Biomedical subjects

S Bertuglia

Publications and source records attributed to S Bertuglia.

At least 19 recordsLinked to original sources

PubMed2006

Polyethylene glycol and a novel developed polyethylene glycol-nitric oxide normalize arteriolar response and oxidative stress in ischemia-reperfusion.

Polyethylene glycol (PEG) has been shown to repair cell membranes and, thus, inhibit free radical production in in vitro and in vivo models. We hypothesized that PEG and newly developed organic nitrate forms of PEG (PEG-NO) could repair endothelial dysfunction in ischemia-reperfusion (I/R) injury in the hamster cheek pouch visualized by intravital fluorescent microscopy. After treatments, we evaluated diameter and RBC velocity and flow in arterioles, as well as lipid peroxides in the systemic blood, perfused capillary length, vascular permeability, leukocyte adhesion, and amount of von Willebrand factor (vWF) in the blood after I/R injury. A control group was treated with 5,000- or 10,000-Da PEG, and three groups were treated with PG1 (1 NO molecule covalently bound to PEG, 5,170 Da), PG8 (8 NO molecules covalently bound to PEG, 11,860 Da), and PG16 (16 NO molecules covalently bound to PEG, 14,060 Da). All animals received 0.5 mg/0.5 ml. Lipid peroxides increased at 5 and 15 min of reperfusion, whereas diameter, RBC velocity, and blood flow decreased in arterioles after I/R injury. Vascular permeability, leukocyte adhesion, and vWF increased significantly. PEG and PG1 attenuated lipid peroxides and vasoconstriction during reperfusion and decreased leukocyte adhesion and vascular permeability. PG8 maintained lipid peroxides at normal levels, increased arteriolar diameter, flow, and perfused capillary length, and decreased vWF level and leukocyte adhesion (P < 0.05). PG16 was less effective than PG1 and PG8. In conclusion, PEG-NO shows promise as a compound that protects microvascular perfusion by normalizing the balance between NO level and excessive production of free radicals in endothelial cells during I/R injury.

Animals↗

PubMed2005

Generalised wavelet analysis of cutaneous flowmotion during post-occlusive reactive hyperaemia in patients with peripheral arterial obstructive disease.

The purpose of the present study was to assess whether the generalised wavelet analysis (GWA) of the leg cutaneous laser Doppler (LD) flowmotion waves recorded during baseline (Bsl) and after skin post-occlusive hyperaemia (POH) can provide information on the leg cutaneous microcirculatory adaptation to stage II peripheral arterial obstructive disease (PAOD). With this aim the flowmotion was characterised in 20 healthy subjects (HS) and 20 stage II PAOD patients by GWA of LDF tracings during Bsl and POH test. The vascular endothelial and smooth muscle function was also evaluated exploring the arm skin vasodilatory response to iontophoretically delivered acetylcholine (Ach) and sodium nitroprusside (SNP) using LD. During Bsl there was no significant difference in leg skin perfusion between HS and PAOD patients (7.3+/-5.6 vs. 5.8+/-2.9 AU, respectively). PAOD patients revealed higher peak powers in the frequency interval of 0.007-0.02 Hz (120+/-82 vs. 85+/-62 AU(2)/Hz; P < 0.05), 0.02-0.06 Hz (116+/-128 vs. 63+/-48 AU(2)/Hz, respectively; P < 0.05) and 0.06-0.2 Hz (39+/-49 vs. 14+/-10 AU(2)/Hz; P < 0.05). These flowmotion frequencies are related to vascular endothelium activity, sympathetic activity and vessel wall myogenic activity, respectively. During POH the mean peak power of the flowmotion waves increased significantly (P < 0.05) in HS respect to Bsl with the only exception of the 0.02-0.06 Hz band. In the PAOD patients, compared to Bsl the amplitude of the flowmotion waves did not significantly change during POH. In addition, the PAOD patients presented an increased time from release to peak-flux (18.25+/-15.5 vs. 2.16+/-1.28 s, respectively; P < 0.05), an increased time from release to recovery of the basal perfusion (90.26+/-39.14 vs. 26.55+/-14.05 s, respectively; P < 0.05) and a lower slope of the POH curve (10+/-15 vs. 54+/-17 degrees , respectively; P < 0.05), compared with HS. The cutaneous arm vasodilatory response to Ach and to SNP was reduced in PAOD patients in comparison with HS (P < 0.001). In conclusion, our findings showed an increased amplitude of the frequency interval 0.007-0.02, 0.02-0.06 and 0.06-0.2 Hz during Bsl in PAOD patients which did not change during the POH test. All data suggest that in stage II PAOD patients the leg skin perfusion is not impaired during Bsl because of a compensatory mechanism related to increased endothelial, myogenic and sympathetic activities. However during reactive hyperaemia these mechanisms appear to be exhausted in accordance with the reduced vasoreactivity to Ach and SNP.

Acetylcholine↗

PubMed2004

Effects of diagnostic cardiac ultrasound on oxygen free radical production and microvascular perfusion during ischemia reperfusion.

Diagnostic ultrasound (US) is reported to increase intracellular oxidative stress in vitro. Increased oxidative stress mediated ischemia-reperfusion injury in the microcirculation. To examine the effects of US in hamster cheek pouch microcirculation during baseline and ischemia and reperfusion (I/R), I/R injury was provoked in the cheek pouch under "sham" (transducer off, group 1) and active US irradiation (group 2) at baseline (15 min) and at the beginning (15 min) of the reperfusion after ischemia (30 min). US transmission was delivered in the harmonic mode (2.5 MHz) with 1.3 mechanical index (MI) and 2.0 peak negative pressure. Microvascular damage was evaluated by measuring arterial diameter, red blood cell velocity, wall shear stress, permeability, perfused capillary length and adherent leukocytes in venules. Lipid peroxides were determined in the systemic blood. US increased permeability (baseline: 0.04 +/- 0.02; after US 0.30 +/- 0.04, p < 0.01) and slightly decreased capillary perfusion by 7% during baseline (p < 0.01). Arteriolar diameter (35 +/- 7 microm vs. 20 +/- 5 microm, p < 0.05), RBC velocity (2.8 +/- 0.4 mm s(-1) vs. 0.75 +/- 0.05 mm s(-1), p < 0.05) and shear stress ( 0.76 +/- 0.09 Pa vs. 0.36 +/- 0.05 Pa, p < 0.05) decreased significantly after reperfusion. These parameters increased by 40, 64 and 33%, respectively after US. Leukocyte adhesion decreased by 31 % (p < 0.05) after US and lipid peroxides decreased by 26% and 51% during baseline and 15 min of reperfusion after US, respectively. In conclusion, diagnostic US increased microvascular permeability during baseline and reperfusion. Moreover, US enhanced wall shear stress and reduced oxidative stress during postischemic reperfusion; thus, increasing capillary perfusion.

Animals↗

PubMed2003

Microvascular oxygenation, oxidative stress, NO suppression and superoxide dismutase during postischemic reperfusion.

Increased formation of reactive oxygen species (ROS) on reperfusion after ischemia underlies ischemia-reperfusion (I/R) damage. We measured, in real time, oxygen tension in both microvessels and tissue and oxidant stress during postischemic reperfusion in the hamster cheek pouch microcirculation. We measured Po2 by using phosphorescence quenching microscopy and ROS production in the systemic blood. We evaluated the effects of a nitric oxide synthase inhibitor (NG-monomethyl-L-arginine, L-NMMA) and SOD on the oxidative stress during reperfusion. Microvascular injury was assessed by measuring diameter change, the perfused capillary length (PCL), and leukocyte adhesion. During early reperfusion, arteriolar Po2 was significantly lower than baseline, whereas capillary Po2 varied between 7 and 0 mmHg. Arterial blood flow did not regain baseline values, whereas Po2 returned to baseline in arterioles and tissue after 30 min of reperfusion. During 5 and 15 min of reperfusion, ROS increased by 72 and 89% versus baseline, respectively, and declined to baseline after 30 min of reperfusion. Pretreatment with SOD maintained ROS at normal levels, increased arteriolar diameter, blood flow, and PCL, and decreased leukocyte adhesion (P < 0.05). L-NMMA decreased ROS only within 5 min of reperfusion, which increased significantly by 72% later during reperfusion. L-NMMA worsened leukocyte adhesion (P < 0.05). In conclusion, our results show that the early reperfusion is characterized by low Po2 linked to increased production of ROS. At early reperfusion both SOD and L-NMMA decreased ROS production, whereas only SOD reduced it during later reperfusion. We suggest that low-flow hypoxia profoundly affects vascular endothelial damage during reperfusion through changes in ROS and nitric oxide production.

Animals↗

PubMed2002

Protective effect of ketoprofen lysine salt on interleukin-1beta and bradykinin induced inflammatory changes in hamster cheek pouch microcirculation.

OBJECTIVE: The purpose of this study was to assess the efficacy of topically applied ketoprofen lysine salt (KLS), a cyclooxygenase inhibitor, against the inflammatory changes induced by interleukin-1beta (IL-1beta) and bradykinin (BK) in hamster cheek pouch microcirculation. In addition, we characterised the pharmacological regulation of IL-1beta activity in this model. MATERIALS AND METHODS: Male Syrian hamsters were used. Microcirculation was visualised by fluorescent microscopy. Leukocyte adhesion, permeability, perfused capillary length (PCL) and capillary red blood cell (RBC) velocity were evaluated. TREATMENTS: KLS (25 microg/ml/min to 1.6 mg/ml/min) was topically applied for 3 min before topically administered IL-1beta (1microg/ml) and BK (10(-4) M). Monoclonal anti-mouse IL-1beta receptor antagonist (200 ng/ml), BK-B2 receptor antagonist (10(-6) M), PAF inhibitor (10(-5) M) and cycloheximide (10 microg/ml) were added topically 15, 10, 15 and 60 min, respectively, before IL-1beta (1 microg/ml). RESULTS: IL-1beta caused a significant increase in microvascular permeability, a decrease in capillary RBC velocity followed by increased leukocyte adhesion in postcapillary venules. BK caused a marked increase in leukocyte adhesion and no decrease in PCL and RBC velocity. Treatment with KLS significantly inhibited both the leukocyte adhesion and microvascular leakage induced by the two mediators. The inflammatory effects induced by IL-1beta were reduced by blockade of IL-1beta receptors and by a BK-B2 receptor antagonist but were not affected by a PAF antagonist and protein synthesis inhibition. CONCLUSIONS: These results demonstrate that KLS is effective in preventing early inflammatory changes induced by both IL-1beta and BK in the capillary network. Prostaglandin release and BK are essential components for IL-beta mediated responses, whereas neither PAF nor new protein synthesis appear to be linked to the early inflammatory changes induced by IL-1beta.

Animals↗

PubMed2001

Phentolamine suppresses the increase in arteriolar vasomotion frequency due to systemic hypoxia in hamster skeletal muscle microcirculation.

Systemic hypoxia (8%, 11% and 15% oxygen gas mixture inspiration) has been shown to increase the frequency of arteriolar rhythmic diameter changes in hamster skeletal muscle microcirculation. The effects of phentolamine on vasomotion frequency during systemic hypoxia were studied in Syrian hamsters implanted with a plastic chamber in the dorsum skin. Phentolamine (50 microg/100 g body wt.) was injected intravenously before the 20-min exposure to 11% oxygen gas mixture. The microvessels were studied with a fluorescent microscopy technique, using fluorescein isothiocyanate bound to dextran (mol. wt. 150,000) as a tracer. Vessel diameters were measured with a shearing method. Fourier transform and autoregressive modeling were used to assess the time variant features of diameter changes. Under baseline conditions, the arterioles were characterized by rhythmic diameter changes with fundamental frequency related to vessel size. The terminal branchings were dominated by order 3 vessel activity (frequency: 0.08-0.16 Hz) spreading downstream to all daughter arterioles. Systemic hypoxia caused an increase in vasomotion frequency of order 3 arterioles up to 0.3-0.5 Hz (average: 0.40 +/- 0.06 Hz) and a significant decrease in mean diameter (-28 +/- 5%). Phentolamine completely suppressed the rhythmic changes in diameter of order 3 arterioles that dilated significantly (+ 30 +/- 4%). Therefore, the effects of systemic hypoxia on arteriolar vasomotion appear to be triggered by an increase in sympathetic nervous discharge that induces a rise in frequency up to 0.3-0.5 Hz.

Animals↗

PubMed2001

Increased viscosity is protective for arteriolar endothelium and microvascular perfusion during severe hemodilution in hamster cheek pouch.

We hypothesized that during severe hemodilution (SH), i.e., hemodilution beyond 50%, the reduced conditions of shear stress result in endothelium dysfunction and subsequent vasoconstriction. To evaluate the endothelial responses associated with the reduction of hematocrit we tested the responsiveness of arterioles to acetylcholine. Infusion with high-molecular-weight dextran 500,000 following SH was characterized by laser Doppler flowmetry (LDF), total perfused capillary length (TPCL), vessel diameter, and red blood cell (RBC) velocity as visualized by fluorescence microscopy in the hamster cheek pouch. Hemodilution was performed by blood removal and simultaneous infusion of 6% dextran 70. LDF increased significantly during hemodilution in arterioles and in venules (100 +/- 20 vs 37 +/- 11 and 34.2 +/- 3.5 vs 28.6 +/- 4.0 perfusion units, PU, respectively). During the final step of hemodilution LDF decreased significantly to 12 +/- 4.5 PU in arterioles and 6.2 +/- 1.5 PU in venules, which correlated with the decrease of arteriolar RBC velocity. Arterioles constricted and TPCL decreased significantly (-35 +/- 5.3%). Hyperviscosity infusion significantly raised arteriolar and venular LDF to 184 +/- 15 and 40.2 +/- 3.5 PU, arterioles dilated, RBC velocity, TPCL, and mean blood pressure. There was an impairment of endothelial-dependent dilation that was not present in the group with dextran 500, which suggests that viscosity was involved in the development of vasoconstriction during SH. In conclusion, an increase in plasma viscosity has beneficial effects on the microcirculation during SH that might preserve arteriolar endothelium and capillary perfusion.

Animals↗

PubMed2001

Glucose-insulin-potassium treatment in combination with dipyridamole inhibits ischaemia-reperfusion-induced damage.

AIMS/HYPOTHESIS: Treatment with intravenous glucose-insulin-potassium has beneficial effects in reperfused patients, reducing mortality in patients with myocardial infarction by 28 %. We hypothesized that insulin response to glucose-insulin-potassium infusion might lead to vasodilation in ischemia/reperfusion (I/R). Hyperglycaemia and hyperinsulinaemia determine oxidative stress. We therefore investigated the microcirculatory changes following I/R after glucose-insulin-potassium or in association with glucose-insulin-potassium dipyridamole in hamster cheek pouch. METHODS: The control (I/R), glucose-insulin-potassium groups with and without dipyridamole were treated with saline, 300 g/l, 50 U/l insulin and 80 meq/l KCl infused at 0.2 ml. 100 g-1. h-1, and GIK plus dipyridamole (0.084 mg. 100 g-1 intravenously) at beginning, 30 min before ischaemia, and continuing through reperfusion. We measured microvessel diameter changes, arteriolar red blood cell velocity, permeability increase, capillary perfused length, leukocyte and platelet adhesion. RESULTS: Hyperglycaemia and hyperinsulinaemia did not cause vasodilation whereas in the glucose-insulin-potassium group with dipyridamole there was a marked arterial vasodilation with increased red blood cell velocity and perfused capillary length at reperfusion. Glucose-insulin-potassium infusion reversed the arterial vasoconstriction caused by I/R at reperfusion. Adhering leukocytes to venules decreased by 56 and 86 % while platelets adhering to microvessels was reduced by 52 and 72 % at reperfusion in glucose-insulin-potassium groups with and without dipyridamole, respectively. The permeability was decreased by GIK and completely suppressed by GIKD after I/R. Conclusion hypothesis: We demonstrated that GIK, when used in combination with dipyridamole, had beneficial effects on the capillary perfusion against I/R-induced injury. There was a marked reduction of leukocyte and platelet adhesion that can be explained by the antioxidant properties of dipyridamole.

Animals↗

PubMed2000

Protective effects of leukopenia and tissue plasminogen activator in microvascular ischemia-reperfusion injury.

Ischemia shifts the anticoaugulant/procoagulant balance of the endothelium in favor of activation of coagulation. We studied whether cheek pouch microcirculation of leukopenic hamsters was protected by tissue plasminogen activator (tPA) (50 microg/100 g body wt) against ischemia-reperfusion injury. Adherent leukocytes, total perfused capillary length (PCL), permeability increase, and arteriolar and venular red blood cell (RBC) velocity were investigated by fluorescence microscopy. Measurements were made at control, 30 or 60 min of ischemia, and at 30 or 60 min of reperfusion. Hamsters were made leukopenic by treatment with cyclophosphamide (20 mg/100 g body wt ip, 4 days before the experiment), which decreased circulating leukocyte count by 85-90%. Leukopenic hamsters undergoing 30 min of ischemia followed by 30 min of reperfusion showed no significant decrease in PCL or increased permeability. Leukopenic hamsters undergoing 60 min of ischemia followed by 60 min of reperfusion presented a significant decrease in microvascular perfusion where PCL was 28 +/- 7% of baseline, low-flow conditions, and increased permeability. In leukopenic hamsters treated with tPA there was complete protection of capillary perfusion with no significant changes in permeability or arteriolar and venular RBC velocity. In conclusion, thrombus formation may be an additional and independent factor that with leukocyte-mediated mechanisms determines ischemia-reperfusion injury.

Animals↗

PubMed1999

Red blood cell velocity and volumetric flow assessment by enhanced high-resolution laser Doppler imaging in separate vessels of the hamster cheek pouch microcirculation.

An enhanced high-resolution laser Doppler imager (EHR-LDI), configured to fit the demands of a measurement area containing separate microvessels, was evaluated for perfusion measurements in hamster cheek pouch preparations during ischemia, reperfusion, and pharmacologically induced vasodilation and vasoconstriction. Measurements in separate microvessels where the laser beam was smaller than the vessel diameter were referred to as red blood cell (RBC) velocity estimates, as previously validated in vitro, whereas a relative flow index, RFI (mean RBC velocity/tissue area), was introduced as a volumetric flow measure. Microvessel diameter and RBC velocity changes during ischemia, reperfusion, as well as during vasoconstriction and vasodilation correlated to the data obtained from the microscope. Correspondingly, during the described provocations anticipated volumetric flow changes were registered as changes in the RFI. When data on intravessel RBC velocity profiles are presented they reflect a parabolic flow profile usually seen in this size microvessel. The EHR-LDI appears a promising tool for investigation of the microvasculature, as it almost simultaneously provides information on relative changes of both in vivo RBC velocity and volumetric flow (RFI), although the latter estimate needs to be further refined.

Adenosine↗

PubMed1999

Time-variant spectral analysis of LDF signals on the basis of multivariate autoregressive modelling.

Time-variant AR-modelling was used to analyse the non-stationary properties of LDF signals during provocation tests. The procedure for the estimation of time-varying AR parameters based on Kalman filtering is presented. The estimates can be used to calculate instantaneous measures, such as peak frequency, spectral band power and coherence. The resulting course of instantaneous peak frequency of a sinusoidal signal with frequency jump was compared to similar parameters derived from short-time FFT and Hilbert transformation. Univariate time-variant spectral analysis was used to investigate LDF measurements in patients with Raynaud's phenomena. The experimental protocol was splitted into phases of different room temperature. The results demonstrate time-dependent variations of spectral components (amplitude and frequency). By means of time-variant coherence analysis of LDF and diameter measurements of vessels in a hamster skin fold the existence of a main rhythm around 0.1 Hz in the LDF signals which is related to vasomotion is shown.

Algorithms↗

PubMed1999

Different flowmotion patterns in healthy controls and patients with Raynaud's phenomenon.

Flowmotion was characterized in healthy controls and 61 Raynaud's phenomenon (RP) patients by spectral analysis of laser-Doppler perfusion monitoring (LDPM) tracings. Healthy subjects flowmotion patterns revealed a main frequency of 3 cycles per min (cpm) with another low frequency and heart rate synchronous components. A first group of RP patients presented a low frequency and heart rate frequency component but no significant difference in blood flow. The second group presented the predominating heart rate related frequency with low microvascular perfusion. The third group presented a flowmotion pattern with overlapping of heart rate and low frequency components. Patients with primary and secondary RP show specific changes in flowmotion, probably related to increased sympathetic nervous activity or vessel wall alterations causing disappearance of arteriolar tone and impairment of microvascular perfusion. The group of patients with overlapping frequency components presents an intermediate flowmotion pattern indicating a different grade of alterations in microvasculature.

Adolescent↗

PubMed1998

Capillary density and leukocyte adhesion in hamsters with hereditary cardiomyopathy.

The aim of this study was to characterize microvascular networks in cheek pouch of cardiomyopathic Syrian hamster (CM) (Bio 14.6), which is an interesting model of idiopathic cardiomyopathy and congestive heart failure. Microcirculation was visualized by fluorescence microscopy. Diameter and length of arterioles, classified according to centrifugal ordering scheme, were measured. A computational method was arranged to determine the density of arterioles and capillaries (total vessel length per unit area, cm-1), fractal dimension of capillaries, and the associated Voronoi tesselation. Furthermore, leukocyte adhesion to venules and arteriolar reactivity to drugs were studied. Increase in the number of terminal arterioles and capillary rarefication characterized CM microvasculature compared with that of age-matched controls (58 +/- 7 versus 25 +/- 5 cm-1, and 128 +/- 15 versus 240 +/- 10 cm-1, respectively). Fractal dimension of capillaries was reduced in CM compared with controls (1. 40 +/- 0.10 versus 1.85 +/- 0.09) and associated with increased avascular spaces, as shown by Voronoi tesselation results. Leukocyte adhesion to venules increased significantly in CM. In CM responsiveness of arterioles to nitric oxide inhibition and propranolol was slighter but more marked to norepinephrine and angiotensin II compared with that of control hamsters. In conclusion, the different geometry, increased leukocyte adhesion, and altered arterial responsiveness may contribute to flow disturbances in the microcirculation of CM hamsters.

Animals↗

PubMed1998

Evaluation of enhanced high-resolution laser Doppler imaging in an in vitro tube model with the aim of assessing blood flow in separate microvessels.

An enhanced high-resolution laser Doppler imaging (EHR-LDI) technique intended for visualization of separate microvessels was evaluated by use of in vitro flow models. In EHR-LDI, a laser beam focused to a half-power diameter less than 40 microm successively scans the tissue under study in steps of 25 microm. Spatial blood flow variations within microvascular structures of 1.5 x 1.5 mm are rendered by 64 x 64 measurement sites. Individual microvessel diameters could be estimated and an average difference of 11 microm compared to microscopic measurements was obtained. For the flow algorithm used, the LDI output signal was found to scale linearly with average velocity (0-3.5 mm/s) when a plastic tube of inner diameter 175 microm was perfused with human blood (correlation coefficient 0.99). The LDI output signal was further found insensitive to hematocrit variations in the range 16-44%. Due to the limited laser light penetration in blood, a reduction in the LDI output signal was observed as the inner tube diameters were successively changed from 280 to 1400 microm.

Animals↗

PubMed1998

Vasomotion and blood flow regulation in hamster skeletal muscle microcirculation: A theoretical and experimental study.

A mathematical model of a microvasculature was used to study the effects of myogenic and flow-dependent stimuli on the characteristics of vasomotion and microvascular perfusion regulation. The model includes three branching orders of arterioles derived from in vivo observations and incorporates a mechanism for terminal arteriolar closure during vasomotion. Simulations were performed to evaluate the effect of vasodilation and vasoconstriction on vasomotion pattern, and the changes in arteriolar effective diameter and flow in response to arterial blood pressure variations triggering the regulatory mechanisms. Vasomotion patterns were studied in the hamster cutaneous muscle, visualized by fluorescent microscopy, in control conditions and after injection of acetylcholine (Ach) or NG-monomethyl-L-arginine (L-NMMA). We have found that vasomotion may be caused by different combinations of feedback mechanisms, including a strong rate-dependent myogenic response or a strong flow-dependent mechanism with no rate-dependent response. Decreasing the rate-dependent component of the myogenic mechanism and increasing the time constant of the flow-dependent mechanism causes vessel stabilization and disappearance of vasomotion. In hamster microcirculation, Ach decreased vasomotion frequency and increased vasomotion amplitude and arteriolar effective diameter, whereas L-NMMA caused a slight increase in vasomotion frequency and decrease in effective diameter. Model simulations, under dilatory and constrictory stimuli, confirmed these results. Moreover, the model predicted that mean blood flow is maintained closer to normal despite arterial pressure changes (+/-15% flow changes versus +/-50% pressure variations) when the vessels were in nonoscillatory than when they are in oscillatory state. In conclusion, a large variety of vasomotion patterns affect arteriolar resistance and microvessel perfusion in skeletal muscle. Furthermore, in the presence of vasomotion the network exhibits a poorer aptitude for regulating blood flow during arterial pressure changes (i.e., worse autoregulation) than the nonoscillatory network.

Animals↗

PubMed1997

Venular oscillatory flow during hemorrhagic shock and NO inhibition in hamster cheek pouch microcirculation.

Blood flow oscillations (flowmotion) during hemorrhagic shock (HS) were recorded with laser Doppler perfusion monitoring (LDPM) and red blood cell (RBC) velocimetry in arterioles and venules in hamster cheek pouch microcirculation. Experiments were carried out after baroceptor denervation or inhibition of nitric oxide (NO) synthesis with NG-monomethyl-L-arginine prior to and during HS. Flowmotion was characterized by spectral analysis with fast Fourier transform and autoregressive modeling. Low frequency flowmotion was detected in LDPM and RBC velocity tracings derived from arterioles while high frequency oscillations dominated in venules under baseline conditions. Venular blood flow was significantly higher compared with arteriolar flow during HS, while large amplitude low frequency flowmotion was found in venules but not in arterioles where dominated small amplitude high frequency oscillations coincident with respiratory or heart rates. Baroceptor denervation did not affect venular blood flow and low frequency flowmotion during HS. NO inhibition reduced significantly venular blood flow compared with control and abolished low frequency flowmotion in venules. High frequency oscillations remained in arterioles during HS. In conclusion, LDPM low frequency flowmotion was not originated by variations in the diameter of vessels, but corresponded to RBC velocity changes. A compensatory higher blood flow and concomitant low frequency flowmotion in venules appeared to be related to NO production during HS, independently of neural mechanism.

Animals↗

PubMed1996

Theoretical analysis of complex oscillations in multibranched microvascular networks.

A mathematical model was used to study the origin of complex self-sustained diameter oscillations in multibranched microvascular networks. The model includes three branching levels (order 3, 2, and 1 arterioles) of a microvascular network derived from in vivo observation in the hamster dorsal cutaneous muscle. The main biomechanical aspects covered by the model are (1) the dependence of the elastic and active wall stress on the inner radius and (2) the static and dynamic myogenic response. Simulations on isolated arterioles indicate that self-sustained periodic diameter oscillations may occur at constant transmural pressure. Conversely, simulations on the entire network reveal different oscillatory patterns, including periodic, quasiperiodic, and chaotic fluctuations. Chaos in the model is revealed by the presence of a broad noise-like component in the frequency spectrum and by the sensitivity dependence of model results on small perturbations. Our results suggest that, owing to the intrinsic nonlinearity of the system, a contracting mechanism, such as the myogenic response, may induce different oscillatory patterns. The change from periodic to chaotic oscillations may be a consequence of a modest variation in a parameter (systemic pressure or arterial resistance) not necessarily related to pathophysiological conditions. Accordingly, our in vivo observations in the skeletal muscle showed that in some instances arteriolar vasomotion is converted from regular to highly irregular patterns in basal conditions. Vasomotion is found to affect mean blood flow compared with the nonoscillatory steady state. Chaotic oscillations tend to maintain a constant ratio of blood flows entering into bifurcation vessels, whereas periodic vasomotion determines a different flow distribution at branches.

Animals↗

PubMed1996

Dynamic coherence analysis of vasomotion and flow motion in skeletal muscle microcirculation.

The aim of our study was to determine the cause of fluctuations in microvascular blood flow measured by laser Doppler perfusion monitoring (LDPM) in microvessels of the hamster skin fold preparation. LDPM flow fluctuations (flow motion) were compared to simultaneous records of diameter changes obtained from arterioles and venules. Time-varying coherence analysis was used to quantify the frequency of flow and diameter changes in awake hamsters in control conditions and during sodium nitroprusside-induced vasodilation. Power spectrum analysis of LDPM signals of order 4 and 3 arterioles indicated frequencies of 0.06 +/- 0.01 and 0.08 +/- 0.02 Hz, respectively. Order 3 arterioles exhibited significant temporal coherence between flow motion and vasomotion signals at a frequency of the order of 0.1 Hz. There was lack of coherence when vasomotion was absent in arterioles. Order 4 arterioles had several coherent frequencies in addition to that around 0.1 Hz. In conclusion, time-variant coherence analysis indicated that spontaneous fluctuations in flow are caused by vasomotion of order 3 arterioles with frequency around 0.1 Hz that appears to coordinate local control processes in the microcirculation. Additional frequency components present in LDPM signals are unrelated to vasomotion.

Animals↗