Monkeys were intubated when necessary, but were usually permitted to breathe spontaneously. Atropine (1 mg kg −1) was intravenously injected to inhibit the parasympathetic reflex and pentazocine (10 mg kg −1) was subcutaneously injected to abolish pain, which is resistant to pentobarbital anesthesia. Stable anesthetic conditions were maintained by additional injections of pentobarbital as needed.
Six Japanese monkeys ( Macaca fuscata both male and female), approximately 10–12 years of age and weighing 8–10 kg, were premedicated with intramuscular injections of 15 mg kg −1 ketamine and anesthetized intravenously with 20 mg kg −1 sodium pentobarbital.
The Animal Care and Use Committee at Shiga University of Medical Science approved the use of monkey blood vessels in this study. Furthermore, a tension-response study was performed to determine whether or not the arteries that irrigate the posterior cerebrum, cerebellum and brain stem, when isolated from the Japanese monkey brain, showed comparable responses to those observed in cerebral angiography studies. In this study, cerebral angiography was performed to measure the diameters of arteries irrigating the cerebrum, cerebellum and brain stem when electrical stimulation of the GPN was performed in anesthetized Japanese monkeys. 9 However, it remains unclear whether or not nitrergic nerves from the PPG innervate other major arteries irrigating the cerebrum, cerebellum and brain stem, including the posterior cerebral artery (PCA), superior cerebellar artery (SCA), anterior inferior cerebellar artery (AICA) and basilar artery (BA).
Furthermore, electrical stimulation of unilateral nerve bundles containing parasympathetic nerves produced an increase of cerebral blood flow in the ipsilateral brain of rats treated with atropine and capsaicin this increase of cerebral blood flow in the temporo-parietal area was abolished by a NOS inhibitor. 8 We have also found that these dilatations are suppressed by a NOS inhibitor. 3, 4, 5, 6 We have reported that electrical stimulation of the unilateral PPG or the greater petrosal nerve (GPN), a preganglionic parasympathetic nerve that synaptically connects to the PPG, dilates the ipsilateral anterior cerebral artery (ACA), and the middle cerebral artery (MCA) in anesthetized monkeys 7 and dogs. 1, 2 Histochemistry has showed that nitric oxide synthase (NOS)-containing nerves originating from the pterygoparatine ganglion (PPG) innervate arteries irrigating the cerebrum in many species. It has been reported that nitric oxide (NO) acts as a neurotransmitter in the vasodilator nerves innervating the cerebral arteries in several mammals. In contrast, circulation in the cerebellum and brain stem might be regulated by nitrergic nerves originating not from the pterygopalatine ganglion, but rather from an unknown ganglion (or ganglia). Therefore, nitrergic nerves derived from the pterygopalatine ganglion appear to regulate cerebral vasomotor function. However, stimulation failed to produce vasodilatation of the superior and anterior–inferior cerebellar arteries and the basilar artery in anesthetized monkeys. Cerebral angiography showed that electrical stimulation of the unilateral greater petrosal nerve, which connects to the pterygopalatine ganglion via the parasympathetic ganglion synapse, produced vasodilatation of the anterior, middle and posterior cerebral arteries in the stimulated side. Relaxation of arteries induced by nicotine was abolished by treatment with N G-nitro- L-arginine, a nitric oxide synthase inhibitor, and was restored by addition of L-arginine. Nicotine produced relaxation of arteries by stimulation of nerve terminals innervating isolated monkey arteries irrigating the cerebrum, cerebellum and brain stem. The functional roles of the nitrergic nerves innervating the monkey cerebral artery were evaluated in a tension-response study examining isolated arteries in vitro and cerebral angiography in vivo.
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