Ograniczanie wyników

Czasopisma help
Autorzy help
Lata help
Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 21

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych:  arterial blood pressure
help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
Lipińska S., Szkudlarek U., Traczyk W. Z.: Hypophysial portal blood flow during preganglionic stimulation of the superior cervical ganglion under condition of systemic arterial blood pressure stabilization in rat. Acta Physiol. Pol. 1990, 41(1-3): 53-61. The presence of hypothalamic hormones in the pituitary portal blood is regarded as the principal factor by which the hypothalamus controls pituitary secretion. In contrast to numerous investigations on hypothalamic hormone release, the regulation of the hypophysial-portal blood flow (HPBF) has been scarcely studied. Hypophysial-portal vessels were exposed according to the Worthington’s method [1966]. The 10-min blood samples were collected before and during unilateral or alternative bilateral electrical stimulation of the preganglionic fibers of the superior cervical ganglia (SCG). During blood samples collection the stable systemic arterial blood pressure was maintained by a barostat. The HPBF was estimated according to the determination of the hemoglobin in samples of washed and collected blood from the cut pituitary portal vessels. The mean HPBF was 3.5 μ /min. Electrical stimulation of SCG. did not change HPBF. This indicates that sympathetic efferents do not participate in the regulation of HPBF under conditions of stabilization of the systemic arterial blood pressure.
The respiratory effects of stimulation of adenosine A1 receptors were studied in spontaneously breathing rats that were either (1) neurally intact and subsequently bilaterally vagotomized in the neck, or (2) neurally intact and subjected to supranodosal vagotomy or (3) midcervically vagotomized before and after pharmacological blockade of A1 receptors. Before neural interventions an intravenous bolus of the A1 receptor agonist N6-cyclopentyladenosine (CPA, 5 µg kg-1) decreased breathing rate, tidal volume, mean arterial blood pressure (MAP) and heart rate. After section of the midcervical vagi, CPA still decreased respiratory rate and tidal volume. Supranodose vagotomy abolished the fall in respiratory rate but did not affect the depression of tidal volume. Blockade of A1 receptors with intravenous doses of DPCPX (100 µg kg-1) eliminated all respiratory effects of CPA challenge. In all the neural states, CPA caused significant falls in mean arterial blood pressure and heart rate. DPCPX pre-treatment prevented these cardiovascular effects. The present data suggest that: (1) CPA-evoked activation of A1 receptors decreases breathing rate and tidal volume and this occurs central to the cervical vagi; (2) supranodosal vagotomy prevents the decrease in breathing rate, which is presumably due to stimulation of nodosal A1 receptor; and (3) depression of tidal volume and the hypotensive response result from the excitation of central nervous A1 expressing neurones.
Different types of adaptation of the cardiovascular system to the gravitational forces (hypokinetic and hyperkinetic) have been described in the healthy and the sick subjects under resting conditions. The aim of the present study was to elucidate whether haemodynamic responses to the dynamic exercise performed under various gravitational conditions are determined by the type of adaptation of the cardiovascular system to the gravitational forces at rest. The study was performed on 249 healthy men, 20-60 years old. To assess the type of regulation of the cardiovascular system arterial blood pressure (MABP), heart rate (HR), stroke volume (SV), cardiac output (CO), and systolic function (SF) of the heart were determined in each subject at rest in the upright (orthostatic state) and in the supine position. Subsequently, the subjects were performing exercise on a cycloergometer in the sitting and the supine position. Four gradually increasing workloads were applied. Measurements of HR, MABP, SV, CO, and SF were repeated at the end of each workload. SV, CO and SF were determined by means of rheography. The results revealed that in the individuals showing at rest the hypokinetic type of orthostatic cardiovascular adaptation the augmentation of CO during exercise in the sitting position was caused by significant increases of HR and SV. In contrast, the subjects with the hyperkinetic type of orthostatic adaptation the increase in CO during exercise in the sitting position was much smaller and resulted predominantly from acceleration of HR. It is concluded that the cardiovascular adaptation to the dynamic exercise depends not only on the position of the body in which the exercise is performed but it is also determined by the type of adaptation of the cardiovascular system to the gravitational forces at rest. In the sitting position the pumping capacity of the heart is significantly greater in the hypokinetic than in the hyperkinetic type of the cardiovascular regulation; this relationship being reversed during exercise in the horizontal position.
Rhythm and conductivity disturbances in heart muscle, change in autonomic system function and raised arterial blood pressure have been described in workers exposed to lead. They may be accompanied by changes in echocardiography test and accordingly we undertook this investigation. The study population included employees of zinc and lead steelworks in the south of Poland that were divided into 2 groups: exposed to lead compounds (n=88) and the reference group - administration workers (n=55) with normal levels of lead concentration in blood (PbB) and zinc protoporphyrin in blood. Left ventricular enddiastolic dimension (LVDd), interventricular septal and posterior wall thickness, right ventricular diastolic, left atrium diameter, aortic diameter and left ventricular ejection fraction (EF) in echocardiograms were performed. Left ventricular mass LVM (g) and left ventricular mass index LVMI (g/m2) was calculated. In the group exposed to lead, EF decreased by 3%, increased LVDd by 6%, and raised LVM by 11% and LVMI by 10%. There was a positive relation between PbB and LVDd (R=0.18) and between PbB and LVM (R=0.14). Decreased EF, enlargement of the left ventricle and raised left ventricle mass in research undertaken, may be a result of raised arterial blood tension.
12
Content available remote

Specific features and roles of renal circulation: angiotensin II revisited

67%
The status of intrarenal circulation determines in part renal excretion, affects body fluid homeostasis and has a role in long term control of arterial blood pressure. The vascular resistance in the renal cortex and medulla is determined by interaction of a vast array of vasoactive hormones and paracrine factors; among these the role of constrictor angiotensin II and dilator prostaglandins and nitric oxide may appear to be dominating. The focus of this review and underlying studies is on the mechanisms whereby the microcirculation of the renal medulla is protected against the vasoconstrictor action of angiotensin II. In anaesthetized normal rats the three mentioned active agents or their inhibitors were applied and total renal blood flow and cortical, outer- and inner medullary laser-Doppler fluxes were determined; in some studies renal tissue nitric oxide was measured using selective electrodes. We conclude that angiotensin II, acting via AT1 receptors, constricts the renal cortical vasculature; in the medulla its action is effectively buffered by prostaglandin E2 but most probably not by nitric oxide.
Calcilytics, antagonists of calcium receptor, decrease sensitivity of this receptor to plasma calcium concentration and increase parathyroid hormone (PTH) secretion. Moreover, it was recently indicated that calcilytic NPS 2143 induces hypertension in rats. This study tested whether the increase of mean arterial blood pressure (MAP) induced by NPS 2143 administration is mediated by calcium channel and angiotensin II type1 (AT1) receptor activity. Wistar rats were anaesthesized with Thiopental i.p. and infused i.v. with saline supplemented with the anaesthetic. Blood pressure was monitored continuously in the carotid artery. Effects of NPS 2143 administered i.v. as bolus on MAP in the presence and absence of felodypine and losartan were investigated. Both, felodipine and losartan pretreatment provoked a persistent MAP decrease by 18±3 and 14±3 mmHg, respectively. Infusion of NPS 2143 at 1 mg/kg b.w. confirmed hypertensive activity of calcilytic and increased blood pressure for 21±4 mmHg. In contrast, administration of NPS 2143 in felodipine as well as in losartan pretreated rats did not change MAP as compared to felodipine/control and losartan/control groups, respectively. Our study indicated that both the blockade of calcium channels and the AT1 receptor activity prevented the hypertensive effect of calcilytic NPS 2143. This finding might be particularly important in understanding the mechanisms that mediated blood pressure changes related to the activity of calcium receptor.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.