasting 15 min. The increase in the venous return and change in the conditions of the peripheral circulation as a result of dextran administration temporarily increased the central venous pressure, caused a lasting increase in the arterial pressure, cardiac output, stroke volume, work of the left ventricle, and total oxygen consumption by the body, and lowered the peripheral vascular resistance. In model experiments on dogs subjected to isolated compression ischemia of the brain for 20 min, a low cardiac output syndrome also developed.Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Fedorov.Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 82, No. 7, pp. 787–789, July, 1976.     

Changes in some hemodynamic,endocrine, and metabolic indices in the early postresuscitation period

Changes in the systemic circulation, the blood flow in the kidney and limb, and certain endocrine and metabolic indices were studied in 24 dogs subjected to circulatory arrest of maximal severity for 17 min in the course of 9 h of the postresuscitation period. Relative compensation and normalization of certain functions and metabolic indices during the first hour after resuscitation were subsequently followed by a new wave of disorders which developed at different times, unequally, and gradually in the body as a whole and in individual peripheral tissues. Disturbances of the peripheral circulation and central hemodynamics were shown to be among the leading pathological manifestations of postresuscitation sickness.Research Laboratory of General Resuscitation, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR V. A. Negovskii.) Translated from Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 87, No. 1, pp. 3–6, January, 1979.     

Hemocoagulation while dying of blood loss and restoration to life after clinical death]

Hemostatic system function was studied in dogs dying of acute blood loss and restoring to life after 4-min clinical death. Phasic changes in hemostatic system of two and three types occurred in the blood loss and reanimation, respectively. Dogs with favorable postresuscitation period exhibited hypercoagulation when dying, hypocoagulation 1 hour after reanimation and normal coagulation 3-6 hours after clinical death.     

Chondriome ultrastructure of rat cardiomyocytes after apparent death and in the postresuscitation period

Twelve-minute blockade of blood circulation caused different changes in cardiomyocyte organelles, particularly in the mitochondria. The initial cardiomyocyte structure was restored within 3.5 h of the postresuscitation period. Ultrastructural changes in cardiomyocytes were observed again 1 month after resuscitation. They disappeared after 5 months. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 127, No. 1, pp. 95–100, January 1999     

Survival of dogs in the recovery period after prolonged hypovolemic hypotension

The survival rate and completeness of neurological recovery of functions of the CNS in the postresuscitation period were investigated in dogs in relation to the duration of hypovolemic hypotension, the arterial pressure level, and subsequent transfusion therapy. Administration of dextran in the early recovery period after hypovolemic hypotension in animals for 4 h increased the number of surviving dogs and led to complete restoration of functions of the CNS.     

Oxygen therapy in the recovery period following clinical death

Summary Forty experiments were carried out on dogs with the employment of oxygen therapy during the period of recovery from clinical death caused by acute hemorrhage. Oxygen therapy was carried out by 3 methods commonly used in the clinic: by an apparatus for artificial circulation, by inhalation of oxygen from a pillow or in an oxygen tent after rehabilitation of spontaneous respiration. The efficacy of oxygen therapy was judged by the general condition of animals, the span of life after the clinical death and by the morphological changes in the brain and internal organs.The animals which are in condition of hypoxia after clinical death possess an increased sensitivity to oxygen and hyperoxia may easily occur, causing their death. Artificial respiration with 100% oxygen in resuscitation during clinical death is not expedient. During the recovery period after clinical death strict dosimetry of oxygen therapy should be observed. Certain favorable effects are obtained only when resuscitation is carried out for 4 hours in a tent with oxygen content of 40–50% in 80–112 minutes after commencing the resucitation.Presented by Active Member AMN SSSR V. N. Chernigovskii     

Changes in serum lysozyme activity in terminal states caused by blood loss

The dynamics of the serum lysozyme activity was investigated in dogs after surviving clinical death for a period of 1 min as a result of blood loss giving rise to hypovolemic hypotension lasting 2 h. A progressive increase in the serum lysozyme activity in the course of hypotension and during the first 30 min of the postresuscitation period was found. Increased lysozyme activity of the serum was detected during the 4 days after resuscitation. The importance of the serum lysozyme activity as an indicator of hypoxic damage to the internal organs in terminal states is discussed.     

The mechanisms of the impact of preliminary immunization with staphylococcus anatoxin on postresuscitation pathology of the myocardium

Chronic experiments lasting for 5 weeks were carried out in 40 nonpedigree mature dogs. It has been detected that preliminary immunization with staphylococcus anatoxin potentiates the compensation mechanisms in the course of postresuscitation period, stimulates cell proliferation by increasing cardiac output that is an adaptive reaction of the cardiovascular system in postresuscitation period and provides optimal metabolism of the organism.     

Structural basis of functional heart failure during the postresuscitation period

Light and electron microscopic study of the myocardium of dogs two weeks after clinical death caused by the loss of blood was carried out and showed that the structural bases of the myocardium contractile function insufficiency during the postresuscitation period included the damage of the contractile apparatus of cardiomyocytes (microlysis and fragmentation of myofibrils, deformation of Z-bands, relaxation of sacromeres) and marked lysis of the sacrotubular system leading to the violation of the excitation-contraction coupling. Cardiomyocyte damages are associated with changes in the microcirculatory channel causing the worsening of transcapillary exchange that provides the tissue homeostasis.     

Correlation between the central hemodynamics of dogs in the early postresuscitation period and the outcome of resuscitation

Changes in the central hemodynamics were compared with the outcome of resuscitation in 18 dogs after circulatory arrest lasting 12 min caused by ventricular fibrillation. In nine animals resuscitated with evidently complete neurological recovery moderate hypertension was observed in the first 10 min after the beginning of the resuscitation measures: The mean arterial pressure (MAP) was 175.0±8.9 mm Hg. In most of the dogs which died subsequently MAP in this period was not higher than initially, but two animals showed severe hypertension (MAP about 200 mm Hg). In this same period differences also were found in other parameters of the central hemodynamics. Moderate hypertension in the first 10 min of the postresuscitation period evidently leads to rapid recovery of an adequate level of the peripheral blood flow in tissues and organs and, as a result, it aids the survival of animals after a long period of circulatory arrest.Research Laboratory of General Resuscitation, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR V. A. Negovskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 88, No. 11, pp. 530–532. November, 1979.     

The status of the erythrocyte membranes and their functional properties in the postresuscitation period

It was found that the deformation properties and peroxidation resistance of erythrocytes deteriorate in the postresuscitation period. On the basis of increase of the level of lipoperoxidation products and reduction of the level of alpha-tocopherol and nonprotein sulfhydryl groups, the authors conclude that lipid peroxidation in the erythrocyte membranes is activated after resuscitation. Disorders of molecular interactions are confirmed by the kinetics of nystatin fluorescent probe insertion and revealed increased cholesterol level in the erythrocyte membranes. It is suggested that the increase of the cholesterol level occurring as a protective response to the activation of lipid peroxidation transforms into a pathological reaction causing disorders of the deformation properties and peroxide resistance, which accelerates considerably the natural death of the erythrocytes after resuscitation.     

Threshold of seizure activity of the brain and higher nervous activity in the postresuscitation period for intracerebral allotransplantation of fetal neocortex tissue

The threshold of seizure activity of the brain, long-term memory, and learning ability are studied in Wistar rats for bilateral transplantation of fetal nervous tissue in area CA1 of the hippocampus. The grafts are performed on the 2nd, 7th, 14th and 30th days after clinical death caused by asphyxia. A neurotransplantation performed on the 2nd day of the postresuscitation period is found to prevent seizure activity, whereas that performed on the 7th–14th days results in a sharp decline or cessation of spontaneous and induced epileptiform convulsive seizures, prolonged preservation of the long-term memory trace, an improvement of learning ability, and a lessening of defensive and phobic behavior in a large proportion of the animals. Translated fromByulleten's Eksperimental'noi Biologii i Meditsiny, Vol. 121, N ^o 2, pp. 234–237, February, 1996 Presented by V. A. Negovskii, Member of the Russian Academy of Medical Sciences     

Role of disorders of metabolism in rat myocardium and endotoxemia in the pathogenesis of post-resuscitation cardiodepression

The model of 4-min clinical death due to acute blood loss was used to study cardiac contractility, myocardial metabolism and causes of endotoxemia in early postresuscitation period. The investigations were made on the whole body, isolated, isovolemically contracting heart and isolated papillary muscle. A marked reduction in functional myocardial reserves, maximal within the first 24 hours of postresuscitation, with dominant defects in relaxation was seen. Pathogenetic factors responsible for cardiodepression are the following: hypoxia, impairment of bioenergetics, hyperactivation of lipid peroxidation, acidosis, membrane destruction, endotoxemia.