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Vascular Pressure (vascular + pressure)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	50%

Selected Abstracts

Functional morphology of the gills of the shortfin mako, Isurus oxyrinchus, a lamnid shark

JOURNAL OF MORPHOLOGY, Issue 8 2010
Nicholas C. Wegner
Abstract This study examines the functional gill morphology of the shortfin mako, Isurus oxyrinchus, to determine the extent to which its gill structure is convergent with that of tunas for specializations required to increase gas exchange and withstand the forceful branchial flow induced by ram ventilation. Mako gill structure is also compared to that of the blue shark, Prionace glauca, an epipelagic species with lower metabolic requirements and a reduced dependence on fast, continuous swimming to ventilate the gills. The gill surface area of the mako is about one-half that of a comparably sized tuna, but more than twice that of the blue shark and other nonlamnid shark species. Mako gills are also distinguished from those of other sharks by shorter diffusion distances and a more fully developed diagonal blood-flow pattern through the gill lamellae, which is similar to that found in tunas. Although the mako lacks the filament and lamellar fusions of tunas and other ram-ventilating teleosts, its gill filaments are stiffened by the elasmobranch interbranchial septum, and the lamellae appear to be stabilized by one to two vascular sacs that protrude from the lamellar surface and abut sacs of adjacent lamellae. Vasoactive agents and changes in vascular pressure potentially influence sac size, consequently effecting lamellar rigidity and both the volume and speed of water through the interlamellar channels. However, vascular sacs also occur in the blue shark, and no other structural elements of the mako gill appear specialized for ram ventilation. Rather, the basic elasmobranch gill design and pattern of branchial circulation are both conserved. Despite specializations that increase mako gill area and efficacy relative to other sharks, the basic features of the elasmobranch gill design appear to have limited selection for a larger gill surface area, and this may ultimately constrain mako aerobic performance in comparison to tunas. J. Morphol. 271:937,948, 2010. © 2010 Wiley-Liss, Inc. [source]

Evidence that the human cutaneous venoarteriolar response is not mediated by adrenergic mechanisms

THE JOURNAL OF PHYSIOLOGY, Issue 2 2002
C. G. Crandall
The venoarteriolar response causes vasoconstriction to skin and muscle via local mechanisms secondary to venous congestion. The purpose of this project was to investigate whether this response occurs through ,-adrenergic mechanisms. In supine individuals, forearm skin blood flow was monitored via laser-Doppler flowmetry over sites following local administration of terazosin (,1 -antagonist), yohimbine (,2 -antagonist), phentolamine (non-selective ,-antagonist) and bretylium tosylate (inhibits neurotransmission of adrenergic nerves) via intradermal microdialysis or intradermal injection. In addition, skin blood flow was monitored over an area of forearm skin that was locally anaesthetized via application of EMLA (2.5 % lidocaine (lignocaine) and 2.5 % prilocaine) cream. Skin blood flow was also monitored over adjacent sites that received the vehicle for the specified drug. Each trial was performed on a minimum of seven subjects and on separate days. The venoarteriolar response was engaged by lowering the subject's arm from heart level such that the sites of skin blood flow measurement were 34 ± 1 cm below the heart. The arm remained in this position for 2 min. Selective and non-selective ,-adrenoceptor antagonism and presynaptic inhibition of adrenergic neurotransmission did not abolish the venoarteriolar response. However, local anaesthesia blocked the venoarteriolar response without altering ,-adrenergic mediated vasoconstriction. These data suggest that the venoarteriolar response does not occur through adrenergic mechanisms as previously reported. Rather, the venoarteriolar response may due to myogenic mechanisms associated with changes in vascular pressure or is mediated by a non-adrenergic, but neurally mediated, local mechanism. [source]

Clenbuterol administration does not attenuate the exercise-induced pulmonary arterial, capillary or venous hypertension in strenuously exercising Thoroughbred horses

EQUINE VETERINARY JOURNAL, Issue 6 2000
M. MANOHAR
Summary The present study was carried out to ascertain whether ,2 -adrenergic receptor stimulation with clenbuterol would attenuate the pulmonary arterial, capillary and venous hypertension in horses performing high-intensity exercise and, in turn, modify the occurrence of exercise-induced pulmonary haemorrhage (EIPH). Experiments were carried out on 6 healthy, sound, exercise-trained Thoroughbred horses. All horses were studied in the control (no medications) and the clenbuterol (0.8 ,g/kg bwt, i.v.) treatments. The sequence of these treatments was randomised for every horse, and 7 days were allowed between them. Using catheter-tip-transducers whose in-vivo signals were referenced at the point of the left shoulder, right heart/pulmonary vascular pressures were determined at rest, sub-maximal exercise and during galloping at 14.2 m/s on a 3.5% uphill grade - a workload that elicited maximal heart rate and induced EIPH in all horses. In the control experiments, incremental exercise resulted in progressive significant increments in right atrial as well as pulmonary arterial, capillary and venous (wedge) pressures and all horses experienced EIPH. Clenbuterol administration to standing horses caused tachycardia, but significant changes in mean right atrial or pulmonary vascular pressures were not observed. During exercise performed after clenbuterol administration, heart rate as well as right atrial and pulmonary arterial, capillary and wedge pressures also increased progressively with increasing work intensity. However, these values were not found to be statistically significantly different from corresponding data in the control study and the incidence of EIPH remained unaffected. Since clenbuterol administration also does not affect the transpulmonary pressure during exercise, it is unlikely that the transmural force exerted onto the blood-gas barrier of exercising horses is altered following i.v. clenbuterol administration at the recommended dosage. [source]

Stroke volume of the heart and thoracic fluid content during head-up and head-down tilt in humans

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2005
J. J. Van Lieshout
Background:, The stroke volume (SV) of the heart depends on the diastolic volume but, for the intact organism, central pressures are applied widely to express the filling of the heart. Methods:, This study evaluates the interdependence of SV and thoracic electrical admittance of thoracic fluid content (TA) vs. the central venous (CVP), mean pulmonary artery (MPAP) and pulmonary artery wedge (PAWP) pressures during head-up (HUT) and head-down (HDT) tilt in nine healthy humans. Results:, From the supine position to 20° HDT, SV [112 ± 18 ml; mean ± standard deviation (SD)], TA (30.8 ± 7.1 mS) and CVP (3.6 ± 0.9 mmHg) did not change significantly, whereas MPAP (from 13.9 ± 2.7 to 16.1 ± 2.5 mmHg) and PAWP (from 8.8 ± 3.4 to 11.3 ± 2.5 mmHg; P < 0.05) increased. Conversely, during 70° HUT, SV (to 65 ± 24 ml) decreased, together with CVP (to 0.9 ± 1.4 mmHg; P < 0.001), MPAP (to 9.3 ± 3.8 mmHg; P < 0.01), PAWP (to 0.7 ± 3.3 mmHg; P < 0.001) and TA (to 26.7 ± 6.8 mS; P < 0.01). However, from 20 to 50 min of HUT, SV decreased further (to 48 ± 21 ml; P < 0.001), whereas the central pressures did not change significantly. Conclusions:, During both HUT and HDT, SV of the heart changed with the thoracic fluid content rather than with the central vascular pressures. These findings confirm that the function of the heart relates to its volume rather than to its so-called filling pressures. [source]