[Guanylate cyclase activity of the rabbit myocardium in normal conditions and in allergic states]. / Issledovanie aktivnosti guanilattsiklazy miokarda krolikov v norme i pri ego allergicheskom povrezhdenii.

Activity of guanylate cyclase, regulation of the enzyme by means of hormones and other biologically active substances as well as level of cGMP were studied in rabbit myocardium of control animals and in animals with allergic impairment of the tissue. The enzyme was shown to exhibit no sensitivity to acetylcholine and histamine, which appears to occur as a result of the hormone-unspecific desensitization of the corresponding receptors in allergic impairment. Decreased basal activity of guanylate cyclase was accompanied by an increase in content of cGMP in myocardial tissue. This phenomenon was apparently also due to a decrease in phosphodiesterase activity, which is observed under the conditions of this pathology. At the same time, the decrease in the basal activity of guanylate cyclase was caused by impairment in active restoration of the enzyme in the allergic tissue. A decrease in the enzyme activation by means of azide and nitroprusside appears to be due to loss of hem, prosthetic group of the cyclase. Physiological functions of guanylate cyclase are discussed.

[Mechanism of disruption in the metabolism of the cyclic AMP system in myocardial tissue in allergic deterioration]. / K mekhanizmu narushenii v sisteme obmena tsiklicheskogo AMP v tkani miokarda pri ego allergicheskom povrezhdenii.

Role of hormones, guanylic nucleotides and sodium fluoride in regulation of adenylate cyclase activity was studied in rabbit heart under conditions of its allergic deterioration caused by repeated administration of horse blood serum. In the allergic injury activation of adenylate cyclase was found to occur simultaneously with a decrease in the rate of the enzyme stimulation by means of either the hormones in presence of guanylic nucleotides or by sodium fluoride. Without guanylic nucleotides the hormones did not stimulate adenylate cyclase activity. At the same time, under conditions of allergic sensitization the hormone stimulated adenylate cyclase was practically not activated by guanylic nucleotides. Unspecific desensitization of membrane receptors to hormones was responsible for impairments in regulation of adenylate cyclase activity under conditions of allergic sensitization. In the allergy the functional activity of N-protein was not altered, whereas its coupling with the catalytic component was impaired by sodium fluoride.

[Acute emotional stress and cyclic nucleotide content of the heart and blood plasma]. / Ostryi émotsional'nyi stress i soderzhanie tsiklicheskikh nukleotidov v serdtse i plazme krovi.

The relationships between the changes in arterial pressure and the content of cyclic nucleotides in the heart and blood plasma were studied on rabbits exposed to acute emotional stress. During 3 hours of the stress program, there were changes in arterial pressure, namely an elevation within the first hour followed by a progressive fall during subsequent 2 hours and death of the animals. The content of cAMP in the heart rose to a greater degree than that of cGMP. The content of cAMP in the blood plasma considerably increased, while the level of cGMP remained unchanged. The data obtained attest to the predominance of activation of adrenergic structures over activation of cholinergic structures.

[Effect of guanyl nucleotides and hyperbaric oxygenation on the adenylate cyclase activity of the heart in rabbits with myocardial hypertrophy]. / Vliianie guanilovykh nukleotidov i giperbaricheskoi oksigenatsii na aktivnost' adenilattsiklazy serdtsa krolikov pri gipertrofii miokarda.

The authors studied the role of guanyl nucleotides and hyperbaric oxygenation (HBO) in desensitization and resensitization of adenylate cyclase of the heart during hypertrophy which was induced by aorta stenosing. The basal activity of the enzyme and the rate of its activation with adrenaline and guanyl nucleotides were discovered to be reduced. In the presence of guanyl nucleotides, HBO gave rise to the recovery of enzyme sensitivity to the hormone. The data obtained indicate that during myocardial hypertrophy, guanyl nucleotides participate both in densensitization of adenylate cyclase to hormonal exposure and in the enzyme resensitization during HBO therapy.

[Changes in the activity of cyclic adenosine monophosphate metabolism enzymes in myocardial hypertrophy and after exposure to hyperbaric oxygenation]. / Izmenenie aktivnosti fermentov obmena tsiklicheskogo adenozinmonofosfata pri gipertrofii miokarda i vozdeistvii giperbaricheskoi oksigenatsii.

Hypertrophy of myocardium, developed within 4 weeks after aorta stenosis, led to alteration in content of adrenaline in heart tissue as well as in some pathways of cAMP turnover: decrease in content of cAMP, an increase in the basal activity of adenylate cyclase, decrease in activation of the enzyme by adrenaline; activity of phosphodiesterase was not distinctly altered. Under conditions of hyperbaric oxygenation hypertrophy of myocardium became less distinct, content of cAMP was increased up to the normal value, the increased basal activity of adenylate cyclase was slightly decreased, whereas sensitivity of the enzyme to adrenaline did not reduce, content of adrenaline was increased.

[Adenylate cyclase system and calcium transport in the cardiac muscle of normal rabbits and rabbits with allergic heart damage]. / Adenilattsiklaznaia sistema i transport kal'tsiia v serdechnoi myshtse krolikov v norme i pri allergicheskom povrezhdenii.

A 2,3-fold increase of cAMP concentration in rabbit myocardium, increase in basal activity of adenylate cyclase and inhibition of phosphodiesterase were found in allergic impairment of heart muscle in response to repeated administration of normal horse blood serum. In presence of adrenaline and NaF the rate of adenylate cyclase activation was distinctly decreased, indicating the "desensitization" of the enzyme. At the same time, parameters of Ca2+ transport were altered; the alterations were expressed as intensification of 45Ca turnover in mitochondria and in the fraction of sarcoplasmic reticulum, as well as distinct increase in the initial rate of Ca2+ penetration into mitochondria and increase in content of calcium in the organelles.

[Effect of succinic semialdehyde on nitrogen metabolism of animal brain tissue during hypoxia]. / Vliianie iantarnogo polual'degida na nekotorye storony azotistogo obmena tkani mozga zhivotnykh pri gipoksii

In examining the content of free ammonia, glutamine and some free amino acid s in the brain tissue of mice under normal conditions, in hypoxia and under the effect of succinic acidsemialdehyde, in hypoxia there was revealed a marked increase in comparison with the normal conditions) of the content of free ammonia, and alpha-alanine, a reduction of glutamine; there was also a slight elevation in the content of gamma aminobutyric acid and no changes in glutamic and asparagic acid content. In case of pretreatment with succinic acid semialdehyde the content of free ammonia, glutamine and alpha-alanine in hypoxia approached the normal value. One of the possible mechanisms of the antihypoxic effect of succinic acid semialdehyde was transformation of this compound as a results of which there occurred synthesis of glutamic acid and glutamine leading to detoxication of free ammonia accumulating in the brain tissue in hypoxia.

[The mechanism of the anticonvulsive action of diazepam]. / K mekhanizmu protivosudorozhnogo deistviia diazepama

Diazepam was shown to be highly efficient in preventing the convulsive siezures induced by thiosemicarbazide and connected with GABA insufficiency. In recording the recovery cycles of the intracortical response of the cat motor cortex it was found that diazepam induced a decrease of the testing respone. These data indicate the enhancement of the inhibitory processes. Using this test an antagonistic relationship was observed between diazepam on the one hand, and biculline and thiosemicarbazide--on the other Diazepam was capable of increasing GABA content in the brain by suppressing GABA-transaminase activity in the mitochondrial fraction of the brain tissue.