[Evaluation of the effect of simultaneous neuralized iliac bone flap on the preservation of lower lip and chin sensation during mandibular reconstruction].

PURPOSE: To evaluate the effect of reconstructing inferior alveolar nerve and preserving the sensation of lower lip and chin in repairing mandibular defect by simultaneous neuralized iliac bone flap. METHODS: Patients with continuous mandibular defects requiring reconstruction were randomly assigned to the innervated(IN) group and the control(CO) group by random number table. In the IN group, the deep circumflex iliac artery and recipient vessels were anastomosed microscopically during mandible reconstruction, and the ilioinguinal nerve(IN), mental nerve(MN) and inferior alveolar nerve(IAN) were anastomosed at the same time. In the CO group, only vascular anastomosis was performed without nerve reconstruction. During the operation, the nerve electrical activity after nerve anastomosis was detected by nerve monitor, and the sensory recovery of lower lip was recorded by two-point discrimination(TPD), current perception threshold (CPT) and Touch test sensory evaluator(TTSE) test. SPSS 26.0 software package was used for data analysis. RESULTS: According to the inclusion and exclusion criteria, a total of 20 patients were included, with 10 patients in each group. All the flaps survived in both groups, and no serious complications such as flap crisis occurred, and no obvious complications occurred in the donor site. The results of TPD test, CPT test and TTSE test all indicated that the degree of postoperative hypoesthesia in the IN group was less(P＜0.05). CONCLUSIONS: Simultaneous nerve anastomosis vascularized iliac bone flap can effectively preserve the feeling of lower lip and improve the postoperative quality of life of patients. It is a safe and effective technique.

Berberine restored nitrergic and adrenergic function in mesenteric and iliac arteries from streptozotocin-induced diabetic rats.

ETHNOPHARMACOLOGICAL RELEVANCE: Perivascular neuropathy was reported to involve in the vascular disorders associated with diabetes. The dried rhizomes of Coptis chinensis Franch. (Latin name: Coptidis Rhizoma; common name: Huang Lian in China), used frequently in Traditional Chinese medicine to treat diabetes (Xiaoke), have been confirmed to possess beneficial effects on diabetic peripheral neuropathy by modern clinical and pharmacological studies. Berberine (BBR), the main effective component of Huang Lian in the treatment of diabetes, is reported to ameliorate diabetic central and peripheral neuropathy. However, the effects of BBR on nerve function of mesenteric and iliac arteries are unclear. AIM OF THE STUDY: To investigate the effects of BBR on the diabetes-induced changes in nitrergic and adrenergic function in mesenteric and iliac arteries. MATERIALS AND METHODS: In this study, the animals were randomized into three groups: control rats, diabetic rats, and diabetic rats gavaged with BBR. We established diabetic rat model using intraperitoneal injection of streptozotocin (STZ, 55 mg kg-1). Two weeks after model establishment, those in the BBR-treated groups were gavaged with berberine chloride (Sichuan Xieli Fharmaceutical. Co., Ltd; 200 mg·kg-1·day-1) diluted in distilled water for another 2 weeks. The superior mesenteric artery and iliac artery were excised. Electric field stimulation (EFS) was used to induce arterial vasoconstriction and explore (1) the diabetes-induced changes in neurogenic function of the superior mesenteric artery and iliac artery; (2) the effects of BBR on neurovascular dysfunction in the early stage of STZ-induced diabetic rats. Nitric oxide (NO) and noradrenaline (NA) released from the nitrergic and adrenergic nerves were quantified using fluorescence assays and ELISA, respectively. RESULTS: EFS induced frequency-dependent vasoconstrictions in both superior mesenteric and iliac artery, and the contractile responses of arteries were abolished by 0.1 µmol·L-1 tetrodotoxin (TTX), or inhibited by 1 µmol·L-1 phentolamine or increased by 0.1 mmol·L-1 Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME). In superior mesenteric artery, but not in iliac artery, the changes of contractile responses with L-NAME were significantly decreased in diabetic rats, and NO release was less also. In contrast, in iliac artery of diabetic rats, but not in superior mesenteric artery, the changes of contractile responses with phentolamine were increased, and NA release was increased significantly. All these changes in diabetic rats on both superior mesenteric artery and iliac artery were reversed by treated with BBR. CONCLUSIONS: In the STZ-induced early diabetic rats, neural control of mesenteric and iliac vasomotor tone are altered differently. The diminished nitrergic nerve in superior mesenteric artery and enhanced adrenergic nerve in iliac artery both contributed to increased vasocontrictor responses. All these changes in diabetic rats were reversed by BBR, suggesting a novel mechanism of BBR in balance of neural regulation of vascular tone.

Neural and humoral control of regional vascular beds via A1 adenosine receptors located in the nucleus tractus solitarii.

Our previous studies showed that stimulation of adenosine A(1) receptors located in the nucleus of the solitary tract (NTS) exerts counteracting effects on the iliac vascular bed: activation of the adrenal medulla and ß-adrenergic vasodilation vs. sympathetic and vasopressinergic vasoconstriction. Because NTS A(1) adenosine receptors inhibit baroreflex transmission in the NTS and contribute to the pressor component of the HDR, we hypothesized that these receptors also contribute to the redistribution of blood from the visceral to the muscle vasculature via prevailing sympathetic and vasopressinergic vasoconstriction in the visceral (renal and mesenteric) vascular beds and prevailing ß-adrenergic vasodilation in the somatic (iliac) vasculature. To test this hypothesis, we compared the A(1) adenosine-receptor-mediated effects of each vasoactive factor triggered by NTS A(1) adenosine receptor stimulation [N(6)-cyclopentyladenosine (CPA), 330 pmol in 50 nl] on the regional vascular responses in urethane/chloralose-anesthetized rats. The single-factor effects were separated using adrenalectomy, ß-adrenergic blockade, V(1) vasopressin receptor blockade, and sinoaortic denervation. In intact animals, initial vasodilation was followed by large, sustained vasoconstriction with smaller responses observed in renal vs. mesenteric and iliac vascular beds. The initial ß-adrenergic vasodilation prevailed in the iliac vs. mesenteric and renal vasculature. The large and sustained vasopressinergic vasoconstriction was similar in all vascular beds. Small sympathetic vasoconstriction was observed only in the iliac vasculature in this setting. We conclude that, although A(1) adenosine-receptor-mediated ß-adrenergic vasodilation may contribute to the redistribution of blood from the visceral to the muscle vasculature, this effect is overridden by sympathetic and vasopressinergic vasoconstriction.

Vasopressin is a major vasoconstrictor involved in hindlimb vascular responses to stimulation of adenosine A(1) receptors in the nucleus of the solitary tract.

Our previous study showed that stimulation of adenosine A(1) receptors located in the nucleus of the solitary tract (NTS) exerts counteracting effects on the iliac vascular bed: activation of the adrenal medulla and beta-adrenergic vasodilation versus vasoconstriction mediated by neural and unknown humoral factors. In the present study we investigated the relative contribution of three major potential humoral vasoconstrictors: vasopressin, angiotensin II, and norepinephrine in this response. In urethane-chloralose anesthetized rats we compared the integral changes in iliac vascular conductance evoked by microinjections into the NTS of the selective A(1) receptor agonist N(6)-cyclopentyladenosine (CPA; 330 pmol in 50 nl) in intact (Int) animals and following: V(1) vasopressin receptor blockade (VX), angiotensin II AT(1) receptor blockade (ATX), bilateral adrenalectomy + ganglionic blockade (ADX + GX; which eliminated the potential increases in circulating norepinephrine and epinephrine), ADX + GX + VX and ADX + GX + VX + ATX. In Int animals, stimulation of NTS A(1) adenosine receptors evoked typical variable responses with prevailing pressor and vasoconstrictor effects. VX reversed the responses to depressor ones. ATX did not significantly alter the responses. ADX + GX accentuated pressor and vasoconstrictor responses, whereas ADX + GX + VX and ADX + GX + VX + ATX virtually abolished the responses. Stimulation of NTS A(1) adenosine receptors increased circulating vasopressin over fourfold (26.4 + or - 10.4 vs. 117.0 + or - 19 pg/ml). These data strongly suggest that vasopressin is a major vasoconstrictor factor opposing beta-adrenergic vasodilation in iliac vascular responses triggered by stimulation of NTS A(1) adenosine receptors, whereas angiotensin II and norepinephrine do not contribute significantly to the vasoconstrictor responses.

Neurogenically derived nitrosyl factors mediate sympathetic vasodilation in the hindlimb of the rat.

Skeletal muscle vasculature of the hindlimb is innervated by a sympathetic noncholinergic vasodilator system. The aim of this study was to determine whether this vasodilator system may represent postganglionic lumbar sympathetic neurons that synthesize and release nitric oxide (NO) or related NO-containing factors. We examined whether NO synthase (NOS)-positive postganglionic lumbar nerves innervate the hindlimb vasculature of the rat and whether the hindlimb vasodilation produced by electrical stimulation of the lumbar sympathetic chain of anesthetized rats is reduced after the systemic administration of the specific inhibitor of neuronal NOS 7-nitroindazole (7-NI). Subpopulations of lumbar sympathetic cell bodies stained intensely for NOS. Postganglionic fibers and varicosities within the iliac and femoral arteries also stained for NOS. Double ligation of the lumbar chain demonstrated that NOS was transported from the cell bodies toward the peripheral terminals. Low-intensity electrical stimulation of the lumbar chain produced a pronounced hindlimb vasodilation that was markedly diminished by pretreatment with 7-NI (45 mg/kg i.v.). In contrast, the vasodilator potency of acetylcholine and S-nitrosocysteine were augmented by 7-NI. These results suggest that postganglionic lumbar sympathetic neurons may synthesize and release NO-containing factors.

Somatostatin receptor expression in rat iliac arteries after balloon injury.

Somatostatin is a general inhibitory hormone that exerts its effects through five functionally distinct receptor subtypes (SSTR1-5). Somatostatin analogues have been shown to be effective in inhibiting intimal hyperplasia after balloon induced vascular injury. However, the exact SSTR subtype responsible for the inhibitory effect of somatostatin on intimal hyperplasia is unknown. The purpose of this study was to define the presence and abundance of SSTR subtypes in a rat iliac balloon injury model of intimal hyperplasia. Transaortic balloon injury of the rat iliac artery was carried out. Rats were sacrificed at 48 h, 1 week, and 1 month postinjury, and perfusion fixed and stained with antibodies against SSTR2, 3, and 5. SSTR2 was identified on the intimal surfaces of normal and injured vessels. SSTR2 immunoreactivity was more prominent at 1 week and 1 month postinjury compared with 48 h postinjury. There was no immunostaining with SSTR3 and SSTR5 antibodies. The results show that SSTR2 is expressed on endothelial cells in normal and injured rat vessels. Its abundance in the injured vessel was increased up to 1 month postinjury.

Neurogenic vasodilation in canine uterine and iliac arteries.

OBJECTIVE: To investigate neurogenic control of uterine and iliac arterial tone with reference to nerve-derived nitric oxide. DESIGN: Mechanisms underlying the response to perivascular nerve stimulation were studied under alpha-adrenoceptor blockade. METHODS: Mechanical responses to nerve stimulation by nicotine were isometrically recorded in isolated canine uterine and iliac arterial strips. Nitric oxide synthase was stained immunohistochemically. RESULTS: The arterial strips responded to nicotine mainly with a contraction, which was reversed to a relaxation by prazosin. The responses were abolished by hexamethonium. The relaxation was not influenced by timolol and atropine but was suppressed by NG-nitro-L-arginine, a nitric oxide synthase inhibitor; the inhibition was reversed by L-arginine. Internal iliac arterial strips also responded to nicotine with a relaxation under prazosin treatment, the magnitude of which was appreciably less than that in the uterine artery. Histochemical study demonstrated that perivascular nerve fibres exhibit nitric oxide synthase immunoreactivity. CONCLUSION: Canine uterine arteries are innervated by adrenergic, vasoconstrictor and nitroxidergic vasodilator nerves, and the neurogenic vasodilation is evidently more marked than that in other canine arteries, including the iliac artery.

Vascular injury augments adrenergic neurotransmission.

BACKGROUND: We have observed persistent desensitization to exogenous norepinephrine after balloon injury. We postulated that this desensitization may be due to a local increase in the release of neuronal norepinephrine. METHODS AND RESULTS: New Zealand White rabbits underwent left iliac artery angioplasty; 4 weeks later, both iliac arteries were harvested. Maximal response to exogenous norepinephrine was reduced in injured compared with noninjured vessels (12.3 +/- 1.0 g versus 10.3 +/- 1.5 g; n = 7, P = .056). By contrast, response to electrical stimulation (to induce neuronal norepinephrine release) was significantly greater in injured tissues (36 +/- 7% versus 14 +/- 3%; values expressed as percent of maximal contraction to exogenous norepinephrine; P = .025). Direct measurement of tissue norepinephrine revealed a threefold increase 4 weeks after injury (1236 +/- 410 versus 466 +/- 97 pg/mg; injured versus noninjured). To determine if desensitization to exogenous norepinephrine was due to a persistent increase in neuronal norepinephrine release, the experiments were repeated after chemical sympatholysis using 6-hydroxydopamine (6-OHDA) (65 mg/kg). To determine if activation of vascular angiotensin II contributed to facilitation of adrenergic neurotransmission, other animals received ramipril (RAM; 1 mg/kg per day). Both treatments were initiated 7 days before angioplasty. In the 6-OHDA group there was no evidence of desensitization, judged by maximal response to exogenous norepinephrine (7.5 +/- 0.6 versus 7.5 +/- 0.8, noninjured versus injured). Similar results were obtained in RAM animals (9.9 +/- 0.8 versus 9.6 +/- 1.2, noninjured versus injured). CONCLUSIONS: This is the first study to demonstrate enhanced adrenergic neurotransmission after balloon injury. The facilitation of adrenergic neurotransmission may be due to increased local concentrations of angiotensin II and is associated with desensitization to exogenous norepinephrine.

[The nerves of the paravasal fatty tissue of the human iliac vessels]. / Nervy paravazal'noi kletchatki podvzdoshnykh sosudov cheloveka.

The aim of the work was to concretize ideas of the anatomy of extraintramural nerve plexuses along the course of large iliac vessels. Three nerves with the diameter 0.6-2 mm were revealed running from the iliac plexus to the paravasal fat. Topographic anatomical characteristics of these formations and their interrelations with the well-known branches of the lumbar plexus are given with special reference to practical value of the results obtained. The relation of nerves of the paravasal fat to adventitia of the vessels, lymph nodes, fascial and muscular formations was studied.

Surgical anatomy of the internal oblique muscle: a practical approach.

In recent years pedicled and microvascular free muscle flaps, myocutaneous flaps, and vascularized bone grafts have become well accepted reconstructive techniques in the management of complex defects. The deep circumflex iliac artery-based internal oblique muscle pedicle flap, internal oblique free muscle pedicle flap, internal oblique free muscle flap, and the internal oblique-iliac crest microvascular free flap are the latest additions to the reconstructive surgeons' armamentarium. This report describes the surgical anatomy of the internal oblique muscle and the deep circumflex iliac artery from a practical viewpoint with particular emphasis on the vascular basis of the above mentioned flaps.

Electrostimulation and penile erection.

Electrostimulation was used to study the neuroanatomy and physiology of penile erection in dogs and monkeys. The canine spinal nuclei responsible for penile erection, identified by the retrograde horseradish peroxidase transport technique after verification of the cavernous nerves with neurostimulation, were mediolateral autonomic neurons at T12-L3 and S1-S3. The erection induced by electrostimulation of the cavernous nerves is the result of increased arterial flow, relaxation of cavernous muscles, and venous outflow restriction. Study of electrostimulation in dogs and monkeys is invaluable for the understanding of the complex neurophysiology of human penile erection.

[Ultrastructure of the nerve plexuses of the arteries of healthy rabbits and rabbits with Brown-Pearce tumors]. / Ul'trastruktura nervnykh spletenii arterii krolika v norme i pri opukholi Brauna-Pirsa.

The neural formations of intact rabbit major arteries and nerves of the same arteries in rabbits with the II and IV stages of the malignant Brown--Pearce tumor have been studied. Periarterial neural fasciculi, fibers and terminal branches have been revealed. According to ultrastructure of their cytoplasmic matrix, they can be divided into adrenergic, cholinergic or sensitive. When the malignant tumor is growing, the arterial neural formations undergo certain distrophic-destructive changes; they are especially pronounced in the membranous structures of the neural elements. Their cytoplasmic and basal membranes are partly or completely destroyed. In mitochondria the matrix is altered, some of them are vacuolized. Neurotubules and vesicles change their form and size and are partly destroyed. Membranous structures of lemmocytes are altered. The electron microscopic investigation adds something new to our data on ultrastructural changes in the arterial neural formations under growth of the malignant tumor previously obtained by means of neurohistological and neurohistochemical methods.

Electrical activity in sympathetic fibres to hind limb muscles of the cat produced by hypothalamic stimulation.

Electrical stimulation of the "Defence Area" of the hypothalamus in anaesthetized cats was accomplished by stereotaxic placement of bipolar stainless steel electrodes; the spinal cord was sectioned at L4. The muscle blood flow in one hind limb was recorded with an electromagnetic flowmeter. Increases of between 100% and 300% were observed during hypothalamic stimulation. Electroneurographic recordings from small nerve filaments supplying tibialis anterior muscle revealed two populations of neurones whose activity was abolished by lumbar sympathectomy. It appears that the increased blood flow in skeletal muscle during stimulation of the hypothalamic "Defence Area" is brought about by a simultaneous inhibition of vasoconstrictor activity and increase in cholinergic vasodilator discharge.