Mm Hg In Arteries Research Articles

Examination of resistance of various methods of pulmonary vessel occlusion to hydrostatic pressure

ObjectiveThe aim of this study was to compare pressure resistance of the most common methods of vessel occlusion during thoracic surgical procedures: ligations, clips, and vascular endostaplers.MethodsPulmonary vessels were obtained during routine thoracic surgeries. A ball-tipped cannula was inserted through an opening in the side wall and secured with a linen ligature from slipping out. Subsequently, saline was infused into the vessel. We recorded the pressure on which a leakage occurred.ResultsA total of 65 vessels, divided between 3 groups, were enrolled in the study. In the endostaplers group, median bursting pressures were 262.5 mmHg and 300 mmHg for arteries and veins, respectively. In the case of clips, it was over 750 mmHg in both types of the vessels. The same results were observed in the ligation group. Minimal bursting pressures in endostapler occlusion were 187.5 mmHg and 225 mmHg in arteries and veins, respectively. In the case of clips, it was 600 mmHg for arteries and 675 mmHg for veins. A total of 525 mmHg (arteries) and 750 mmHg (veins) were the minimal leaking values observed in vessels occluded with ligations. Comparative analysis showed statistically significant differences in endostapler-clips and endostapler-ligations pairs (p < 0.001). There were no differences between clips and ligations.ConclusionsThe examined methods are capable of occluding pulmonary vessels under physiological conditions. Furthermore, ligations and clips are resistant to pressures highly exceeding physiological values.

Chronic hypoxia induces Rho kinase-dependent myogenic tone in small pulmonary arteries

Myogenic tone in the pulmonary vasculature of normoxic adult animals is minimal or nonexistent. Whereas chronic hypoxia (CH) increases basal tone in pulmonary arteries, it is unclear if a portion of this elevated tone is due to development of myogenicity. Since basal arterial RhoA activity and Rho kinase (ROK) expression are augmented by CH, we hypothesized that CH elicits myogenic reactivity in pulmonary arteries through ROK-dependent vascular smooth muscle (VSM) Ca(2+) sensitization. To test this hypothesis, we assessed the contribution of ROK to basal tone and pressure-induced vasoconstriction in endothelium-disrupted pulmonary arteries [50-300 microm inner diameter (ID)] from control and CH [4 wk at 0.5 atmosphere (atm)] rats. Arteries were loaded with fura-2 AM to continuously monitor VSM intracellular Ca(2+) concentration ([Ca(2+)](i)). Basal VSM [Ca(2+)](i) was not different between groups. The ROK inhibitor, HA-1077 (100 nM to 30 microM), caused a concentration-dependent reduction of basal tone in CH arteries but had no effect in control vessels. In contrast, PKC inhibition with GF109203X (1 microM) did not alter basal tone. Furthermore, significant vasoconstriction in response to stepwise increases in intraluminal pressure (5-45 mmHg) was observed at 12, 15, 25, and 35 mmHg in arteries (50-200 microm ID) from CH rats. This myogenic reactivity was abolished by HA-1077 (10 microM) but not by GF109203X. VSM [Ca(2+)](i) was unaltered by HA-1077, GF109203X, or increases in pressure in either group. Myogenicity was not observed in larger vessels (200-300 microm ID). We conclude that CH induces myogenic tone in small pulmonary arteries through ROK-dependent myofilament Ca(2+) sensitization.

Acute and chronic effects of relaxin on vasoactivity, myogenic reactivity and compliance of the rat mesenteric arterial and venous vasculature

We investigated the effect of relaxin on vasodilation, myogenic reactivity, and compliance of small mesenteric arteries and veins. In acute experiments, small (second order) mesenteric arteries and veins from female rats were mounted in a pressure myograph, perfused intraluminally with relaxin, and exposed to incremental increases in intraluminal pressure (20–120 mm Hg for arteries, 2–12 mm Hg for veins). We expressed myogenic reactivity as the ratio of active to passive diameter at each pressure step. In chronic experiments, relaxin was administered to rats (4 μg/h) for 3 days prior to isolating the vessels and measuring myogenic reactivity. Arteries were more sensitive than were veins to the acute vasodilatory activity of relaxin (EC 50: arteries = 1.32 ± 0.18 × 10 − 8 M; veins = 3.19 ± 0.88 × 10 − 8 M, P < 0.05). Acute relaxin reduced myogenic reactivity of mesenteric arteries, but not veins. Chronic pretreatment with relaxin did alter the pressure/diameter relationship in Ca 2+-containing medium, but this was due to increased passive compliance (control: 2.96 ± 0.14 μm mm Hg − 1 , n = 5; relaxin: 3.72 ± 0.16 μm mm Hg − 1 , n = 5) rather than to reduced myogenic reactivity. Chronic relaxin did not alter myogenic reactivity or compliance (control: 43.8 ± 1.4 μm mm Hg − 1 , n = 5; relaxin: 46.1 ± 2.3 μm mm Hg − 1 , n = 5) of veins. Thus, although relaxin reduces total peripheral resistance, it does not affect splanchnic venous capacitance or tone. In the face of elevated plasma relaxin levels, such as during pregnancy, cardiac preload may thus be maintained, concurrent with a reduction in cardiac afterload and blood pressure. We caution that, if an experimental treatment alters compliance, myogenic reactivity must be expressed as the ratio of active : passive diameter.

Contribution of 20-HETE to Augmented Myogenic Constriction in Coronary Arteries of Endothelial NO Synthase Knockout Mice

Previous studies suggested an important role for 20-HETE in the regulation of myogenic responses. Thus, pressure-diameter relationships were investigated in isolated, cannulated coronary arteries (approximately 100 microm) from male endothelial NO synthase knockout (eNOS-KO) and wild-type (WT) mice. All arteries constricted in response to step increases in perfusate pressure from 20 to 100 mm Hg. This constriction was significantly enhanced from 40 to 100 mm Hg in arteries of eNOS-KO compared with those of WT mice. For example, at 60 and 100 mm Hg, respectively, the normalized diameter (expressed as a percentage of the corresponding passive diameter) of arteries of eNOS-KO mice was 10% and 12% smaller than that of WT mice. Removal of the endothelium did not significantly affect the responses of vessels from either strain of mice. However, N-methylsulfonyl-12,12-dibromododec-11-enamide (5x10(-6) M), an inhibitor of cytochrome P-450 (CYP)/omega-hydroxylase, significantly attenuated the greater myogenic constriction of arteries from eNOS-KO mice by approximately 12% at each pressure step but did not significantly affect responses of those from WT mice, leading to a comparable myogenic response in the 2 strains. Western blot analysis demonstrated a comparable CYP4A protein content in coronary arteries of the 2 strains of mice. However, production of 20-HETE, measured by fluorescent high-performance liquid chromatography assay was approximately 2.7-fold greater in eNOS-KO compared to WT mice. Thus, as a function of eNOS deficiency, the enhanced coronary artery constriction to pressure is attributable to an increased activity of omega-hydroxylase, which, consequently, increases the synthesis of 20-HETE in vascular smooth muscle.

Endothelial dysfunction in uterine circulation in preeclampsia: Can estrogens improve it?

Objective: The purpose of this study was to evaluate whether a 3-hour incubation with 17β-estradiol will enhance blood flow- and bradykinin-mediated dilatation and alter pressure-induced basal tone in myometrial resistance arteries from women with preeclampsia and to evaluate the role of nitric oxide in the responses that were observed. Study Design: Blood flow- and bradykinin-mediated dilatation and responses to intraluminal pressure of 60 and 80 mm Hg were compared before and after 3 hours of incubation with 17β-estradiol (10−8 mol/L) in isolated myometrial arteries with the pressure myography technique. In separate experiments, the role of nitric oxide on 17β-estradiol-induced responses was evaluated in the presence of the nitric oxide synthase inhibitor (10−4 mol/L). Endothelial morphologic condition was evaluated by scanning electron microscopy. Results: Incubation with 17β-estradiol significantly improved blood flow-mediated dilatation compared with initial blood flow-mediated response in arteries from women with preeclampsia. This effect was nitric oxide mediated, because the nitric oxide synthase inhibitor abolished the response. Arteries from women with preeclampsia demonstrated impaired bradykinin-mediated dilatation compared with that obtained in arteries from normal pregnant women. The 17β-estradiol had no effect on bradykinin-mediated dilatation in arteries from women with preeclampsia. The enhanced pressure-induced tone at 80 mm Hg compared with the tone that developed at 60 mm Hg in arteries from women with preeclampsia was reduced after incubation with 17β-estradiol. This reduction was also nitric oxide mediated. Morphologic signs of endothelial dysfunction were evident in arteries from women with preeclampsia. Conclusion: The 17β-estradiol improved impaired blood flow-mediated dilatation and reduced basal tone through a nitric oxide-mediated pathway in isolated myometrial arteries from women with preeclampsia. (Am J Obstet Gynecol 2002;187:1608-16.)

Chronic cerebral arterial spasm. The role of intracranial pressure.

The author used isolated rabbit common carotid and femoral arteries perfused at a constant pressure of 90 mm Hg to examine the variation of flow (F) with transmural pressure (TMP). When the TMP was reduced below 50 to 60 mm Hg in arteries with normal smooth muscle tone, arterial resistance increased significantly causing a reduction in flow. It is suggested that the diffuse arterial narrowing that occurs in patients with severe intracranial hypertension may be the result of a similar reduction in TMP. In the presence of active vasoconstriction, any increase in extraluminal (intracranial) pressure (ICP) resulted in a substantial increase in arterial resistance and subsequent reduction of flow. This F-TMP relationship depended only on the initial degree of constriction and was independent of the vasoconstrictor used to achieve this constriction and of the artery in which this constriction was produced. A review of the literature suggests that human cerebral arteries normally exhibit only mild constrictions in response to subarachnoid blood during the chronic phase of spasm. In the present study, a mild constriction in the absence of increased ICP or a moderate increase in ICP (45 mm Hg) in the absence of constriction produced minor reductions in arterial diameter and an average flow reduction of only 5% to 10%. However, when ICP was increased to 45 mm Hg in the presence of a mild constriction, severe arterial narrowing resulted and flow was reduced by 50%. Therefore, it is suggested that chronic arterial spasm is the result of a mild constriction which is amplified by the simultaneous occurrence of increased ICP. Phenoxybenzamine was found to be effective in reversing and preventing these contractions. The improvement in flow produced by phenoxybenzamine decreased as the TMP was reduced below 60 mm Hg. The effects of both diffuse and local spasm on cerebral blood flow are discussed.