Nasal Mucosal Blood Flow Research Articles

Premedication with clonidine before TIVA optimizes surgical field visualization and shortens duration of endoscopic sinus surgery - results of a clinical trial

During functional endoscopic sinus surgery (FESS), intraoperative bleeding can significantly compromise visualization of the surgical field. Clonidine constricts peripheral blood vessels and reduces systemic blood pressure, which in combination decrease nasal mucosa blood flow. This dual effect can potentially reduce bleeding during FESS and stabilize the intraoperative hemodynamic profile of the patient. The aim of this prospective study was to assess if the quality of the surgical field visualization during FESS was improved when clonidine was used as a premedication agent. A group of 44 patients undergoing FESS for chronic sinusitis and polyp removal were enrolled and randomly assigned to receive either oral clonidine or midazolam as preoperative premedication. During the operation, the quality of the surgical field was assessed and graded by the operating surgeon using the scale proposed by Boezaart. The evaluations were done during surgery at 15 minutes (K1), 30 minutes (K2), 60 minutes (K3) and 120 minutes (K4) after incision. The duration of the surgical procedure was significantly shorter in the clonidine group: mean time of surgery: 80 vs. 96 min in the clonidine and midazolam groups, respectively. Also better quality of surgical field was observed at all time points in the clonidine group. Premedication with clonidine before FESS results in shortening of the surgical time and a better quality of the surgical field.

Using dynamic analysis of Laser-Doppler blood flowmetry to measure nasal mucosa bloody flow in postural changes

The regulation of nasal mucosa blood flow (NMBF) is affected by multiple factors, such as the autonomic nervous system, medications, temperature, humidity, endocrine, even emotional stress and vision. The effects of postural changes on NMBF have been described in numerous studies. However, the results are far from consistent due to different experimental designs. Dynamic analysis of Laser-Doppler blood flowmetry (LDBF) is employed to recognize the effect of postural changes on NMBF. NMBF was continuously measured by LDBF in 14 participants with changing postures (sitting and supine). NMBF was measured in Blood Perfusion Unit (BPU), equivalent to the number of red blood cells multiplied by their mean velocity in a measured volume. NMBF increases significantly in a supine posture compared with that in a sitting posture. Our study demonstrates that NMBF is significantly influenced after initial postural change, suggesting that changes in posture may be regarded as an important factor regulating NMBF.

Oxymetazoline Superior to Cocaine and Lidocaine for Nosebleeds

Oxymetazoline Superior to Cocaine and Lidocaine for Nosebleeds

Ambient cold air decreased nasal mucosa blood flow measured by laser Doppler flowmeter

With its potentially conflicting physiological roles of both air-conditioning and body-heat recovery, the response of nasal mucosa blood flow (NMBF) to ambient cold air is not well understood. To evaluate the NMBF in response to cold ambient air. The NMBF was continuously measured by laser Doppler flowmetry in nine participants exposed to different air temperatures (24 degrees C and 4 degrees C). The NMBF significantly decreased at 4 degrees C compared with that at 24 degrees C (p < 0.01). The response to ambient cold air in the nasal microcirculation is similar to that of the body-surface blood vessels, suggesting that body-heat recovery rather than air-conditioning is the predominant function.

Effect of Nitric Oxide Synthase Inhibitor on Increase in Nasal Mucosal Blood Flow Induced by Sensory and Parasympathetic Nerve Stimulation in Rats

Neural control of nasal blood flow (NBF) has not been systematically investigated. The aim of the present study was to evaluate the effect of electrical stimulation of both sensory and parasympathetic nerves innervating the nasal mucosal arteries on NBF in rats. In anesthetized rats, nasociliary (sensory) nerves and postganglionic (parasympathetic) nerves derived from the right sphenopalatine ganglion were electrically stimulated. We measured NBF with a laser-Doppler flowmeter. The nerve stimulation increased NBF on both sides and increased the mean arterial blood pressure. The increase in NBF was larger on the ipsilateral side than on the contralateral side. Hexamethonium bromide, a ganglion blocker, abolished the stimulation-induced pressure effect and the increase in NBF on the contralateral side, but did not abolish the increase in NBF on the ipsilateral side. The remaining increase in NBF was abolished by N(G)-nitro-L-arginine, a nitric oxide synthase inhibitor. Histochemical analysis with nicotinamide adenine dinucleotide phosphate-diaphorase showed neuronal nitric oxide synthase-containing nerves that innervate nasal mucosal arteries. Nitric oxide released from parasympathetic nitrergic nerves may contribute to an increase in NBF in rats. The afferent impulses induced by sensory nerve stimulation may lead to an increase in mean arterial blood pressure that is partly responsible for the increase in NBF.

Effects of Nasal Application of an Epinephrine and Lidocaine Mixture on the Hemodynamics and Nasal Mucosa in Oral and Maxillofacial Surgery

Our purpose was to investigate the influences of nasal pretreatment with a mixed solution of epinephrine and lidocaine (E-L pretreatment) on the systemic hemodynamics and the mucosa of the inferior nasal concha, which is carried out for expansion of the nasal cavity and the prevention of mucosal injury before nasotracheal intubation. Subjects included 29 adult patients undergoing oral and maxillofacial surgery. This study consisted of 2 parts. In part 1 (n = 18), the effects of E-L pretreatment on the systemic hemodynamics were studied before (pre-Anesth group, n = 10) and after (post-Anesth group, n = 8) induction of anesthesia. Changes of the mucosal volume and the blood flow of the inferior nasal concha also were observed by optic bronchoscopy and noncontact type laser-Doppler flowmetry, respectively. In part 2 (n = 11), changes in the serum concentrations of epinephrine and lidocaine after the E-L pretreatment were determined by high performance liquid chromatography and enzyme immunoassay, respectively. The heart rate increased at 2 and 3 min after E-L pretreatment in pre-Anesth group (P < .05), but not in post-Anesth group. The cross section of the nasal cavity decreased from 66% to 42% (n = 8, P < .05). The mucosal blood flow decreased from 60 to 22 AU (n = 8, P < .01). The serum epinephrine concentration increased from 24 to 185 pg/mL. The E-L pretreatment provided characteristic evidence for useful expansion of the nasal cavity and for reduction of the nasal mucosal blood flow with less systemic hemodynamic effects, although further investigation is needed for the determination of the proper epinephrine concentration in E-L pretreatment.

Inflammatory mediators in allergic rhinitis

Allergic rhinitis (AR) is part of a systemic disease complex. There is a close relationship between AR and asthma, which has led to the "one airway, one disease" concept. Both conditions share common immunopathology and pathophysiology. In patients with AR, allergen-triggered early and late responses are mediated by a series of inflammatory cells. Within minutes of contact with allergen, IgE-sensitized mast cells degranulate, releasing both preformed and newly synthesized mediators. Immunologic processes in both nasal and bronchial tissue involve T H 2 lymphocytes and eosinophils. Eosinophils are the predominant cell in the chronic inflammatory process characteristic of the late-phase allergic response. Eosinophils release an array of proinflammatory mediators, including cysteinyl leukotrienes, cationic proteins, eosinophil peroxidase, and major basic protein, and might serve as a major source of IL-3, IL-5, GM-CSF, and IL-13. Neuropeptides also appear to contribute to the pathophysiology of AR symptoms. Both AR and asthma exhibit marked day-night variation in symptom severity. Acknowledging both the chronobiology of AR and circadian rhythm-dependent attributes of antiallergy medications might enhance the beneficial effects of allergy therapies.

Sensory nitrergic meningeal vasodilatation and non-nitrergic plasma extravasation in anaesthesized rats

The aim of the present study was to evaluate the role of nitric oxide (NO) of sensory neural origin in neurogenic inflammatory response in the trigeminovascular system. Antidromic vasodilatation and plasma extravasation in response to electrical stimulation (15 V, 5 Hz, 0.5 ms, 100 impulses) of the trigeminal ganglion were investigated in the dura mater and nasal mucosa/upper eyelid by laser Doppler flowmetry and [ 125I]-labelled bovine serum albumin, respectively. Electrical stimulation of the trigeminal ganglion of rats elicited a reproducible ipsilateral enhancement of both meningeal and nasal mucosal blood flow. N ω-nitro- l-arginine ( l-NNA; 4, 8, and 16 mg/kg, i.v.), a nonselective inhibitor of nitric oxide synthase (NOS), inhibited antidromic vasodilatation both in the dura mater (15.86±2.05%, 22.82±2.51%, and 36.28±4.37%) and nasal mucosa (35.46±8.57%, 58.72±9.2%, and 89.99±8.94%) in a dose-dependent manner. Specific inhibitors of neuronal NOS, 7-nitroindazole (7-NI; 20 mg/kg, i.v.) and 3-bromo-7-nitroindazole (3Br-7NI; 10 mg/kg, i.v.) were administered to assess the possible role of NO released from the trigeminal sensory fibres. The meningeal vasodilatation was inhibited by both 3Br-7NI and 7-NI (63.36±7.7% and 49±6.5%, respectively). The nasal hyperaemic response was also reduced by 3Br-7NI (78.26±8.7%). Plasma extravasation in the dura mater and upper eyelid evoked by electrical stimulation of the trigeminal ganglion (25 V, 5 Hz, 0,5 ms, 5 min), expressed as extravasation ratios (ERs) of the stimulated vs. nonstimulated sides, was 1.80±0.8 and 4.63±1.24, respectively. This neurogenic oedema formation was not inhibited by neither l-NNA nor 3Br-7NI. It is concluded that neural nitrergic mechanisms are involved in the meningeal vasodilatation evoked by electrical stimulation of the trigeminal ganglion.

Responses to nasal bradykinin challenge in normal and allergic subjects

Problem: Neurally mediated secretory hyper-reactivity is well-documented in allergic rhinitis; however, congestive responses to nasal challenge in allergic subjects are less well characterized. Methods: Normal subjects (n = 13), and subjects with seasonal allergic rhinitis (SAR) (n = 16), perennial allergic rhinitis (PAR) (n = 24), and nonallergic rhinitis (NAR) (n = 9) underwent unilateral nasal challenge with Hartman’s solution, bradykinin 50 mcg, and bradykinin 100 mcg. Acoustic rhinometry was performed at baseline and after each challenge. Values for the first, second, and third minimum cross-sectional areas (csa 1, 2, 3), and the volumes to csa 2, csa 3, and to 4 cm inside the nasal cavity (vol 2, 3, 4) were recorded on each side. Results: Challenge with the first dose (50 mcg) of bradykinin in normal subjects led to ipsilateral congestion. A tendency to decongest was seen after the second (100 mcg) dose. Significant changes were not seen in contralateral parameters. In contrast, subjects with SAR and PAR demonstrated significant contralateral congestion after control challenge, which persisted after both bradykinin challenges. Subjects with SAR also demonstrated significant ipsilateral congestion after challenge with bradykinin 50 mcg; however, this was not the case for subjects with PAR. Subjects with NAR did not demonstrate any significant ipsilateral or contralateral congestive responses. Conclusion: Acoustic rhinometry may be used to measure congestive responses to nasal bradykinin challenge. Allergic subjects demonstrate congestive hyper-reactivity, which is more pronounced on the contralateral side. Subjects with PAR had a less pronounced ipsilateral congestive response than did normal subjects or subjects with SAR, which may reflect greater baseline nasal congestion or disturbed regulation of nasal mucosal blood flow. Significance: The present study is the first to investigate nasal congestive responses to bradykinin challenge using acoustic rhinometry in a large number of subjects. Our findings suggest that hyper-reactive congestive reflexes may contribute to the symptoms of allergic rhinitis. Support: None reported.

Efficacy of ice packs in the management of epistaxis.

There are no uniformly accepted criteria for the management of epistaxis. The usefulness of ice application in the treatment of epistaxis as a first aid method is not generally accepted, but is widespread. In order to evaluate the effect of cold application on the blood vessels of the nasal mucosa, their blood flow and blood content were investigated on 56 healthy volunteers before and after exposure to cold in the neck area. Nasal mucosal microcirculatory blood flow was measured directly by non-invasive laser Doppler flowmetry in Kiesselbach's area. Changes in the nasal mucosal blood content were estimated using a conventional computer-aided rhinomanometer by measuring alterations in nasal airflow. After ice application in the neck area, no statistically significant effects on the blood vessels of the nasal mucosa were seen. These results do not support the usefulness of this manoeuvre in the treatment of epistaxis.

The Effect of Topical Xylometazoline on the Mucosal Temperature of the Nasal Septum

The purpose of this study was to determine the short-term influence of the alpha2-adrenoreceptor agonist xylometazoline on the nasal mucosal temperature. Thirty healthy subjects were enrolled into the study. Fifteen of these subjects got xylometazoline and 15 subjects, matched to age, got saline solution as control. A miniaturized thermocouple was used for continuous detection of the septal mucosal temperature without interruption of nasal breathing before and after application of nose spray. In the anterior nasal segment, the mucosal temperatures before decongestion were significantly higher than after decongestion (p < 0.05). These changes could not be found in the control group after saline solution. The mean end-expiratory mucosal temperatures were significantly higher than the end-inspiratory ones in both study groups (p < 0.005). The reduction of the nasal mucosal bloodflow because of vasoconstriction and the increase of the nasal cavity volume after decongestion with xylometazoline seem to cause a significant decrease of the septal mucosal temperature in the anterior nasal segment. This might be one possible causative factor of the common symptom of the "dry nose" in patients with nasal decongestant abuse.

Nasal nitric oxide.

Nasal nitric oxide.

Functional effects of neuropeptide Y receptors on blood flow and nitric oxide levels in the human nose.

The aim of this study was to examine dose-dependent effects of intranasal application of neuropeptide Y (NPY) on nasal mucosal blood flow, blood content, and intranasal nitric oxide (NO) concentration. Blood flow was measured by laser Doppler flowmetry (LDF) and blood content by rhinomanometry. Mucosal biopsies were taken for investigation of Y1 and Y2 receptor mRNA expression, using the reverse transcriptase-polymerase chain reaction (RT-PCR). Intranasal application of NPY evoked a dose-dependent reduction of nasal mucosal blood flow. Maximal vasoconstriction, seen at 12 nmol, was -37.5 +/- 6.2%, p < 0.05 (n = 9). The vasoconstrictive effect developed within 2 to 4 min and lasted > 17 min. NPY evoked a dose-dependent reduction of nasal airway resistance (NAR) on the ipsilateral side. Maximal decrease was -24.0 +/- 10.0% at 12 nmol, p < 0.05 (n = 9). There was a decrease in nasal NO production on the ipsilateral side after application of NPY 12 nmol (-7.4 +/- 1.2%, p < 0.05, n = 8). RT-PCR products corresponding to Y1 receptor but not Y2 receptor mRNA were obtained from biopsies of the nasal mucosa. In conclusion, NPY is a potent vasoconstrictor in the human nose reducing mucosal blood flow, as well as the blood content. The effect is probably mediated via Y1 receptors. NPY receptor agonists may prove beneficial in the treatment of the congested nose in allergic or vasomotor rhinitis.

Effect of internal maxillary arterial occlusion on nasal blood flow in swine.

The precise effects of therapeutic occlusion of the internal maxillary artery (IMA) on distal nasal mucosal perfusion are unknown. A better understanding of these effects has important implications regarding the rationale and expected efficacy of certain therapeutic interventions for epistaxis management. The authors developed an animal model to assess these issues. The effects of "proximal" and progressively more "distal" occlusions of the IMA on nasal mucosal blood flow (NBF) were assessed in anesthetized swine using continuous laser Doppler flowmetry. The levels of arterial occlusion were selected to simulate clinical therapeutic occlusions used for the management of epistaxis. Nineteen swine were entered into one of four experimental groupings: proximal IMA occlusion using platinum micro-coils (n = 6), mid-grade distal IMA occlusion with polyvinyl alcohol particulate (PVA) suspensions (300 to 500 microns, n = 5), high-grade distal IMA occlusion with polyvinyl alcohol particulate suspensions (50 to 150 microns, n = 5), and sham control (n = 2). All embolizations resulted in acute decreases in average NBF from 120 mL/min per 100 g to 40 mL/min per 100 g (P < .05 for all groups). NBF returned to baseline in all three treated groups within 2 to 8 days after therapeutic embolization, depending on the level of occlusion (coils, 2 d; mid-grade PVA, 2-3 d; high-grade PVA, 8 d). Follow-up angiography showed recanalization and collateralization as possible methods of reestablishing NBF. This study supports the rationale for performing distal IMA occlusion with transarterial particulate embolization, in order to provide a longer period of time of diminished NBF. This theoretically should promote hemostasis within an injured portion of the nasal mucosa by decreasing perfusion pressure within the capillary bed. However, the benefits of distal IMA embolization must be balanced against potential ischemic complications, as may be more commonly seen with high-grade particulate embolization.

Laser-Doppler blood flowmetry measurement of nasal mucosa blood flow after injection of the greater palatine canal

Laser-Doppler blood flowmetry1 was used to measure the mucosal blood flow of the inferior turbinate before and after injection of the greater palatine canal with 2 ml of a 0.5% bupivicaine hydrochloride solution. Injection of the greater palatine canal is a useful technique in the control of posterior epistaxis.2 The arterial blood supply to the inferior turbinate is via a single descending branch of the sphenopalatine artery. We conjectured that injection of the pterygopalatine fossa, via the greater palatine canal, would result in a reduction of blood flow to the inferior turbinate.2 A cohort of 14 healthy volunteers who were to undergo routine nasal surgery was recruited to this study, each subject acted as their own control. Their age ranged from 28–52 years. In the study injection of the pterygopalatine fossa caused only a 4.7% decrease in blood flow to the inferior turbinate mucosa (P = 0.571). Elevation of the head by an angle of 20° reduced nasal mucosal blood flow by 38.3% (P < 0.0001). Depression of the head by an angle of 20° increased nasal mucosal blood flow by 74.7% (P < 0.0001). We conclude that there is an adequate collateral blood circulation to the anterior portion of the inferior turbinate.

Increased nasal mucosal blood flow, airway resistance and secretion induced by electrical stimulation of the superior salivatory nucleus in cats

We studied the effects of electrical stimulation of the superior salivatory nucleus (SSN) on the nasal blood flow, nasal airway resistance, and nasal secretion in ketamine or pentobarbital anesthetized cats. The blood flow of the nasal mucosa was measured by laser Doppler flowmetry. Similar to the effects of stimulation of the parasympathetic nerve innervating the nasal mucosa, the SSN stimulation increased the nasal blood flow, nasal airway resistance, and nasal secretion on the ipsilateral side. These responses were not accompanied by changes in contralateral nasal blood flow, ipsilateral forelimb blood flow, blood pressure, or orofacial movement. Atropine administration partially inhibited the SSN-induced nasal vasodilatation without interfering with the effect on the nasal airway resistance. This vasodilatation was not affected by sympathectomy or guanethidine administration, but it was abolished by hexamethonium administration. It is suspected that the cells in the SSN control both nasal vasodilatation and secretion, and that the SSN output fibers responsible for the nasal parasympathetic control consist of both cholinergic and non-cholinergic fibers.

Increased nasal mucosal blood flow, airway resistance and secretion induced by electrical stimulation of the superior salivatory nucleus in cats

Increased nasal mucosal blood flow, airway resistance and secretion induced by electrical stimulation of the superior salivatory nucleus in cats

Nasal vasoconstriction and decongestant effects of nitric oxide synthase inhibition in the pig.

The effects of systemic administration of the nitric oxide synthase inhibitor N omega-nitro-L-arginine on the vasculature of the pig nasal mucosa were compared with the effects of alpha-adrenoceptor agonists and of sympathetic nerve stimulation. A novel in vivo pig model was used in which standard measurements of nasal mucosal blood flow were complemented with measurements of nasal cavity volume using an acoustic rhinometer. The vasodilatory effects of capsaicin, substance P. acetylcholine, vasoactive intestinal polypeptide and nitroprusside, before and after nitric oxide synthase inhibition, were also investigated. N omega-nitro-L-arginine evoked a marked, slowly developing, long-lasting reduction in nasal vascular conductance with a parallel increase in nasal cavity volume (by approximately 30%) comparable in magnitude with the response upon alpha-adrenoceptor stimulation. L-Arginine partly reversed the N omega-nitro-L-arginine-evoked vasoconstriction, although nasal cavity volume was unaffected. Nasal vasodilation and decrease in nasal cavity volume resulting from capsaicin-evoked activation of sensory nerves were unaltered after administration of N omega-nitro-L-arginine. Nitric oxide synthase inhibition did not attenuate the vasodilator responses evoked by either substance P. acetylcholine, vasoactive intestinal polypeptide or nitroprusside. The present data suggest that nitric oxide synthase activity is of importance both for basal nasal vascular conductance and nasal cavity volume in the pig in vivo. In contrast, nitric oxide synthase inhibition does not reduce the vascular effects of a variety of vasodilating agents, including capsaicin, acetylcholine and substance P.

Capsaicin-, resiniferatoxin-, and lactic acid-evoked vascular effects in the pig nasal mucosa in vivo with reference to characterization of the vanilloid receptor.

Nasal cavity volume, mucosal and superficial skin blood flow as well as renal splenic vascular effects of capsaicin, resiniferatoxin and lactic acid were investigated, using a novel in vivo pig model. The present results show that locally intraarterially injected capsaicin, resiniferatoxin and lactic acid evoke similar vasodilatory responses, although with different duration, in the nasal mucosa and superficial skin as well as an increase in heart rate and mean arterial blood pressure. Nasal vascular responses evoked by capsaicin, resiniferatoxin and lactic acid were unaffected by the cyclooxygenase inhibitor diclofenac. Moreover, chlorisondamine did not alter the nasal vasodilatory responses evoked by capsaicin and lactic acid. However, chlorisondamine abolished sympathetic reflex-mediated vasoconstrictor effects of capsaicin in the spleen and kidney. Lactic acid-evoked vasodilation in the nasal mucosa and skin was inhibited by the 8-37 fragment of calcitonin gene-related peptide, a calcitonin gene-related peptide-receptor antagonist. Lactic acid-evoked vasoconstriction in the spleen and kidney was reduced but not abolished by chlorisondamine, suggesting that the effects of lactic acid are not exclusively reflex-mediated. Capsazepine did not inhibit the vasodilatation in the nasal mucosa evoked by capsaicin and lactic acid. [3H]Resiniferatoxin bound to pig nasal mucosa membranes with an affinity of 134 pM in a non-cooperative fashion; this binding behaviour contrasted to the apparent positive cooperativity (a Hill coefficient of 2.2) of specific resiniferatoxin binding to pig spinal cord preparations. Specific [3H]resiniferatoxin binding to nasal mucosa membranes was fully inhibited by capsaicin (Ki = 5 microM) and lactic acid (IC50 at pH 5.0) but not by capsazepine (up to 10 microM), in accord with the physiological findings. Capsazepine, by contrast, displaced [3H]resiniferatoxin from spinal vanilloid receptors with an affinity of 3 microM. These findings show the presence of vanilloid receptors in the pig nasal mucosa and suggest heterogeneity in the properties of vanilloid receptors in the pig. Furthermore, lactic acid evokes vascular effects similar to those of capsaicin and resiniferatoxin, possibly via interaction of protons and/or proton-generated substances at vanilloid receptors with a subsequent release of calcitonin gene-related peptide.

Nasal mucosal vasodilatation in response to passive hyperthermia in humans.

The present study was conducted to measure nasal mucosal blood flow (NMBF) during body warming. Five subjects [mean (SD) 24 (2) years], wearing only shorts and a thick felt hat with ear flaps, were immersed to the neck in a bath at 40 (0.5) degrees C. Tympanic (Tty), esophageal (Tes), mean unweighted skin (Tsk), nose skin and ear pinna skin were recorded at 1-min intervals. NMBF on the lower septal wall was estimated using a laser Doppler flow meter. At rest Tty and Tes were both 36.5 degrees C. Tty dropped significantly below Tes during body warming, despite impeded heat loss from the head due to the felt hat. Tty increased to 37.3 degrees C and Tes increased to 37.5 degrees C during the immersion. During the immersion all skin temperatures were steady or increasing, ruling out the possibility of a contamination of Tty from Tsk. Body warming significantly (P = 0.001) increased NMBF by approximately three times from resting values at the end of immersion. During the period of increasing core temperatures NMBF was significantly correlated to Tty (r = 0.93, P = 0.0001) and Tes (r = 0.97, P = 0.0001), suggesting the blood flow change in this tissue was a thermoregulatory response. The increased NMBF during hyperthermia supports the hypothesis of respiratory cooling involvement in selective brain cooling of humans.