Biomedical subjects

F Bari

Publications and source records attributed to F Bari.

35 records · Page 2Linked to original sources

PubMed1996

Global ischemia impairs ATP-sensitive K+ channel function in cerebral arterioles in piglets.

BACKGROUND AND PURPOSE: Indirect evidence from studies in which calcitonin gene-related peptide was used indicates that anoxic stress suppresses functioning of cerebral vascular ATP-sensitive K+ channels. The purpose of this study was to directly examine effects of total global ischemia on cerebral arteriolar dilator responses to activators of ATP-sensitive K+ channels. METHODS: We measured pial arteriolar diameters in anesthetized piglets using a closed cranial window and intravital microscopy. Baseline diameters were approximately 100 microns. Arteriolar responses to aprikalim (10(-8) and 10(-6) mol/L), a pharmacological activator of ATP-sensitive K+ channels, and iloprost (0.1 and 1 microgram/mL), a physiological activator of these channels, were determined before and 1, 2, and 4 hours after a 10-minute period of total global ischemia. Ischemia was caused by increasing intracranial pressure. RESULTS: Before ischemia, aprikalim dilated cerebral arterioles by 7 +/- 2% at 10(-8) mol/L and by 25 +/- 4% at 10(-6) mol/L (n = 5). At 1 hour after ischemia, aprikalim did not cause significant dilation at either dose (3 +/- 2% at 10(-8) mol/L and 7 +/- 4% at 10(-6) mol/L; P < .05 compared with corresponding preischemic response). Arteriolar dilation returned toward normal values at 2 and 4 hours. Similar results were found with iloprost. Furthermore, prior treatment with indomethacin (5 mg/kg) preserved normal arteriolar dilation to aprikalim and iloprost after ischemia. In contrast, arteriolar dilator responses to prostaglandin E2 were intact after ischemia. CONCLUSIONS: Ischemia transiently eliminates cerebral arteriolar dilation to activation of ATP-sensitive K+ channels; arteriolar responses are suppressed at 1 hour and return toward normal over 2 to 4 hours. In addition, reduced responsiveness can be prevented by prior treatment with indomethacin.

Adenosine Triphosphate↗

PubMed1996

Differential effects of short-term hypoxia and hypercapnia on N-methyl-D-aspartate-induced cerebral vasodilatation in piglets.

BACKGROUND AND PURPOSE: Recent studies in piglets show that either asphyxia or global cerebral ischemia, which combines effects of hypoxia and hypercapnia, transiently attenuates N-methyl-D-aspartate (NMDA)-induced pial arteriolar dilation. The purpose of this study was to determine individually the effects of hypoxic hypoxia and normoxic hypercapnia on NMDA-dependent cerebrovascular reactivity. In addition, we examined mechanisms involved in reduced cerebral vascular dilation to NMDA. METHODS: In anesthetized piglets, we examined pial arteriolar diameters using a cranial window and intravital microscopy. Arteriolar responses to topically applied NMDA were determined under control conditions and after arterial hypoxia or arterial hypercapnia. In addition, arteriolar responses to NMDA were examined in animals given indomethacin (10 mg/kg IV) or superoxide dismutase (100 U/mL, topical application) before hypoxia. RESULTS: Under control conditions, application of NMDA produced a dose-related dilation of pial arterioles (eg, 9 +/- 1% to 10(-5), 15 +/- 2% to 5 x 10(-5), and 28 +/- 5% to 10(-4) mol/L NMDA above baseline, respectively, in the hypoxic group; n = 6, P < .05). After transient exposure to 15 minutes of hypoxic hypoxia, arteriolar responses to NMDA were reduced at 30 minutes and at 60 minutes (10(-4) mol/L NMDA dilated by 12 +/- 5% and 18 +/- 5%, respectively; n = 6, P < .05). Five minutes of hypoxic hypoxia also reduced dilatation to NMDA. Indomethacin or superoxide dismutase preserved arteriolar responses to NMDA after 15 minutes of hypoxia. Pial arteriolar responses to NMDA remained unimpaired during and after hypercapnia. CONCLUSIONS: Short-term severe hypoxic hypoxia and reventilation impair the NMDA-induced dilatation of pial arterioles. Respiratory acidosis alone does not modify pial arteriolar reactivity to NMDA. The reduced responsiveness of the cerebral blood vessels to NMDA caused by hypoxia appears to be due to action of oxygen radicals.

Acute Disease↗

PubMed1996

Induction of cyclooxygenase-2 following anoxic stress in piglet cerebral arteries.

OBJECTIVE: Ischemic stress causes damage to cerebrovascular endothelium and alters arteriolar responses to prostanoid-dependent stimuli. However, effects of ischemic stress on cyclooxygenase (COX) levels in endothelium are unclear. We examined the effect of ischemia and reperfusion and asphyxia and reventilation on production of COX isoforms in cerebral vascular endothelium. METHODS: Neonatal pigs were exposed to global ischemia (n = 4) or asphyxia (n = 3) for 5-10 min. Following 2-6 h of recovery, the animals were killed, and the cerebral arteries and arterioles were removed. Cerebral arteries and arterioles were also removed from untreated control animals (n = 1) and from time control animals (n = 3). Cerebral vessels were fixed in 4% formalin and paraffin embedded, and constitutive and inducible COX (COX-1 and COX-2, respectively) levels were assessed using indirect immunofluorescence. RESULTS: Hemotoxylin and eosin staining indicated that anoxic stress leads to enlargement of endothelial cells. Immunofluorescence for COX-1 in endothelium was minimal in cerebral arteries and arterioles from control animals and did not show an increase in animals exposed to anoxic stress. Similarly, cerebral vessels from control animals showed little immunostaining for COX-2. In contrast, immunofluorescence for COX-2 was greatly increased in cerebral arteries and arterioles from animals exposed to asphyxia or ischemia. CONCLUSIONS: We concluded that anoxic stress increases COX-2 but not COX-1 levels in cerebral endothelium.

Animals↗

PubMed1994

Ruthenium red antagonism of capsaicin-induced vascular changes in the rat nasal mucosa.

Mechanisms of capsaicin-induced vascular changes were examined in the nasal mucosa of anesthetized adult rats. Intra-arterial infusions of capsaicin at doses of 20-100 pmol/min into the external carotid artery resulted in a dose-dependent increase in nasal blood flow as assessed by laser-Doppler flowmetry. Intra-arterial infusion of ruthenium red (RR, 2.5-10 mumol) prior to the administration of capsaicin significantly inhibited the capsaicin-evoked response. The technique of vascular labelling was used to examine nasal mucosal vascular permeability. Intravenous administration of colloidal silver solution prior to capsaicin infusion resulted in accumulation of colloid in the walls of small blood vessels, indicative of enhanced vascular permeability. Vascular labelling was largely abolished after RR pretreatment. These findings suggest that neuropeptides released from trigeminal sensory nerve endings play a significant role in the local vascular and inflammatory reactions of the nasal mucosa. The experimental approach utilized in this study provides a promising model for defining the roles of capsaicin-sensitive afferent nerves in the mechanisms of allergic and/or inflammatory diseases affecting the nasal mucosa.

Animals↗

PubMed1994

Possible involvement of capsaicin-sensitive sensory nerves in the regulation of cochlear blood flow in the guinea pig.

Capsaicin-induced microcirculatory changes in the cochlea of anaesthetized guinea pigs were examined by laser-Doppler flowmetry. Close intraarterial capsaicin infusion into the anterior inferior cerebral artery at doses of 10-50 pmol/min was followed by dose-dependent vasodilatation. Capsaicin infused in a dose of 150-200 pmol/min or above resulted in vasoconstriction in the region examined. Topical capsaicin administration into the cochlea (50-150 pmol) resulted in very moderate vasodilation with a latency of 1-2 min. Perivascular capsaicin application onto the anterior inferior cerebellar artery elicited an elevated blood flow in the cochlea, too. It is concluded that the release of vasoactive substances from capsaicin-sensitive nerve fibres in the inner ear of the guinea pig may play a role in the control of the local microcirculation. These nerves may also be involved in the neurogenic inflammatory processes in the region.

Animals↗

PubMed1994

The measurement of cardiac output in dogs by impedance cardiography with different electrode arrangements.

This study was performed to compare cardiac output (CO) values determined by means of impedance cardiography (ICG) with the conventional four-band electrode array and with different spot electrode arrays in anaesthetised dogs. CO values determined at end-expiratory apnoea with hand-calculation (ICG1) and during several respiratory cycles with a computer program (ICG2) were compared with values obtained via simultaneous thermodilution (TD) measurements. Changes in CO during isoproterenol infusion, bleeding and reinfusion were also studied by means of ICG1, using one of the spot electrode arrays and TD. Band voltage electrodes yielded a significantly lower CO, whereas spot electrodes on the left thorax gave a significantly higher CO than that measured with TD. In spite of the high correlation coefficients in the different electrodes arrays, the bias between ICG1 and TD, and that between ICG2 and TD CO in the SL1-SL8 and BN-BX electrode arrays showed differences statistically significant from zero. The percentage changes in CO measured with ICG1 in the SN-SX electrode array and TD during isoproterenol infusion, bleeding and reinfusion also showed a high correlation. These results indicate that band voltage electrodes can be replaced by the more convenient spot electrodes in certain arrays. Further CO may be measured during several respiratory cycles by using a computer program. Thus, ICG is a reproducible, non-invasive method for the measurement of CO in anaesthetised dogs.

Animals↗

PubMed1993

Lack of short-term autoregulation in the cochlear microcirculation in guinea pigs.

To determine the relationship between the dynamics of mean arterial blood pressure (MABP) elevation and possible changes in the cochlear microcirculation the cochlear blood flow (CBF) was measured in guinea pigs by a laser Doppler method. The MABP was elevated at rates ranging from 0.02 mmHg/s to 4 mmHg/s by intravenous infusions of norepinephrine or epinephrine in various concentrations. A fall in MABP was induced by exsanguination of the animals. The purpose of the experiments was to record the time of onset and course of an expected autoregulation in the cochlea in response to slow or rapid changes in MABP. The data suggest that there is no short-term autoregulation in the cochlear microcirculation reflecting the increase of the MABP, but a slight compensation occurs when the MABP declines. These latter changes could be attributed to the high CO2 sensitivity of the cochlear blood vessels.

Animals↗

PubMed1993

Dexmedetomidine-induced decrease in cerebral blood flow is attenuated by verapamil in rats: a laser Doppler study.

This study was performed to examine the changes in local cortical blood flow (CoBF) after simultaneous administration of an alpha 2 adrenergic agonist (dexmedetomidine) and a calcium channel antagonist (verapamil) to urethane-anaesthetized rats. Dexmedetomidine (100 micrograms.kg-1) given intraperitoneally alone resulted in decreases in mean arterial blood pressure (MABP) (F[27,140] = 3.43; P < 0.01) and CoBF (F[27,140] = 4.22; P < 0.01), whereas the heart rate (HR) was increased (F[27,140] = 2.33; P < 0.01). Verapamil (2.5 mg.kg-1) given subcutaneously reduced the MABP (F[27,140] = 3.41; P < 0.01), but the HR and CoBF were not changed. Combined administration of the drugs decreased MAPB (F[27,140] = 5.37; P < 0.01), with no changes in CoBF and HR. The present data indicate that the calcium channel antagonist verapamil did not potentiate the haemodynamic effects of dexmedetomidine in rats, but rather attenuated the effect of dexmedetomidine on CoBF. This favourable interaction suggests a potential therapeutic role of these agents in maintaining cardiovascular stability during surgical interventions.

Adrenergic alpha-Agonists↗

PubMed1993

Significance of the rate of systemic change in blood pressure on the short-term autoregulatory response in normotensive and spontaneously hypertensive rats.

Cerebral autoregulation, the physiological regulatory mechanism that maintains a constant cerebral blood flow (CBF) over wide ranges of arterial blood pressure, was investigated in normotensive and spontaneously hypertensive rats by means of laser-Doppler flowmetry. Systemic arterial hypertension was produced at rates ranging from 0.02 mm Hg/second to 11 mm Hg/second by constant infusion of epinephrine and norepinephrine. Systemic arterial hypotension was produced at rates ranging from -0.03 mm Hg/second to -12 mm Hg/second, either by bleeding the animals into a reservoir or by compressing the abdomen. In those cases with a low rate of change in systemic arterial blood pressure (SABP), the measurements lasted for 5 +/- 2 minutes, and in those with a high rate of change in SABP, measurements lasted for 40 +/- 30 seconds. The purpose was to record the time of onset and course of autoregulation in the basal ganglia in response to slow or rapid changes in SABP. CBF in the basal gray matter remained at baseline values (i.e., autoregulation was functioning) if the rate of increase of SABP did not exceed a critical value (0.10 mm Hg/second in the normotensive rats; 0.35 mm Hg/second in the spontaneously hypertensive rats). When hypertension was produced at faster rates, CBF followed arterial blood pressure passively, and no autoregulatory response was observed for 2 +/- 1 minutes. Hypotension did not change the baseline CBF when it was not produced at a rate faster than -0.4 mm Hg/second in normotensive rats and -0.15 mm Hg/second in spontaneously hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1982

Elevation of thermoregulatory vasodilatation threshold in the rat after capsaicin treatment.

In control and capsaicin-treated (300 mg/kg) rats tail skin vasodilatation was studied while the body temperature was raised to 38 degrees C, 39 degrees C or 40 degrees C and held at these levels. In the capsaicin-treated rats, at 38 degrees C vasodilatation was weaker than in the controls but at temperatures of 39 degrees C and 40 degrees C a delayed increase in tail vasodilatation occurred to the level observed in the controls. It is concluded that the threshold of vasodilatation response to heat is elevated after capsaicin treatment.

Animals↗

PubMed1981

Analysis of ultradian sleep rhythms in rats, using stage transition functions.

To analyse intrinsic sleep rhythms, transition probability functions were calculated from rat hypnograms. The method can be regarded as a generalization of Globus' binary autocorrelation analysis of sleep periodicity. It is useful for studying the construction of sleep cycles. The main advantage of the method is its insensitivity to random disturbances.

Animals↗

PubMedDate not supplied

Histamine responsiveness of the various vascular beds of facial and nasal tissues in the dog.

The effects of the close arterial infusion of histamine upon the microcirculation of facial and nasal tissues were examined in dogs. Blood flow through arteriovenous anastomoses (AVA flow), capillaries (CAP flow) and collaterals (COL flow) were determined by electromagnetic flowmetry and the tracer-microsphere technique following an infusion of histamine at doses ranging from 0.5 to 50 nmol/min. Low doses of histamine (0.5-5.0 nmol/min) resulted in an increase in blood flow through the ipsilateral internal maxillary artery (IMA), which could be mainly attributed to a significant elevation of the CAP flow. A concomitant marked increase in AVA flow was observed only after the administration of higher doses (20-50 nmol/min). Significant changes in systemic blood pressure, heart rate and cardiac output occurred only after the infusion of histamine at doses of 20 and 50 nmol/min. Significant increases in the CAP flow of tissues with relatively low perfusion were observed after the infusion of histamine at lower doses. The CAP flow of structures which play an essential role in conditioning the inspired air and exhibit high perfusion rates under control conditions exhibited significant increases only after the administration of higher doses. The present experiments provide direct evidence for a dose-dependent vasodilatory effect of histamine on different microcirculatory compartments of cutaneous and mucosal vascular beds supplied by the IMA in the dog. The results indicate that at low blood histamine levels, an increase in CAP flow predominates, and at higher doses, both elevated CAP flow and elevated AVA flow contribute to the vasodilatory response to histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Circulatory effects caused by intra-arterial infusion of AMP, ADP and ATP in the canine facial and nasal vascular beds.

The effects of the intra-arterial infusion of ATP, ADP and AMP into the internal maxillary artery (IMA), which provides the blood supply to the nasal and forehead regions of the dog, were analyzed. Total blood flow and perfusion pressure measurements in the IMA after administration of each adenyl compound indicated dose-dependent and active vasodilatory responses that were restricted to the ipsilateral vessels. The rank order of potency was ADP > or = ATP > AMP. In order to determine the microcirculatory effects caused by ADP, the tracer microsphere technique combined with absolute blood flow measurement was used. Intra-arterial infusion of ADP in the range 1-200 nmol/min produced elevations in the IMA flow on the stimulated side that ranged between 11 and 74%. The responses to low doses of ADP were mainly confined to the capillaries (CAP), whereas the arteriovenous anastomoses too were sensitive to high doses. The relative contributions of the anatomically and functionally different compartments of the forehead and nose to ADP-produced relaxations of the CAP were dependent upon their location. The CAP flows in the tissues which play a crucial role in conditioning the inspired air increased significantly, while the compartments of the furred surfaces were less sensitive to ADP. The results suggest that, since ATP, ADP and AMP are effective vasodilatory agents in all the regions examined, purines could have a regulatory or modulatory role in the complex vascular regulation of the nasal and forehead regions.

Adenosine Diphosphate↗

PubMedDate not supplied

Influence of hypoxia/ischemia on cerebrovascular responses to oxytocin in piglets.

We examined the effects of hypoxic/ischemic stress on cerebral arteriolar responses to oxytocin in anesthetized piglets. Pial arteriolar diameters were measured using a cranial window and intravital microscopy. First, we evaluated arteriolar responses to topical application of oxytocin during normoxic conditions. We then determined whether 5-10 min of arterial hypoxia, ischemia, or asphyxia alters oxytocin-induced responses. Arterial hypoxia was produced by inhalation of 7.5% O2-92.5% N2 for 10 min. Ischemia was achieved by increasing intracranial pressure for 10 min. Asphyxia was achieved by turning off the ventilator for 5 min. During normoxic conditions, oxytocin dilated pial arterioles by 9 +/- 1% at 10(-8) and by 16 +/- 1% at 10(-6) mol/l (n = 47, p < 0.05). Arteriolar responses to oxytocin did not change with repeated applications (n = 10). Following hypoxia, dilator effect of oxytocin was not changed at 10(-8) (8 +/- 2%) but it was reduced at 10(-6) mol/l (7 +/- 2%; p < 0.05, n = 8). After asphyxia or ischemia, oxytocin did not dilate arterioles at 10(-8) mol/l, whereas 10(-6) mol/l resulted in a mild vasoconstriction (-4 +/- 3 to -6 +/- 4%, n = 6 and 8). Topically applied superoxide dismutase did not preserve arteriolar responses to oxytocin after asphyxia although the arterioles did not constrict to 10(-6) mol/l oxytocin (n = 5). Dilatation of cerebral arterioles in response to oxytocin was reversed to constriction by N(omega)-nitro-L-arginine methyl ester (L-NAME) (15 mg/kg, i.v.; n = 5) and by endothelial impairment by intra-arterial infusion of phorbol ester (10[-5] mol/l; n = 5). We conclude that the absence of pial arteriolar dilation to oxytocin after ischemia and asphyxia indicates endothelial dysfunction which may be involved in the pathology of perinatal brain injury.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMedDate not supplied

Effects of calcium channel blockers on cold-induced vasodilatation and elevated sympathetic tone in the canine internal maxillary artery bed.

This study was concerned with the interactive effects of cold-induced vasodilatation, blockade of voltage-sensitive Ca2+ channels and sympathetic nerve stimulation in the nasal vascular bed of anesthetized dogs. To estimate the distribution of the internal maxillary artery blood flow to capillaries and to arteriovenous anastomoses (AVA), the microsphere technique in combination with electromagnetic flowmetry was used. Intraarterial infusion of verapamil resulted in a dose-dependent vasodilatation and a redistribution of the internal maxillary artery blood flow. Simultaneously applied electrical stimulation of the cervical sympathetic trunk resulted in a significant fall in blood flow, caused mainly by a decrease in capillary flow. Verapamil infusion combined with cold exposure led to a simultaneous elevation of the AVA and capillary flows. When electrical stimulation of the cervical sympathetic trunk was also applied, the AVA and capillary flows were affected in different manners, depending on the sequence of the stimulations. Analysis of capillary flow data in the various nasal and facial tissue compartments indicates that cold exposure, blockade of the voltage-dependent Ca2+ channels and an elevated sympathetic tone modify the local nutritive blood flow.

Animals↗

PubMedDate not supplied

Isometric handgrip exercise-induced muscarinic vasodilation in the human skin microvasculature.

The existence of an active vasodilator system in the human skin microvasculature is well documented, but its physiological role and the underlying mechanisms are not completely understood. Cutaneous blood flow increases during isometric handgrip exercise. To examine whether this response is mediated by active vasodilation, isometric handgrip exercise testing was performed in nine healthy subjects. Local iontophoresis of atropine was applied to the forearm skin. Skin blood flow (SBF) monitoring by means of laser Doppler flowmetry was combined with continuous noninvasive blood pressure monitoring. SBF monitoring was performed at a site pretreated with atropine and an adjacent control area. Mean arterial pressure (MAP) was recorded noninvasively. Cutaneous vascular resistance (CVR) was calculated as MAP/SBF for the atropine treated and the control areas. Changes in CVR were expressed as percent deviation from the baseline (dCVR). Isometric handgrip exercise resulted in a marked reduction in CVR at the control site (dCVR: -66 +/- 4%). In contrast, the CVR was not significantly altered at the atropinetreated site (2.4 +/- 7%). It is concluded that isometric exercise induces an atropine-sensitive vasodilation which is mediated by muscarinic receptors in the human skin.

Adult↗

PubMedDate not supplied

Short-term monitoring of the vascular resistance of the human skin microvasculature.

OBJECTIVE AND METHOD: Laser Doppler flowmetry is a non-invasive tool in assessing the temporary changes of skin microcirculation. Another non-invasive equipment the Finapres 2300 finger blood pressure monitor provides a continuous blood pressure signal. The combination of the two devices allows short-term monitoring of the changes in the resistance of skin microvasculature. In order to assess the role of skin blood vessels in physiological responses to complex reflex tests Valsalva manoeuvre was performed by 12 healthy volunteers. For comparison a thermal stimulation (cold pressor) test was also done. RESULTS: The two tests resulted in skin blood flow responses of similar magnitude. The changes in calculated regional peripheral resistance (dRPR) indicated that both responses involved active vasoconstrictor mechanisms. It is of importance that the active vasoconstriction could be documented only at the late strain phase (V2) but not in the early strain phase (V1) of the Valsalva manoeuvre (%dRPR in V1 = 0.14 vs. V2 = 0.96, p < 0.05). CONCLUSIONS: In conclusion our findings support the theory that changes in the tone of the skin blood vessels parallel the changes in systemic vasculature in response to complex reflex tests. This is the first report which documents the feasibility of the continuous monitoring of the regional peripheral resistance.

Adolescent↗