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Arteriolar Vasoconstriction (arteriolar + vasoconstriction)
Selected AbstractsRetinal arterioles have impaired reactivity to hyperoxia in type 1 diabetesACTA OPHTHALMOLOGICA, Issue 4 2010Birgitte L. Justesen Abstract. Purpose:, Diabetes has adverse effects on the retinal microvasculature. The purpose of this study was to compare the effects of inhalation of hypoxic, hyperoxic and normoxic,hypercapnic gas mixtures on retinal vessel diameter in people with and without diabetes. Methods:, Sixty-one participants (aged 24,50 years) 29 with (male : female ratio 2.6 : 1) and 32 without (male : female ratio 0.7 : 1) diabetes, inhaled hypoxic, hyperoxic and normoxic,hypercapnic gas mixtures for 3,5 mins. The diameters of arterioles and venules were measured using digital retinal images taken before and after gas inhalation. Results:, There was no significant difference in the diameters of arterioles and venules prior to gas inhalation in people with and without diabetes. Inhalation of the hyperoxic gas mixture caused a statistically significant decrease in arteriolar and venular diameters without altering mean arterial pressure significantly. Arteriolar vasoconstriction in response to the hyperoxic gas mixture was significantly reduced in people with diabetes (3.95% versus 7.75%; p = 0.04), but venular vasoconstriction did not differ significantly. A hypoxic gas mixture caused increased arteriolar and venular diameter and a normoxic,hypercapnic gas mixture had no significant effect on vessel diameter. Responses to hypoxic and normoxic,hypercapnic gas did not differ significantly between diabetes and non-diabetes subjects. Conclusions:, Type 1 diabetes impairs retinal arteriolar responses to hyperoxia. Abnormalities in retinal arteriolar reactivity in response to oxygen may play a role in the development of diabetic retinopathy and this technique may represent a simple means of identifying early abnormalities in the reactivity of retinal arterioles in diabetes. [source] Tubular reabsorption and diabetes-induced glomerular hyperfiltrationACTA PHYSIOLOGICA, Issue 1 2010P. Persson Abstract Elevated glomerular filtration rate (GFR) is a common observation in early diabetes mellitus and closely correlates with the progression of diabetic nephropathy. Hyperfiltration has been explained to be the result of a reduced load of sodium and chloride passing macula densa, secondarily to an increased proximal reabsorption of glucose and sodium by the sodium-glucose co-transporters. This results in an inactivation of the tubuloglomerular feedback (TGF), leading to a reduced afferent arteriolar vasoconstriction and subsequently an increase in GFR. This hypothesis has recently been questioned due to the observation that adenosine A1 -receptor knockout mice, previously shown to lack a functional TGF mechanism, still display a pronounced hyperfiltration when diabetes is induced. Leyssac demonstrated in the 1960s (Acta Physiol Scand58, 1963:236) that GFR and proximal reabsorption can work independently of each other. Furthermore, by the use of micropuncture technique a reduced hydrostatic pressure in Bowman's space or in the proximal tubule of diabetic rats has been observed. A reduced pressure in Bowman's space will increase the pressure gradient over the filtration barrier and can contribute to the development of diabetic hyperfiltration. When inhibiting proximal reabsorption with a carbonic anhydrase inhibitor, GFR decreases and proximal tubular pressure increases. Measuring intratubular pressure allows a sufficient time resolution to reveal that net filtration pressure decreases before TGF is activated which highlights the importance of intratubular pressure as a regulator of GFR. Taken together, these results imply that the reduced intratubular pressure observed in diabetes might be crucial for the development of glomerular hyperfiltration. [source] Effects of hyperbaric oxygen exposure on experimental hepatic ischemia reperfusion injury: Relationship between its timing and neutrophil sequestrationLIVER TRANSPLANTATION, Issue 12 2005Kenji Kihara Recent studies have shown that hyperbaric oxygen therapy (HBOT) reduces neutrophil endothelial adherence in venules and also blocks the progressive arteriolar vasoconstriction associated with ischemia-reperfusion (I-R) injury in the extremities and the brain. In order to elucidate the effects of HBOT after I-R in digestive organs, particularly in the liver, we evaluated the following: 1) the relationship between timing of HBOT and tissue damage; and 2) HBOT's effects on neutrophil sequestration. Using a hepatic I-R (45 minute) model in male rats, survival rate, liver tissue damage, and neutrophil accumulation within the sinusoids in the HBOT-treated group (Group H) were compared to those in the nontreated group (Group C). For the HBOT-treated group, HBOT was administered as 100% oxygen, at 2.5 atm absolute, for 60 minutes. When HBOT was given 30 minute after I-R, the survival rate was much better in Group H than in Group C. HBOT performed within 3 hours of I-R markedly suppressed increases in the malondialdehyde level in tissues of the liver and lessened the congestion in the sinusoids. In addition, HBOT just after I-R caused decreased number of cells stained by the naphthol AS-D chloroacetate esterase infiltrating into the sinusoids. HBOT 3 hours after reperfusion, however, showed no clear effects upon neutrophil sequestration compared to Group C. These results indicate that HBOT performed within 3 hours of I-R alleviates hepatic dysfunction and improves the survival rate after I-R. Herein, we propose 1 possible mechanism for these beneficial effects: early HBOT given before neutrophil-mediated injury phase may suppress the accumulation of neutrophils after I-R. In conclusion, we believe that the present study should lead to an improved understanding of HBOT's potential role in hepatic surgery. (Liver Transpl 2005;11:1574,1580.) [source] Losartan and Ozagrel Reverse Retinal Arteriolar Constriction in Non-Obese Diabetic MiceMICROCIRCULATION, Issue 5 2008Seungjun Lee ABSTRACT Objective: Reductions in retinal blood flow are observed early in diabetes. Venules may influence arteriolar constriction and flow; therefore, we hypothesized that diabetes would induce the constriction of arterioles that are in close proximity to venules, with the constriction mediated by thromboxane and angiotensin II. Methods: Using nonobese diabetic (NOD) mice, retinal measurements were performed three weeks following the age at which glucose levels exceeded 200 mg/dL, with accompanying experiments on age-matched normoglycemic NOD mice. The measurements included retinal arteriolar diameters and red blood cell velocities and were repeated following an injection of the thromboxane synthase inhibitor, ozagrel. Mice were subdivided into equal groups and given drinking water with or without the angiotensin II receptor antagonist, losartan. Results: Retinal arterioles were constricted in hyperglycemic mice, with a significant reduction in flow. However, not all arterioles were equally affected; the vasoconstriction was limited to arterioles that were in closer proximity to venules. The arteriolar vasoconstriction (mean arteriolar diameters = 51 ± 1 vs. 61 ± 1 , m in controls; p < 0.01) was eliminated by both ozagrel (61 ± 2 , m) and losartan (63 ± 2 , m). Conclusions: Venule-dependent arteriolar vasoconstriction in NOD mice is mediated by thromboxane and/or angiotensin II. [source] Inspiration-induced vasoconstrictive responses in dominant versus non-dominant handsCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 2 2005Harvey N. Mayrovitz Summary Single rapid and deep inspirations (inspiratory gasps, IG) result in arteriolar vasoconstriction with concomitant transient decreases in skin blood flow that are most prominent in fingers and toes. Vascular responses (inspiratory gasp responses, IGR) are determined as the maximum percentage reduction in blood flow and have been used to assess sympathetic neurovascular function in several conditions. Previous studies have described various features of the response but there has been no reported systematic investigation of the degree of similarity between IGR obtained on dominant and non-dominant hands. This aspect is important in procedures that may use IGR to evaluate suspected unilateral sympathetic dysfunction of a limb-pair or to test the effectiveness of physiological interventions imposed on a single limb of a pair. Thus, the goal of our study was to compare IGR magnitudes that were simultaneously determined in paired-fingers of dominant and non-dominant hands. In 30 healthy seated subjects, skin blood perfusion via laser-Doppler (SBF) was measured on the dorsum of the middle finger of both hands while subjects performed three sequential IG at 3-min intervals. Analysis of variance for repeated measures revealed no significant difference in IGR between dominant (79·3 ± 11·2%) and non-dominant hands (81·9 ± 11·6%, P = 0·965) with an overall IGR of 80·6 ± 11·4%. These results indicate that hand-dominance is not a factor that is likely to significantly effect IGR differentials determined in paired-limbs. [source] Angiotensin II enhances the afferent arteriolar response to adenosine through increases in cytosolic calciumACTA PHYSIOLOGICA, Issue 4 2009E. Y. Lai Abstract Aims:, Angiotensin II (Ang II) is a strong renal vasoconstrictor and modulates the tubuloglomerular feedback (TGF). We hypothesized that Ang II at low concentrations enhances the vasoconstrictor effect of adenosine (Ado), the mediator of TGF. Methods:, Afferent arterioles of mice were isolated and perfused, and both isotonic contractions and cytosolic calcium transients were measured. Results:, Bolus application of Ang II (10,12 and 10,10 m) induced negligible vasoconstrictions, while Ang II at 10,8 m reduced diameters by 35%. Ang II at 10,12, 10,10 and 10,8 m clearly enhanced the arteriolar response to cumulative applications of Ado (10,11 to 10,4 m). Ado application increased the cytosolic calcium concentrations in the vascular smooth muscle, which were higher at 10,5 m than at 10,8 m. Ang II (10,11 to 10,6 m) also induced concentration-dependent calcium transients, which were attenuated by AT1 receptor inhibition. Simultaneously applied Ang II (10,10 m) additively enhanced the calcium transients induced by 10,8 and 10,5 m Ado. The transients were partly inhibited by AT1 or A1 receptor antagonists, but not significantly by A2 receptor antagonists. Conclusion:, A low dose of Ang II enhances Ado-induced constrictions, partly via AT1 receptor-mediated calcium increase. Ado increases intracellular calcium by acting on A1 but not A2 receptors. The potentiating effect of Ang II on Ado-induced arteriolar vasoconstrictions may involve calcium sensitization of the contractile machinery, as Ang II only additively increased cytosolic calcium concentrations, while its effect on the arteriolar constriction was more than additive. The potentiating effect of Ang II might contribute to the resetting of TGF. [source] | ||||||||||