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Total Vascular Resistance (total + vascular_resistance)
Selected AbstractsSustained increase in arterial blood pressure and vascular resistance induced by infusion of arachidonic acid in ratsACTA PHYSIOLOGICA, Issue 1 2000Kirkebų The haemodynamic responses to arachidonic acid (AA) have been investigated in seven groups of anaesthetized rats. Sodium arachidonate was infused intravenously for 4 or 20 min, and arterial blood pressure was recorded continuously. Cardiac output and organ blood flow were measured by microspheres. Infusion of arachidonate caused first a fast drop in arterial blood pressure, thereafter it increased steadily for 5,15 min towards a pressure about 25 mmHg above control level. The high pressure was maintained for at least 1 h. Repeated infusions of arachidonate gave similar responses. Inhibition of cyclo-oxygenase by indomethacin prevented the initial pressure drop to arachidonate, but not the sustained increase in pressure. Arterial pressure, total vascular resistance and blood flow in the kidneys, adrenals and spleen were significantly reduced, whereas cardiac output was not changed 4 min after start infusion of arachidonate. However, average blood pressure was significantly increased 22 and 35 min after start infusion (from 103.9 ± 2.9 to 128.1 ± 6.1 and 135.8 ± 4.6 mmHg). Mean vascular resistance increased simultaneously (from 3.5 ± 0.2 to 4.7 ± 0.4 and 5.2 ± 0.4 mmHg 100 mL,1), while cardiac output, stroke volume and heart rate were maintained or slightly reduced. The renal blood flow was significantly lowered (from average 4.9 ± 0.1 to 3.3 ± 0.2 and 4.0 ± 0.2 mL min,1). Indomethacin did not prevent the changes in vascular resistance or organ blood flow recorded after 20,35 min. On the other hand, inhibition of both cyclo-oxygenase, lipoxygenase and the cytochrome P450 pathways by eicosatetrayonic acid (ETYA) normalized all haemodynamic parameters. Likewise, the rise in pressure was prevented by 17-octadecynoic acid (17-ODYA), an inhibitor of the cytochrome P450 enzyme activity. Thus, arachidonate infusion caused a transient decrease, and then a sustained increase in arterial pressure and vascular resistance, and a long-lasting reduction in renal blood flow, possibly owing to release of a cytochrome P450 dependent vasoconstrictor metabolite of AA. [source] Maternal cardiac function and uterine artery Doppler at 11,14 weeks in the prediction of pre-eclampsia in nulliparous womenBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 3 2008A Khaw Objective, To assess maternal cardiac function in nulliparous women in the first trimester of pregnancy and evaluate its potential role for predicting pre-eclampsia and small for gestational age (SGA). Design, Prospective, observational, cross-sectional study. Setting, Maternity unit of a teaching hospital. Population, Nulliparous women with singleton pregnancies presenting consecutively for routine antenatal care (n= 534). Methods, Two-dimensional and M-mode echocardiography and uterine artery Dopplers were carried out at 11-14 weeks. Main outcome measures, Cardiac output (CO), stroke volume (SV), mean arterial pressure (MAP), total vascular resistance and uterine artery pulsatility index (UAPI) were compared in four outcome groups according to the development of pre-eclampsia and/or SGA. Results, Compared with the normal outcome group (n= 457), in those with pre-eclampsia but not SGA (n = 8), CO and MAP were increased; in the group with pre-eclampsia and SGA (n= 19) MAP, TRP and UAPI were increased and in the group with SGA but no pre-eclampsia (n= 50) total peripheral resistance and UAPI were increased. Independent predictors of pre-eclampsia were MAP, SV and UAPI and of SGA SV and UAPI. Conclusions, Alterations in maternal cardiac function and UAPI are observed in the first trimester of pregnancy in nulliparous women that subsequently develop pre-eclampsia and/or SGA. [source] Intrinsic vasomotricity and adrenergic effects in a model of isolated rabbit eyeACTA OPHTHALMOLOGICA, Issue 4 2009Esmeralda Delgado Abstract. Purpose:, We aimed to investigate the responsiveness of the ocular arteries to adrenergic drugs in a model of perfused isolated rabbit eye. Methods:, Rabbit external ophthalmic arteries (n = 15) in a head-mounted preparation were cannulated and the retinal and uveal vasculature perfused at a constant flow with warmed tyrode. The three-way polypropylene catheter was further connected to a pressure transducer and intraluminal pressure was taken as a measure of vascular resistance. Effects of intra-arterial injections of phenylephrine (group A, n = 5), prazosin (group B, n = 5) and phentolamine (group C, n = 5) on the recorded pressure were obtained. Student's paired- t test and one-way analysis of variance were used for statistical analysis (p < 0.05). Results:, Intrinsic vasomotricity was observed in all preparations prior to any drug administration. Phenylephrine produced an increase in total vascular resistance. Intrinsic vasomotricity became more evident, showing a lower frequency but higher amplitude of oscillations. Evoked vasomotor responses with phenylephrine (250 ,g/ml) were inhibited by intra-arterial administration of the selective ,1 -adrenergic antagonist, prazosin (0.5 mg/ml), as well as the non-selective ,-adrenergic antagonist phentolamine (6 mg/ml). Conclusions:, Rabbit external ophthalmic arteries showed spontaneous contractions under constant perfusion. Phenylephrine elicited a vasoconstrictor response that was inhibited by adrenergic antagonists. In addition, the intrinsic vasomotricity was enhanced by phenylephrine and blocked by adrenergic antagonists. These results show that under in vitro perfusion the territory presents similar responses to adrenergic drugs to those observed in in vivo models and also provides evidence of myogenic autoregulatory properties in the rabbit ophthalmic artery and/or choroid. [source] Does caffeine impair cerebral oxygenation and blood flow velocity in preterm infants?ACTA PAEDIATRICA, Issue 9 2010MB Tracy Abstract Aim:, The aim of the study is to assess the effects of an intravenous 10 mg/kg loading dose of caffeine base in cerebral oxygenation, cerebral Doppler blood flow velocity and cardiac output in preterm infants. Methods:, Preterm neonates <34 weeks gestation were investigated at 1 and 4 h following the loading dose of caffeine using Doppler cerebral sonography, cardiac echocardiography and cerebral spatially resolved near-infrared spectroscopy. Results:, Forty infants were studied with a mean gestational age (mean ± standard deviation) of 27.7 (±2.5) weeks, birth weight of 1155 (±431) g and a postnatal age of 2.8 (±2.2) days. Mean Anterior Cerebral Artery peak and time average mean blood flow velocity fell significantly by 14% and 17.7%, respectively at 1 h post-caffeine loading dose, which recovered partially by 4 h. Cerebral Tissue Oxygenation Index fell from pre-dose levels by 9.5% at 1 h with partial recovery to 4.9% reduced at 4 h post-dose. There were no significant changes in left or right ventricular output, transcutaneous oxygen saturation, transcutaneous PCO2 or total vascular resistance. Conclusions:, A loading dose of 10 mg/kg caffeine base resulted in significant reduction at 1 h post-dose in cerebral oxygenation and cerebral blood flow velocity with partial recovery at 4 h. [source] | ||||||||||