Variant Inferior Alveolar Nerves and Implications for Local Anesthesia.

A sound knowledge of anatomical variations that could be encountered during surgical procedures is helpful in avoiding surgical complications. The current article details anomalous morphology of inferior alveolar nerves encountered during routine dissection of the craniofacial region in the Gross Anatomy laboratory. We also report variations of the lingual nerves, associated with the inferior alveolar nerves. The variations were documented and a thorough review of literature was carried out. We focus on the variations themselves, and the clinical implications that these variations present. Thorough understanding of variant anatomy of the lingual and inferior alveolar nerves may determine the success of procedural anesthesia, the etiology of pathologic processes, and the avoidance of surgical misadventure.

Neurogenic vasodilatation of canine isolated small labial arteries.

Mechanisms underlying vasodilatation to nerve stimulation by electrical pulses and nicotine were analyzed in isolated canine small labial arteries. Transmural electrical stimulation (5 and 20 Hz) produced a contraction followed by a relaxation in labial arterial strips denuded of the endothelium, partially contracted with prostaglandin F2alpha. The contraction was abolished by prazosin or combined treatment with alpha, beta-methylene ATP. In the treated strips, neurogenic relaxation was abolished by NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthase inhibitor, and restored by L-arginine. The D-enantiomers were without effect. Nicotine (10(-4) M) also relaxed the arteries, in which the contractile response was abolished by prazosin and alpha, beta-methylene ATP. The relaxant response was attenuated but not abolished by L-NA; the inhibition was reversed by L-arginine. The remaining relaxation by nicotine was abolished by calcitonin gene-related peptide (CGRP)-[8 to 37], a CGRP1 receptor antagonist. Relaxations elicited by a lower concentration of nicotine (2 x 10(-5) M) sufficient to produce similar magnitudes of response to those induced by 5-Hz electrical nerve stimulation were also inhibited partially by L-NA. Histochemical study with the NADPH-diaphorase method demonstrated positively stained nerve fibers and bundles in the arterial wall, suggesting the presence of neuronal NO synthase. It is concluded that the relaxation induced by electrical nerve stimulation of small labial arteries is mediated exclusively by NO synthesized from L-arginine in nerve terminals, whereas nicotine in the concentrations used evokes relaxations by a mediation of nerve-derived NO and also CGRP, possibly from sensory nerves. The reason why nicotine but not electrical pulses stimulates sensory nerves and elicits vasorelaxation remains unsolved.

Effects of the neuropeptide YY1 receptor antagonist SR 120107A on sympathetic vascular control in pigs in vivo .

The possible involvement of neuropeptide Y in sympathetic vasoconstriction in various vascular beds in anesthetized pigs in vivo was studied using the neuropeptide Y Y1 receptor antagonist SR 120107A. Single impulse sympathetic nerve stimulation evoked rapid vasoconstrictor responses in hind limb and nasal mucosa which were not affected by SR 120107A (1.5 mg kg-1). Vascular responses to high frequency stimulation was measured in kidney, spleen (three 1 s bursts at 20 Hz or 300 impulses at 10 Hz), hind limb and nasal mucosa (three 1 s bursts at 20 Hz). High frequency stimulation evoked rapid vasoconstriction in all vascular beds studied. This was followed by a long-lasting phase of reduced blood flow in hind limb and nasal mucosa. SR 120107A (1.5 mg kg-1) attenuated the vasoconstriction evoked by the 20 Hz stimulation in the kidney, whereas a higher dose (a total of 6.0 mg kg-1) was required to reduce the vascular response in kidney to the 10 Hz simulation. SR 120107A (1.5 mg kg-1) did not inhibit the vascular responses in spleen, hind limb or nasal mucosa to the 20 Hz stimulation or the vasoconstriction in the spleen to the 10 Hz stimulation (a total of 6 mg kg-1). Subsequent addition of the adrenoceptor antagonists phenoxybenzamine (5 mg kg-1) plus timolol (2 mg kg-1) strongly reduced the vascular responses to single impulse stimulation and high frequency stimulation (20 Hz series) in all vascular beds. We conclude that endogenous neuropeptide Y acting on the neuropeptide Y Y1 receptor, as revealed by SR 120107A, is likely to account for part of the sympathetic vasoconstriction upon high frequency stimulation in the kidney.

SR 120107A antagonizes neuropeptide Y Y1 receptor mediated sympathetic vasoconstriction in pigs in vivo.

The effects of the neuropeptide Y Y1 receptor antagonist SR 120107A (1-[2-[2-(2-naphtylsulfamoyl)-3-phenylpropionamido]-3-[4-[N- [4- (dimethylaminomethyl)-cis-cyclohexylmethyl]amidino]phenyl]propiony l] pyrrolidine, (S,R) stereoisomer) on sympathetic non-adrenergic vasoconstriction in a variety, of vascular beds were studied in reserpinized anesthetized pigs in vivo. The rapid vasoconstrictor response evoked by single impulse stimulation, in hind limb and nasal mucosa, was not affected by SR 120107A (1.5 mg kg-1 i.v.). In contrast, SR 120107A potently inhibited the long-lasting phase of vasoconstriction evoked by high frequency (60 impulses at 20 Hz) sympathetic nerve stimulation, in the main and deep femoral, the saphenous and the internal maxillary arteries, leaving merely the initial rapid peak of vasoconstriction in these vessels. Furthermore, the vasoconstrictor response was nearly abolished in the kidney and was attenuated in the spleen and main femoral artery, despite maintained neuropeptide Y overflow. The vasoconstrictor response evoked in the kidney by peptide YY, a neuropeptide Y Y1 and Y2 receptor agonist, was also nearly abolished in the presence of SR 120107A. This inhibitory effect on the response to exogenous agonist correlated well with the long-lasting inhibition of the response to nerve stimulation in the same tissue. The peptide YY-evoked vasoconstriction in the spleen was not altered by SR 120107A, in accordance with the view that the neuropeptide Y receptor population in this organ consists mainly of neuropeptide Y Y2 receptors. SR 120107A did not influence the vasoconstrictor effects of alpha, beta-methylene ATP (mATP) or phenylephrine in any of the tissues studied. We conclude that SR 120107A is a potent neuropeptide Y Y1 receptor antagonist with long duration of action in vivo. Endogenous neuropeptide Y acting on the neuropeptide Y Y1 receptor is likely to account for the long-lasting component of the reserpine-resistant sympathetic vasoconstriction upon high frequency stimulation in hind limb and nasal mucosa. Furthermore, the peak vasoconstriction in kidney, and to some extent in spleen, is also neuropeptide Y Y1 receptor mediated.

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.

Sympathetic control of blood flow to AVAs and capillaries in nasal and facial tissues supplied by the internal maxillary artery in dogs.

Total blood flow and perfusion pressure (PP) of the internal maxillary artery (IMA) were recorded bilaterally during electrical stimulation (8 V, 2ms) of the right cervical sympathetic nerve at frequencies (f) of 0.3, 0.5, 1.0 and 3.0 Hz in anesthetized, paralyzed and artificially ventilated dogs. Distribution of IMA-FLOW to precapillaries (CAP-FLOW) and arteriovenous anastomoses (AVA-FLOW) was determined by the tracer microspheres technique. During electrical stimulation (ES) IMA-FLOW was affected only unilaterally and decreased in a hyperbola-like fashion with the increase of f, while contralateral IMA-FLOW remained unchanged. Systemic blood pressure as well as PP of both IMA remained unchanged while heart rate was only increased during ES at maximal f. The reduction of IMA-FLOW was mainly due to marked vasoconstrictor responses of the AVAs, which were already attained at low f while significant vasoconstrictor responses of precapillaries occurred at higher f and were less pronounced. The early response of AVAs to increasing sympathetic activation enables IMA-FLOW to be adjusted in a physiological range of sympathetic activities, before CAP-FLOW is substantially reduced. The predominance of AVA-FLOW in blood flow control of the IMA was also supported by the conformity in their hyperbolic relationship with maxillary resistance at rest and during enhanced levels of sympathetic vasoconstrictor activity.

The effects on respiration in the cat of the sudden excitation of cerebral vascular nociceptors by carbon dioxide.

1. Injection of CO2-saturated saline in a distal direction into either a vertebral artery or an internal maxillary artery in pentobarbitone-anaesthetized cats produced abrupt changes in respiration. Vertebral-artery injections produced a transient inhibition of respiration, followed by a stimulation of it. Internal-maxillary-artery injections produced only the inhibition. 2. Injections during inspiration usually shortened that inspiration, reduced its volume and prolonged the following expiration. In the first 30% of an expiration they prolonged that expiration, but given in the next 50% they shortened it. In the last 20% of expiration internal-maxillary-artery injections again slightly prolonged the expiration. 3. Phenyl diguanide injected into either a vertebral or an internal maxillary artery also produced abrupt effects on respiration. 4. The effects of CO2-saturated saline were abolished by intravenous acetazolamide, suggesting that nociceptors may be affected by a change in local pH. 5. The effects may arise from the excitation of vascular nociceptors, and our observations may suggest a way of studying in animals the receptors responsible for headache.