Biomedical subjects

F Bari

Publications and source records attributed to F Bari.

At least 19 recordsLinked to original sources

PubMed1997

Calcium-activated K+ channels in cerebral arterioles in piglets are resistant to ischemia.

Our previous studies indicate that function of ATP-dependent K+ channels (K(ATP)) in cerebral arterioles is suppressed after ischemia. In the current study, we examined pial arteriolar responses to forskolin, dibutyryl-cAMP, NS-1619, and methionine (met)-enkephalin, activators of calcium-dependent K+ channels (K(Ca)) before and 1 hour after 10 minutes of total, global ischemia in anesthetized piglets. Arteriolar diameters were measured using a closed cranial window and intravital microscopy. All pharmacologic agents were given topically. Baseline diameters were approximately 100 microm, and diameters had returned to normal by 1 hour after ischemia. Forskolin dilated arterioles by 9 +/- 3%, 18 +/- 4%, and 31 +/- 12% at 5 x 10(-8), 5 x 10(-7), and 10(-6) mol/L, respectively (P < 0.05, n = 10). In addition, dibutyryl-cAMP dilated arterioles by 8 +/- 2% at 10(-4) mol/L and 14 +/- 2% at 3 x 10(-4) mol/L (P < 0.05, n = 6). Also, NS-1619 increased diameter of arterioles by 9 +/- 2% at 10(-7) mol/L and 17 +/- 9% at 10(-5) mol/L (P < 0.05, n = 5). Finally, met-enkephalin dilated arterioles by 9 +/- 2% at 10(-8) mol/L and 16 +/- 3% at 10(-6) mol/L (P < 0.05, n = 5). At 1 hour after ischemia, arteriolar dilator effects to forskolin, dibutyryl-cAMP and NS-1619, and met-enkephalin were intact. Thus, in contrast to K(ATP), K(Ca) in cerebral arterioles are resistant to ischemic stress.

Animals↗

PubMed1997

Kainate-induced cerebrovascular dilation is resistant to ischemia in piglets.

BACKGROUND AND PURPOSE: Cerebral arteriolar dilation to N-methyl-D-aspartate (NMDA) is drastically reduced by anoxic stress. The effects of anoxic stress on cerebrovascular dilation to activation of other types of glutamate receptors are unknown. The purpose of this study was to examine the effects of ischemia on cerebral arteriolar responses to kainate in anesthetized piglets. METHODS: Arteriolar responses to 5 x 10(-5) mol/L and 10(-4) mol/L kainate were evaluated before and 10 minutes after total, global ischemia. Ischemia was induced by increasing intracranial pressure. We measured pial arteriolar diameters (approximately 100 microns) using a cranial window and intravital microscopy. RESULTS: Before ischemia, kainate dilated arterioles by 16 +/- 2% at 5 x 10% mol/L and 30 +/- 2% at 10(-4) mol/L (mean +/- SEM; n = 6). After ischemia, the diameter of arterioles increased by 17 +/- 3% and 26 +/- 3% to 5 x 10% and 10(-4) mol/L kainate, respectively (P > .05). We also investigated the mechanisms involved in mediating arteriolar dilation to kainate. Intravenous administration of N omega-nitro-L-arginine methyl ester (L-NAME) (15 mg/kg) (n = 7) or indomethacin (10 mg/kg) (n = 6) individually reduced arteriolar dilation to kainate by approximately one half. Coadministration of L-NAME and indomethacin almost completely eliminated arteriolar dilation to kainate (n = 10). Administration of theophylline (20 mg/kg IV) did not affect dilator responses to kainate (n = 7). Blockade of NMDA receptors by MK801 had minimal effects on arteriolar dilation to kainate (n = 6). CONCLUSIONS: There are three main findings from this study: (1) kainate is a potent dilator agent in the neonatal cerebral circulation; (2) nitric oxide and prostaglandins both participate in the vasodilator response to kainate; and (3) in contrast to NMDA, cerebral arteriolar dilator responses to kainate are resistant to ischemic stress.

Animals↗

PubMed1996

Interaction between ATP-sensitive K+ channels and nitric oxide on pial arterioles in piglets.

The interaction between ATP-sensitive K+ channels (KATP) and nitric oxide (NO) was studied in pial arterioles of piglets. We examined the effects of N omega-nitro-L-arginine methyl ester (L-NAME), a general inhibitor of nitric oxide synthase (NOS), and 7-nitroindazole (7-NI), a selective inhibitor of neuronal NOS, on aprikalim-induced cerebral vasodilation. Topically applied, aprikalim, a selective activator of KATP, dilated arterioles by 11 +/- 7% at 10(-8) M and 17 +/- 6% at 10(-6) M. After L-NAME treatment (15 mg/kg, i.v.), the response was reduced (4 +/- 4% and 12 +/- 7%, respectively; n = 8, p < 0.05). Administration of 7-NI (50 mg/kg, i.p.) did not change pial arteriolar responsiveness to aprikalim. However, both L-NAME and 7-NI reduced the vasodilator responses to 10(-4) M N-methyl-D-aspartate (NMDA) (by 73% and by 36%, respectively). Furthermore, 7-NI treatment abolished the glutamate-induced dilatation of pial arterioles. Administration of L-NAME reduced the NOS activity in the cerebral cortex by 88%, whereas the reduction after the 7-NI treatment was 44%. Pre-treatment and coadministration of 10(-5) M glibenclaminde, a specific inhibitor of KATP or L-NAME administration, did not change the dilatory response to sodium nitroprusside. We conclude that NO may be involved in aprikalim-induced dilation of pial arterioles.

Animals↗

PubMed1996

Effect of nitric oxide synthase inhibition on myocardial contractility in anesthetized normal and endotoxemic dogs.

Nitric oxide (NO) produced by the induced NO synthase (NOS) enzyme has been implicated in the mechanisms of the circulatory changes that occur in the later stages of sepsis. As NO produced by the constitutive form of the enzyme is known to play a role in the regulation of normal circulation, we have performed a series of experiments to study the early circulatory effects of inhibition of NOS in a hyperdynamic endotoxemic dog model. Pentobarbital-anesthetized animals were used. Cardiac output (CO) was measured by thermodilution. Myocardial contractility (MC) was estimated from the slope of the left ventricular end-systolic pressure-diameter relationship obtained from sonomicrometer- and catheter-tip manometer signals in closed chest animals. All animals received a 15 mL/kg/h infusion of Ringer's lactate. A hyperdynamic response was elicited by a 2 h infusion of a total dose of 5.3 micrograms/kg Escherichia coli O55:B5 endotoxin (ETX). CO increased initially by about 25%, and total peripheral resistance decreased by 35%. These changes subsided in 60-90 min, after which a sustained decrease in CO occurred. MC elevated transiently by 25% after the first 30 min of ETX infusion, then decreased gradually below the control level. Administration of 2 mg/kg of the NOS inhibitor N-nitro-L-arginine (NNA) between the 45th and 55th min of the ETX infusion increased MC to the level in the control group, but accelerated the decline of the initially increased CO and caused a sustained increase in total peripheral resistance to about 50% above the control level. In normal (nonendotoxin treated) dogs, NNA also caused a similar increase in MC which, however, lasted at least 3 h. Left ventricular diameter increased in the NNA-treated groups. This increase also occurred in the endotoxin-only group but with a delay of about 2.5 h. Our results demonstrate the participation of constitutive NOS-produced NO in the early hyperdynamic response of endotoxemia. Suppression of NO is associated with increased myocardial contractility. NNA treatment may be favorable for the restoration of depressed cardiac contractility during endotoxemia, but this treatment is probably detrimental for the compensatory systemic flow (CO) increase.

Anesthesia↗

PubMed1996

Effects of ischemia on cerebrovascular responses to N-methyl-D-aspartate in piglets.

We examined the effects of total global ischemia on cerebral arteriolar responses to N-methyl-D-aspartate (NMDA) in anesthetized newborn pigs. Arteriolar responses to 10(-4) M NMDA were determined before and after 10 to 20 min of ischemia caused by increasing intracranial pressure. Before ischemia, NMDA dilated arterioles by 30 +/- 5% (baseline = 88 +/- 2 microns; n = 6). However, after 10 min of ischemia, arteriolar dilation was reduced to 10 +/- 3% at 1 h (P < 0.05). At 2 and 4 h, NMDA-induced dilation was not different from preischemia values. Twenty minutes of ischemia had similar effects. Coadministration of 100 U/ml of superoxide dismutase did not restore arteriolar dilation to NMDA at 1 h after ischemia. Sodium nitroprusside dilated by 14 +/- 3 and 40 +/- 5% at 10(-6) and 10(-5) M before ischemia, respectively, and arteriolar responsiveness was not changed by ischemia (n = 6). Cortical nitric oxide synthase (NOS) activity, measured by the in vitro conversion of L-[14C]arginine to L-[14C]citrulline, was unaffected by ischemia (n = 12). We conclude that decreases in cerebral arteriolar responsiveness to NMDA are not due to impairment of NOS activity, enhanced degradation or chelation of nitric oxide (NO), or reduced vascular smooth muscle responsiveness to NO.

Animals↗

PubMed1996

Ischemia reduces CGRP-induced cerebral vascular dilation in piglets.

BACKGROUND AND PURPOSE: Effects of anoxic stress on cerebrovascular responses to calcitonin gene-related peptide (CGRP) have not been examined previously. We determined the effects of total global ischemia on cerebral arteriolar responses to CGRP in newborn pigs. METHODS: Piglets were anesthetized and ventilated with a respirator. Pial arteriolar diameter was determined using a closed cranial window and intravital microscopy. Baseline arteriolar diameters ranged from 80 to 100 microns. Arteriolar responses to 10(-9) and 10(-8) mmol/L CGRP applied topically 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, CGRP dilated arterioles by 14 +/- 2% (n = 6) and 24 +/- 3% (n = 7) at 10(-9) and 10(-8) mmol/L, respectively. However, after ischemia, arteriolar responses to 10(-9) mmol/L CGRP were reduced at 1 hour to 4 +/- 1%, at 2 hours to 3 +/- 2%, and at 4 hours to 5 +/- 4% (P < .05 for all comparisons). Similarly, arteriolar responses to 10(-8) mmol/L CGRP were reduced to 5 +/- 2% at 1 hour, 5 +/- 2% at 2 hours, and 10 +/- 6% at 4 hours (P < .05 for all comparisons). In time control animals, arteriolar responses to CGRP did not change over time. In other animals, we examined effects of pretreatment with indomethacin (5 mg/kg IV) on ischemia-induced decreases in arteriolar responses to CGRP. Indomethacin administration did not preserve arteriolar dilation to CGRP at 1 hour after ischemia, but responses were normal at 2 hours. CONCLUSIONS: Total global ischemia leads to prolonged attenuated dilator responses of cerebral arterioles to CGRP. In addition, indomethacin treatment alters effects of ischemia on CGRP-induced dilation.

Animals↗

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↗