Dilatation Of Capacitance Vessels Research Articles

Состояние барьеров микробной колонизации зубочелюстной системы в условиях имитированной невесомости

Введение. Условия космического полета приводят к изменению функциональных показателей многих органов и систем организма человека. Накопленный опыт показывает, что с увеличением длительности полета большое значение приобретают комплексные исследования состояния зубочелюстной системы. Цель исследования - изучение анаэробной составляющей микробиоты, иммунологических показателей ротовой жидкости и скорости кровотока в микроциркуляторном русле пародонта при моделировании невесомости. Методика. Наиболее адекватной моделью, воспроизводящей эффекты факторов полета в земных условиях, является «сухая» иммерсия. Было проведено комплексное обследование 20 мужчин добровольцев, в возрасте от 19 до 26 лет. В качестве модели микрогравитации использовали 5-суточную «сухую» иммерсию. Изучение состояния тканей пародонта включало микробиологические, иммунологические и микроциркуляторные исследования. Исследования выполняли в 1-е сут (фон), на 5-е сут иммерсии (выход) и на 7-е сут по окончании иммерсии. Качественный состав основных пародонтопатогенных видов микроорганизмов определяли методом полимеразной цепной реакцией. Концентрацию иммуноглобулинов (sIgA, IgA, IgМ) в ротовой жидкости - методом ИФА с помощью соответствующих наборов реагентов ЗАО «Вектор-Бест». Оценку кровотока в тканях пародонта проводили методом высокочастотной ультразвуковой допплеровской флуометрии ультразвуковым допплерографом «Минимакс-Допплер-К» (г. Санкт-Петербург) с датчиком непрерывного излучения, рабочая частота - 20 МГц. Результаты. Во время эксперимента в составе микробиоты пародонта обнаружено появление 5 основных пародонтопатогенных видов микроорганизмов (Aggregatibacter actinomycetemcomitans, Tannerella forsythia, Prevotella intermedia, Porphyromonas gingivalis, Treponema denticola). Отмечен рост концентрации в десневой жидкости sIgA, что связано с появлением пародонтопатогенной микробиоты. На 5-е сут и 7-е сут после «сухой» иммерсии у 12 человек отмечено статистически значимое снижение скорости кровотока в микроциркуляторном русле тканей пародонта как нижней, так и верхней челюсти. У 6 человек наблюдалась морфофункциональная перестройка микроциркуляторного русла в виде дилатации емкостных сосудов (венул) с частичным обеднением капиллярного звена, что свидетельствует о реакции венулярной компоненты на моделируемую микрогравитацию. Заключение. Комплексное исследование показало предрасположенность тканей пародонта в условиях «сухой» иммерсии к развитию воспалительных заболеваний и снижению барьерных функций пародонта.Comprehensive evaluation of 20 male volunteers aged 19-26 was conducted during exposure to 5-day “dry” immersion (DI). The aim was to examine periodontal tissues in the conditions of 5-day “dry” immersion, specifically, to study the anaerobic component of periodontal microbiota, immunological parameters of the oral fluid, and blood flow velocity in the periodontal microcirculation (PMC). Methods. Microgravity was modeled with the 5-day DI. Evaluation of the condition of periodontal tissues included microbiological, immunological, and microcirculatory studies. The studies were performed on day 1 (baseline), day 5 of immersion (completion), and day 7 upon the end of immersion. All studies were performed in the fasting state, before toothbrushing, in the supine position in the immersion bath, and in the sitting position 7 days after the immersion. PMC was studied at the same time points as in the immunoglobulin study. Blood flow in periodontal tissues was measured using the high-frequency ultrasonic Doppler fluorimetry (HFUDF) with a Minimax-Doppler-K ultrasonic dopplerograph (St. Petersburg) with a continuous radiation sensor at an operating frequency of 20 MHz. Results. Five major periodontopathogenic bacteria (Aggregatibacter actinomycetemcomitans, Tannerella forsythia, Prevotella intermedia, Porphyromonas gingivalis, and Treponema denticola) emerged as a part of the periodontal microbiota during the experiment. An increased concentration of sIgA was observed in the gingival fluid, which was associated with the emergence of periodontopathogenic microbiota. On day 5 of SI and day 7 following SI, 12 subjects had a statistically significant decrease in blood flow velocity in PMC of both the lower and upper jaws. 6 subjects showed morphological and functional rearrangement of the PMC, including dilation of capacitance vessels (venules) with partial capillary depletion, which indicated a venular component response to the conditions of modeled microgravity. Conclusion. This comprehensive study showed predisposition of periodontal tissues to development of inflammatory diseases and impaired functioning of the periodontal barrier under the conditions of DI.

Effect of the platelet‐activating factor antagonist, TCV‐309, and the cyclo‐oxygenase inhibitor, ibuprofen, on the haemodynamic changes in canine experimental endotoxic shock

1. The present study was conducted in order to examine the effects of the platelet-activating factor (PAF) antagonist, TCV-309, and the cyclo-oxygenase inhibitor, ibuprofen, on the acute haemodynamic responses to endotoxin in anaesthetized dogs. 2. Endotoxin (2 mg kg-1, i.v.) induced a severe hypotension by decreasing both total peripheral resistance (TPR) and cardiac output. Endotoxin also decreased central venous pressure and increased effective vascular compliance (EVC), indicating a blood pooling in the capacitance vessels. 3. The endotoxin-induced hypotension but not the fall in cardiac output, was markedly attenuated by ibuprofen. Ibuprofen abolished the decrease in TPR and even caused a systemic vasoconstriction. Ibuprofen abolished the increase in EVC. 4. The hypotension caused by endotoxin was attenuated by TCV-309 to a lesser extent than ibuprofen. However, the reduction in cardiac output produced by endotoxin was markedly attenuated by the PAF antagonist. TCV-309 also abolished the increase in EVC. In contrast to ibuprofen, TCV-309 did not affect the decrease in TPR caused by endotoxin. 5. Combined treatment with ibuprofen and TCV-309 markedly attenuated the endotoxin-induced hypotension, but not the fall in cardiac output. Nevertheless, when compared with animals treated with ibuprofen alone, treatment with ibuprofen and TCV-309 partly attenuated the endotoxin-induced reduction in cardiac output and systemic vasoconstriction. 6. These data indicate that dilatation of both resistance vessels and capacitance vessels contributes to the endotoxin-induced hypotension. It is suggested that (i) both prostanoids and PAF are involved in dilatation of capacitance vessels, (ii) prostanoids, but not PAF cause dilatation of resistance vessels and(iii) PAF may partly contribute to prostanoid-independent reduction in cardiac output in acute canine experimental endotoxin shock.

Prostacyclin effect on blood pressure in pig with aortic obstruction

Cardiovascular effects of infused prostacyclin (PGI2 )were investigated in hypertensive anesthetized pigs in the steady state and at 1,2,3,4,5,10,15,20 and 30min after the beginning of the infusion PGI2 was perfused at the rate of 2 μg/Kg/min for 4 min before and after vagosympathectomy. We measured the mean arterial pressure, heart rate, cardiac output, stroke volume, mean pulmonary arterial pressure,mean pulmonary wedge pressure and calculated total systemic resistance and total pulmonary resistance. Our findings suggest that prostacyclin lowers pulmonary and systemic blood pressure in hypertensive animal by vasodilatation. The decrease in mean arterial pressure does not produce any change in heart rate probably because the substance also has a vagal effect. Finally, it might reduce venous return by dilatation of capacitance vessels. PGI 2, appears to be a powerful vasodilator agent acting both afterload and preload without influencing heart rate or stroke volume.

Neural and non-neural mechanisms influencing circulation during sleep.

IN the past few years there has been increasing interest in cardiovascular changes during sleep, on the assumption that they might provide some insight into the neural control of circulation in a natural condition. The hypothesis that all cardiovascular events that occur during sleep are neurally mediated has never been crucially proved, however. Furthermore, sleep is accompanied by various haemodynamic phenomena which may well have different mechanisms. In the cat the greatest cardiovascular changes occur during desynchronized sleep (DS)1,2, a stage of sleep characterized by a desynchronized electroencephalogram and bursts of rapid eye movements, and in man associated with dreaming. We have shown recently that the arterial hypotension occurring during DS is dependent chiefly on a decreased peripheral resistance, change in cardiac output being small3. This is particularly true for animals subjected to sino-aortic deafferentation3, whose hypotension during DS is greatly exaggerated because of the removal of a buffer action exerted by arterial chemoceptors4. But in the few DS episodes during which hypotension is so profound as to cause electroencephalographic signs of cerebral anoxia (a phenomenon observed in deafferented animals only), the very large decrease in arterial pressure seems to be exclusively a consequence of a dramatic fall in cardiac output3. It has been suggested3, though not demonstrated, that the decrease in peripheral resistance might result from a reduction of sympathetic vasoconstrictor activity. The decrease in cardiac output, which is independent of cardiac innervation3,5, may also be a consequence of a reduction of sympathetic activity resulting in a dilatation of capacitance vessels and a decreased venous return, although non-neural mechanisms may well be involved.