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M Kumada

Publications and source records attributed to M Kumada.

At least 91 records · Page 5Linked to original sources
PubMed1986

Barosensory neurons in the ventrolateral medulla in rabbits and their responses to various afferent inputs from peripheral and central sources.

In 55 anesthetized and paralyzed adult rabbits, 161 spontaneously active neurons which responded to electrical stimulation of A-fibers of the aortic nerve were found within the ventrolateral medulla (VLM). They were termed barosensory VLM neurons, since the aortic nerve A-fibers were considered to consist exclusively of afferents from arterial baroreceptors. Forty percent of barosensory VLM neurons tested (49/123) were activated antidromically by stimulation of the dorsolateral funiculus indicating that they send descending bulbospinal projections. Spontaneous discharges of barosensory VLM neurons were invariably inhibited by stimulation of aortic nerve A-fibers. Ninety-three percent of 80 neurons tested also responded to stimulation of aortic nerve C-fibers, a mixture of barosensory and nonbarosensory afferents. Natural stimulation of carotid sinus baroreceptors by an intravenous injection of phenylephrine in 19 vagotomized rabbits with aortic nerves disrupted inhibited spontaneous activity of all the 50 barosensory VLM neurons tested. By contrast, pharmacological stimulation of right or left carotid body chemoreceptors by close arterial injection of NaCN into the carotid sinus augmented activity of 93% of barosensory VLM neurons tested (41/44). The neuronal response was always greater to stimulation of chemoreceptors in the contralateral carotid sinus. Seven out of 8 barosensory VLM neurons tested (88%) were orthodromically excited by stimulation of the posterior hypothalamic area. In 74% of the 97 neurons examined in 29 vagotomized animals, a distinct respiratory-related rhythm, locked to that of phrenic nerve activity, was discerned. Thus, spontaneous activity of barosensory VLM neurons is inhibited by afferent inputs from aortic and carotid sinus baroreceptors, but is excited by incoming signals from carotid body chemoreceptors and the posterior hypothalamic area. It is also subject to the influence of the central mechanism generating the respiratory rhythm.

Afferent Pathways↗
PubMed1985

The aortic nerve-sympathetic reflex in the rat.

The effects of stimulation of aortic nerve A- and C-fibers on the renal and cardiac sympathetic nerve activities in anesthetized and immobilized Sprague-Dawley rats were investigated. A separate aortic nerve was found in 46 rats (90%) out of 51. Activation of A- and C-fiber groups, alone or in combination, resulted in an inhibition of renal and cardiac nerve activities. However, an excitatory component preceding the inhibitory component, representing the reflex response to stimulation of non-barosensory afferent fibers contained in the carotid sinus or aortic nerve, was never observed. This result provides electrophysiological evidence supporting the view that the rat's aortic nerve does not contain a significant amount of functionally active non-barosensory afferents. As with the aortic nerve reflex in the rabbit and cat, the sympatho-inhibitory action of C-fibers was more powerful and longer-lasting than that of A-fibers. Furthermore, the C-fiber reflex was elicited at stimulus frequencies as low as 2 Hz. No significant difference was found between the reflex response of cardiac and renal nerves. On the other hand, stimulation of the superior laryngeal nerve, which constitutes an important pathway carrying arterial baroreceptor fibers, caused a reflex sympathetic response typically consisting of excitatory and inhibitory components. Thus, the rat's aortic nerve provides a useful experimental means to activate selectively central neural structures associated with barosensory afferents and to elicit the reflex response homologous to that in the arterial baroreceptor reflex in rabbits and cats.

Animals↗
PubMed1985

Sympathoinhibition by A1-noradrenergic neurons is mediated by neurons in the C1 area of the rostral medulla.

In anesthetized, paralyzed rats, bilateral microinjections of kainic acid (KA) into an area of caudal ventrolateral medulla containing A1 noradrenergic neurons of the A1 group (A1 area) first reduced and then elevated arterial pressure (AP), heart rate (HR) and sympathetic renal nerve activity. These effects are attributable to initial excitation and then paralysis of local neurons by KA. The microinjection of tetrodotoxin into an area of rostral ventrolateral medulla containing adrenaline neurons of the C1 group (C1 area) and which is innervated by neurons in A1 area abolished all the effects of KA. The pretreatment of the C1 area with 6-hydroxy-dopamine (6-OHDA) also abolished all the effects of KA. In contrast interruption of projections of the A1 area to the hypothalamus or nucleus tractus solitarii had no effects. The latency for response evoked in renal nerve by stimulation of A1 area was about 10 ms longer than that elicited from C1 area. Tyramine microinjected into the C1 area elicited a dose-dependent decrease in AP prevented by local application of desmethylimipramine. We conclude that neurons of the A1 area tonically inhibit sympathetic activity by inhibiting neurons of the C1 area probably by release of NA.

Adrenergic Fibers↗
PubMed1983

Physiological and pharmacological properties of the three subsystems constituting the aortic nerve-renal sympathetic reflex in rabbits.

Electrical stimulation of the aortic nerve of anesthetized rabbits reflexly evoked both excitation and inhibition of renal nerve activity. The excitatory component of the reflex, observed in about 75% of the animals, was elicited by activation of aortic C-fibers. It was selectively suppressed by chronic treatment of the animal with capsaicin. Intracisternal injection of either [D-ala2]-met-enkephalinamide or beta-endorphin markedly attenuated this excitatory component, although neither affected the excitatory component mediated by chemoreceptor fibers in response to stimulation of the carotid sinus nerve. It seems most likely that nociceptive C-fibers of the rabbit's aortic nerve were responsible for the excitatory component. On the other hand, the inhibitory component was reflexly elicited by stimulation of the aortic A- or C-fiber group activated separately or in combination. In agreement with previous reports, the sympatho-inhibitory action of C-fibers was more powerful and longer-lasting than that of A-fibers. We found that the inhibitory component induced by C-fibers was markedly attenuated by the two opioid peptides mentioned above, but was resistant to pentobarbital. On the contrary, the component mediated by A-fibers was suppressed by pentobarbital but was relatively resistant to the opioid peptides. Thus, the rabbit's aortic nerve-renal sympathetic reflex consists of the following 3 subsystems characterized by different physiological and pharmacological properties: sympatho-inhibitory systems activated by barosensory A- or C-fibers and a sympatho-excitatory system attributable to C-fibers probably of nociceptive modality.

Action Potentials↗
PubMed1982

Reevaluation of projections from the mesencephalic trigeminal nucleus to the medulla and spinal cord: new projections. a combined retrograde and anterograde horseradish peroxidase study.

Microinjection of horseradish peroxidase (HRP) into the medullary parvocellular reticular formation (NPvc) resulted in retrograde labeling of neurons throughout the mesencephalic trigeminal nucleus (Mes V). Labeled cells were large and ovoid and were distributed primarily in the expanded pontine part of the nucleus. However, none of the small neurons in Mes V were labeled. Injections of HRP made into adjacent brainstem structures including the nucleus gigantocellularis, ventrolateral reticular formation, vestibular complex, and the spinal trigeminal nucleus failed to label neurons in Mes V. Injections made into the medullary raphe and into regions reported to receive inputs from Mes V--spinal cord, nucleus tractus solitarius, hypoglossal nucleus, and facial nucleus--were also not followed by transport to Mes V. Anterograde axonal transport of HRP from the region of reticular formation innervated by Mes V also labeled axons projecting to Mes V and to visceral and somatic sensorimotor nuclei in the lower brainstem. Recent reports of afferents from the amygdala to Mes V suggest that reflexes involving the mesencephalic trigeminal nucleus might be modulated by signals from limbic and autonomic as well as somatic centers in the brain.

Animals↗
PubMed1982

Role of the nucleus parabrachialis in cardiovascular regulation in cat.

Electrical stimulation of the nucleus parabrachialis (NPB) and surrounding areas of the dorsolateral pons in anesthetized immobilized cats elicits a rise of arterial pressure (AP) and tachycardia: the parabrachial pressor response (PBPR). The most excitable sites were concentrated within the intermediate one-third of the NPB in its medial and lateral subdivisions. The magnitude of pressor responses and their stimulus sensitivity were substantially greater in NPB than in adjacent areas of the dorsal pons including nucleus locus coeruleus and brachium conjunctivum, suggesting that cardiovascular responses heretofore attributed to locus coeruleus may have been due to excitation of the NPB. The PBPR persisted after chronic cerebellectomy, acute transection of the brain stem at the lower midbrain, or acute bilateral lesions of the nucleus tractus solitarii (NTS), the latter abolishing baroreceptor reflexes. Thus the PBPR cannot be attributed to antidromic or orthodromic stimulation or from NTS. Change in blood flow and regional vascular resistances during the PBPR were measured by electromagnetic flow meters placed on the thoracic aorta, superior mesenteric, renal and femoral arteries. When elicited with stimuli 5 times threshold, the PBPR was associated with an 80% increase in AP, 14+ increase in heart rate, 25% increase in cardiac output, and a 42% increase in total peripheral resistance. There was a differentiated vasoconstriction in the order of superior mesenteric greater than renal greater than femoral arteries. The baroreflex elicited by electrical stimulation of the carotid sinus nerve was reduced during stimulation of the NPB. The tachycardia was abolished by bilateral vagotomy, combined with beta-adrenergic blockade. Such treatment attenuated but did not abolish the hypertension which was only eliminated by subsequent alpha-adrenergic blockade. Thus the hypertension caused by stimulation of NPB is a result both of an increase of total peripheral resistance and of cardiac output. The cardiovascular pattern of the PBPR differ from other responses elicited from the dorsal pons, including the defense response, and the response to cerebral ischemia. We conclude that a powerful cardiovascular response pattern is organized within intrinsic neurons of the NPB. This nucleus may play an important role in organization of cardiovascular control by brain.

Animals↗
PubMed1982

Two types of hypotensive effect of beta-blocking agents.

In anesthetized and immobilized rats, an hour-long continuous intravenous injection of dl-propranolol (PR; 3 mg/kg), pindolol (PI; 1 mg/kg), oxprenolol (OX; 3 mg/kg) or atenolol (AT; 3 mg/kg) invariably resulted in moderate hypotension. When the drug-induced hypotension was plotted against the control arterial pressure (AP), two types of correlation were found. The hypotension induced by PR or PI, both known to accumulate in the brain at a high concentration was positively correlated to the control AP, whereas the hypotension produced by OX or AT, both known to penetrate the blood-brain-barrier poorly, was not. To test the hypothesis that the observed difference was attributable to the presence or lack of sympathoinhibitory action of the drug, the effect of these agents on the renal nerve activity (RNA) was examined. PR or PI diminished the tonic and reflexly evoked RNA, when the evoked RNA was elicited by sciatic nerve stimulation. No such changes were induced by OX or AT. These results demonstrate a modulatory role of sympathoinhibitory effect of beta-blocking agents in their hypotensive action.

Adrenergic beta-Antagonists↗
PubMed1981

Identification of the primary afferent fiber group and adequate stimulus initiating the trigeminal depressor response.

In anesthetized and immobilized rabbits we sought to identify the adequate stimulus and the primary afferent fiber group initiating hypotension and inhibition of sympathetic vasoconstrictor discharges in the trigeminal depressor response (TDR). In the first series of experiments we investigated the effects of electrical stimulation of different fiber groups of the infraorbital nerve on arterial pressure (AP) and renal sympathetic nerve activity (RNA). Stimulation of A-beta-fibers at frequencies between 1 and 200 Hz caused little or no reduction in AP or RNA. Recruitment of A-delta-fibers at stimulus frequencies between 1 and 30 Hz always resulted in falls in AP and RNA (by up to 30 mm Hg, and 75% of control, respectively). Decreases in AP and RNA were augmented to some extent by additional excitation of C-fibers over the same frequency range. In the second series of experiments we applied noxious or innocuous mechanical or thermal stimuli to the hairy skin of the upper lip. Hypotension and inhibition of RNA were elicited by any of the following noxious stimuli of the facial skin: (a) pricking by pins; (b) pinching by serrated forceps, (c) heating above 43% C by a contact thermoprobe; and (d) actual burning of the skin. In contrast, innocuous mechanical or thermal (below 40 degrees C) stimuli failed to diminish AP and RNA. These results indicate that noxious stimuli to the face initiate hypotension and inhibition of the sympathetic nerve activity in the TDR through activation of the A-delta primary afferent fiber group, alone or in combination with the C-fiber group.

Afferent Pathways↗
PubMed1981

Thymocytotoxic autoantibodies found in mice infected with Schistosoma japonicum.

Thymocytotoxic autoantibodies were demonstrated in sera of C3H/HeJms, C57BL/6J, and ddY mice infected with 50 cercariae of Schistosoma japonicum, using C57BL/6J thymocytes as target cells in the trypan blue dye exclusion test. Kinetic study revealed that thymocytotoxic activity began to increase at week 6 of infection, reached a maximum at 8 weeks, and thereafter decreased gradually. Thymocytotoxic antibodies had an optimal reactivity at 4 degrees C and were sensitive to 2-mercaptoethanol treatment, suggesting that they were immunoglobulin M in nature. The cytotoxicity was completely abolished by absorption with C57BL/6J thymocytes but not with S. japonicum parasites or eggs. The antigen reacting with thymocytotoxic antibodies was found in the thymus, brain, spleen, and, to a lesser extent, kidney and liver. In parallel with the appearance of thymocytotoxic antibodies, the increase of background plaque-forming cells to trinitrophenyl, polyvinyl pyrrolidone, and sheep erythrocytes in the spleen of S. japonicum-infected mice suggested that te induction of thymocytotoxic antibodies may be the consequence of polyclonal B-lymphocyte stimulation by the infection.

Animals↗
PubMed1981

Hypertrophy of acridine orange granules in Toxoplasma gondii.

The hypertrophy of acridine orange (AO) granules is found in the cytoplasm of living tachyzoites of Toxoplasma gondii stained with AO under special conditions and observed by means of the fluorescent microscope. Large acid phosphate (Ac Pase) granules appear in the cytoplasm when the above-mentioned tachyzoites are treated more by Gomori's method for Ac Pase. It was confirmed in this investigation that the hypertrophied AO granules are identical to the hypertrophied Ac Pase one by following both granules in the same single tachyzoite throughout the test.

Acid Phosphatase↗
PubMed1981

[Antihypertensive effect of guanfacine in rats].

Effects of an antihypertensive drug, guanfacine, on blood pressure and heart rate were studied in comparison with findings in a related drug, clonidine. Conscious rats (normotensive rat, SHR, DOCA-hypertensive rat and renal hypertensive rat), anesthetized rats and pithed rats were used. Effects of guanfacine resembled those of clonidine but were about 10 times less potent. Both drugs produced an initial transient increase in blood pressure and a prolonged decrease then followed. In the SHR, a decrease in blood pressure occurred. The vasopressor effect of guanfacine was inhibited by phentolamine (1 mg/kg i.v.) and potentiated after previous treatment of the rats with reserpine (5 mg/kg i.p. 24 hr prior to drug administration, indicating that the effect was produced through activation of peripheral alpha-adrenoceptors. The vasodepressor effect of guanfacine was clearly dose-dependent, and was more marked when the initial level of the blood pressure was high, while that of clonidine was dose-dependent, only within a limited dosage range. Vasodepressor effects of guanfacine were associated with a decrease in the efferent discharges of the renal sympathetic nerve. Guanfacine, when given intracisternally produced a greater fall of blood pressure and a greater inhibition of the renal nerve activity than when given intravenously. It is concluded that the antihypertensive effects of guanfacine are due to stimulation of alpha-adrenoceptors within the central nervous system.

Anesthesia↗
PubMed1978

Hemodynamic similarities between the trigeminal and aortic vasodepressor responses.

The hemodynamic changes associated with hypotension elicited by electrical stimulation of the spinal trigeminal complex (trigeminal depressor response, TDR) or the aortic nerve (aortic depressor reflex, ADR) were compared in rabbits anesthetized with urethan. The hypotension associated with each response was accompanied by bradycardia, a marked fall in total peripheral resistance, a small decrease in cardiac output, and a nonuniform decrease in regional vascular resistances, with the order of magnitude of the decrease being femoral greater than mesenteric greater than renal arterial resistance. In individual experiments the percent decrease in heart rate, total peripheral resistance, or regional resistances was plotted against the percent fall in arterial pressure to obtain a pair of regression lines during the TDR and ADR. There was no significant difference in the slope or y-intercept of the regression line between the TDR and ADR for all of the hemodynamic variables examined. In both responses, however, the slope of the femoral resistance/arterial pressure relationship was significantly greater than that of the renal resistance/arterial pressure relationship. We conclude that the TDR is characterized by a pattern of hemodynamic changes similar to that of the ADR.

Animals↗
PubMed1977

The trigeminal depressor response: a novel vasodepressor response originating from the trigeminal system.

Electrical stimulation within discrete sites of the spinal trigeminal complex in anesthetized or decerebrated rabbits results in arterial hypotension, often over 50 mm Hg, bradycardia of up to 60 beats/min, apnea, and gastric hypermotility, collectively termed the trigeminal depressor response (TDR). The threshold for the TDR is less than or equal to 10 muA and is graded up to 3-6 times threshold. It can only be elicited by trains of stimuli of low frequency (0.5-20 Hz); at 50 Hz the response disappears or becomes pressor. The bradycardia is only abolished by bilateral vagotomy combined with beta-adrenergic blockade, and thus results from combined excitation of cardio-vagal and inhibition of cardiac sympathetic nerves. The hypotension is unassociated with changes in cardiac output, does not change after blockade of the bradycardia, but disappears after alpha-adrenergic blockade and hence is entirely attributable to inhibition of ongoing sympathetic vasoconstrictor nerve activity. Below threshold stimulation the TDR can only be elicited from the root entry zone of the Vth nerve, from dorsal portions of the spinal tract of the Vth nerve, and to portions of the nucleus of the spinal tract, notably the nucleus caudalis. A TDR of reduced magnitude can also be elicited by low frequency stimulation of numerous branches of the Vth nerve arising from all three divisions and including the supra- and infra-orbital, the inferior alveolar, and lingual nerves. Bilateral electrolytic lesions of the nucleus tractus solitarii at the obex, with complete abolition of baroreceptor reflexes from carotid sinus and aortic depressor nerves, fail to alter the TDR elicited from the brain or from branches of the Vth nerve, or the vasodepressor responses elicited by electrical stimulation of the central ends of the IXth and Xth cranial nerves transescted distal to the branches of baro-receptor nerves. In contrast, caudal lesions of the trigeminal complex abolish the TDR elicited from brain and Vth nerve and substantially reduces the vasodepressor responses from the IXth and Xth nerves, without altering baroreceptor reflexes. We conclude that the TDR represents a heretofore recognized vasodepressor response dependent upon the spinal trigeminal complex which is at least in part anatomically distinct from pathways subserving arterial baroreceptor and somatic vasodepressor reflexes. The TDR can be reflexly elicited from widely distributed but yet unidentified receptors innervated by branches of the Vth and of the IXth and Xth cranial nerves other than those innervating arterial baroreceptors. It is of unknown function, but may be related to pain mechanisms.

Animals↗