Arterial baroreflex control of the sinus node during dobutamine exercise stress testing.
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The contributions of increases in circulating catecholamines, changes in central command, and muscle afferents on baroreflex control of the sinus node during exercise are unclear. We used a dobutamine infusion to induce hemodynamic changes comparable to those of moderate physical exercise in the absence of changes in central command and muscle afferents in 13 healthy subjects. Dobutamine (up to 9 microg/kg body weight per minute) increased systolic blood pressure, shortened the RR interval, increased systolic blood pressure variability, but blunted RR interval variability (P<0.05 versus placebo). Consequently, dobutamine decreased the coherence between variations in systolic blood pressure and RR interval and decreased arterial baroreflex sensitivity from 12+/-2 to 3+/-1 ms/mm Hg (P<0.01). The largest increases in systolic blood pressure with dobutamine were paralleled by the greatest impairments in arterial baroreflex sensitivity (0. 50+info)
Central adrenomedullin augments the baroreceptor reflex in conscious rabbits.
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We examined the roles of central adrenomedullin, proadrenomedullin N-terminal 20 peptide (PAMP), and calcitonin gene-related peptide (CGRP) on the baroreceptor reflex in conscious rabbits. Intracerebroventricular injection of adrenomedullin (0.2 and 1 nmol/80 microL) elicited dose-related increases in arterial pressure and renal sympathetic nerve activity. On the other hand, a subpressor dose of intracerebroventricular infusion of adrenomedullin (1 nmol/300 microL per hour) caused significant increases in baroreflex sensitivities assessed by renal sympathetic nerve activity and heart rate compared with vehicle infusion (Gmax; -14.9+/-1.7 versus -8.0+/-0.7%/mm Hg, P<0.01, and -8.1+/-0.8 versus -5.1+/-0.5 bpm/mm Hg, P<0.01, respectively). Intracerebroventricular infusion of CGRP (1 nmol/300 microL per hour), which is structurally homologous to adrenomedullin, also enhanced the baroreflex controls of renal sympathetic nerve activity and heart rate. However, the intracerebroventricular infusion of PAMP (30 nmol/300 microL per hour) failed to alter the baseline levels of arterial pressure and baroreflex sensitivities. These results suggest that central adrenomedullin and CGRP, but not PAMP, participate in cardiovascular regulation to augment the baroreflex controls of renal sympathetic nerve activity and heart rate in conscious rabbits. (+info)
Upregulation of tumor necrosis factor alpha transport across the blood-brain barrier after acute compressive spinal cord injury.
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Tumor necrosis factor alpha (TNF) is a cytokine that is involved in the inflammatory process after CNS injury and is implicated in neuroregeneration. A saturable transport system for TNF located at the blood-brain barrier (BBB) is responsible for the limited entry of TNF from blood to the CNS in normal mice. After partial disruption of the BBB by compression of the lumbar spinal cord, permeability to TNF was increased not only in the lumbar spinal cord but also in brain and distal spinal cord segments, where the BBB remained intact. The increase in the entry of TNF to the CNS followed a biphasic temporal pattern, with a first peak immediately after injury and a second peak starting on day 3; these changes lasted longer than the mere disruption of the BBB. The increased entry of TNF was abolished by addition of excess unlabeled TNF, showing that the transport system for TNF remained saturable after spinal cord injury (SCI) and providing evidence that the enhanced entry of TNF could not be explained by diffusion or leakage. This study adds strong support for our concept that the saturable transport system for TNF across the BBB can be upregulated in the diseased state, and it suggests that the BBB is actively involved in the modulation of the processes of degeneration and regeneration after SCI. (+info)
Inhibition of inspiratory motor output by high-frequency low-pressure oscillations in the upper airway of sleeping dogs.
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1. We utilized a chronically tracheostomized, unanaesthetized dog model to study the reflex effects on inspiratory motor output of low-amplitude, high-frequency pressure oscillations (HFPOs) applied to the isolated upper airway (UA) during stable non-rapid eye movement (NREM) sleep. 2. HFPOs (30 Hz and +/-2 to +/-4 cmH2O) were applied via a piston pump during eupnoea, inspiratory resistive loading and tracheal occlusion. 3. When applied to the patent UA during expiration, and especially during late expiration, HFPOs prolonged expiratory time (TE) and tonically activated the genioglossus muscle EMG. When applied to the patent UA during inspiration, HFPOs caused tonic activation of the genioglossus muscle EMG and inhibition of inspiratory motor output by either: (a) a shortening of inspiratory time (TI), as inspiration was terminated coincident with the onset of HFPOs; or (b) a prolonged TI accompanied by a decreased rate of rise of diaphragm EMG and rate of fall of tracheal pressure. These effects of HFPOs were observed during eupnoea and inspiratory resistive loading, but were maximal during tracheal occlusion where the additional inhibitory effects of lung inflation reflexes were minimized. 4. During eupnoea, topical anaesthesia of the UA abolished the HFPO-induced prolongation of TE, suggesting that the response was mediated primarily by mechanoreceptors close to the mucosal surface; whereas the TE-prolonging effects of a sustained square wave of negative pressure (range, -4.0 to -14.9 cmH2O) sufficient to close the airway were preserved following anaesthesia. 5. These results demonstrate that high-frequency, low-amplitude oscillatory pressure waves in the UA, similar to those found in snoring, produce reflex inhibition of inspiratory motor output. This reflex may help maintain UA patency by decreasing the collapsing pressure generated by the inspiratory pump muscles and transmitted to the UA. (+info)
Cortical control of spinal pathways mediating group II excitation to human thigh motoneurones.
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1. The possibility was investigated that cortical excitation to human thigh motoneurones is relayed via lumbar premotoneurones. 2. Test responses were evoked by transcranial magnetic stimulation (TMS) in voluntarily contracting quadriceps (Q) and semitendinosus (ST) muscles: either a motor evoked potential (MEP) in surface recordings or a peak of cortical excitation in the post-stimulus time histogram (PSTH) of single motor units was used. These test responses were conditioned by stimuli to the common peroneal (CP) or gastrocnemius medialis (GM) nerves. 3. CP stimulation evoked a large biphasic facilitation of the Q MEP, with early, short-lasting, low-threshold (0.6-0.8 x motor threshold (MT)) and late, longer lasting and higher threshold (1.2-1.5 x MT) peaks separated by a period of depression. GM nerve stimulation evoked a similar early depression and late facilitation in the ST MEP. 4. CP-induced effects in the Q H reflex were different (smaller late facilitation not preceded by any depression), suggesting that CP and cortical volleys interact at a premotoneuronal level to modify the Q MEP. 5. Peaks of cortical excitation evoked by TMS in single motor unit PSTHs were modulated by the conditioning volley like the MEPs with, in Q motor units, early and late CP-induced facilitations separated by a depression, and in ST motor units a late GM-induced facilitation. Facilitations on combined stimulation (i) were greater than the sum of effects by separate stimuli and (ii) never affected the initial part of the cortical peak. 6. It is concluded that the features of the reported facilitatory interactions between cortical and peripheral volleys are consistent with interactions in a population of lumbar excitatory premotoneurones co-activated by group I and group II afferents. The potency of the effects suggests that a significant part of the cortical excitation to motoneurones of thigh muscles is relayed via these interneurones. 7. It is argued that the early depression in ST motoneurones and the separation of the two peaks of facilitation in Q motoneurones reflect a cortical facilitation of spinal inhibitory interneurones projecting on excitatory premotoneurones. (+info)
Mechanism of biphasic response of renal nerve activity during acute cardiac tamponade in conscious rabbits.
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Renal sympathetic nerve activity (RSNA) responses to acute cardiac tamponade were studied in conscious rabbits with all reflexes intact (Int) or after either surgical sinoaortic denervation (SAD) or administration of intrapericardial procaine (ip-Pro) or intravenous procaine (iv-Pro). In Int rabbits, the mean arterial pressure (MAP) remained relatively constant until the pericardial volume reached 7. 7 ml, whereas the RSNA increased to 226% [compensated cardiac tamponade (CCT)], then, at a pericardial volume of 9.3 ml, the MAP fell sharply and RSNA decreased to 34% [decompensated cardiac tamponade (DCT)]; 1 min after cessation of pericardial infusion, an intravenous injection of naloxone resulted in increases in both MAP and RSNA. In SAD rabbits, RSNA did not alter throughout CCT and DCT, but increased on injection of naloxone. In ip-Pro rabbits, RSNA increased during CCT but did not decrease during DCT, whereas, in iv-Pro rabbits, the RSNA response was similar to that in Int rabbits. These results indicate that RSNA responses to cardiac tamponade are biphasic, with an increase during CCT and a decrease during DCT. Sinoaortic baroreceptors are involved in mediating the increase in RSNA, whereas cardiac receptors may be involved in mediating the decrease in RSNA. An endogenous opioid may be responsible for the decrease in RSNA seen during DCT. (+info)
Sex differences in morphine-induced ventilatory depression reside within the peripheral chemoreflex loop.
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BACKGROUND: This study gathers information in humans on the sites of sex-related differences in ventilatory depression caused by the mu-opioid receptor agonist morphine. METHODS: Experiments were performed in healthy young men (n = 9) and women (n = 7). Dynamic ventilatory responses to square-wave changes in end-tidal carbon dioxide tension (7.5-15 mmHg) and step decreases in end-tidal oxygen tension (step from 110 to 50 mmHg, duration of hypoxia 15 min) were obtained before and during morphine infusion (intravenous bolus dose 100 microg/kg, followed by 30 microg x kg(-1) x h(-1)). Each hypercapnic response was separated into a fast peripheral and slow central component, which yield central (Gc) and peripheral (Gp) carbon dioxide sensitivities. Values are mean +/- SD. RESULTS: In carbon dioxide studies in men, morphine reduced Gc from 1.61 +/- 0.33 to 1.23 +/- 0.12 l x min(-1) x mmHg(-1) (P < 0.05) without affecting Gp (control, 0.41 +/- 0.16 and morphine, 0.49 +/- 0.12 l x min(-1) x mmHg(-1), not significant). In carbon dioxide studies in women, morphine reduced Gc, from 1.51 +/- 0.74 to 1.17 +/- 0.52 l x min(-1) x mmHg(-1) (P < 0.05), and Gp, from 0.54 +/- 0.19 to 0.39 +/- 0.22 l x min(-1) x mmHg(-1) (P < 0.05). Morphine-induced changes in Gc were equal in men and women; changes in Gp were greater in women. In hypoxic studies, morphine depressed the hyperventilatory response at the initiation of hypoxia more in women than in men (0.54 +/- 0.23 vs. 0.26 +/- 0.34 l x min(-1) x %(-1), respectively; P < 0.05). The ventilatory response to sustained hypoxia (i/e., 15 min) did not differ between men and women. CONCLUSIONS: The data indicate the existence of sex differences in morphine-induced depression of responses mediated via the peripheral chemoreflex pathway, with more depression in women, but not of responses mediated via the central chemoreflex pathway. In men and women, morphine did not change the translation of the initial hyperventilatory response to short-term hypoxia into the secondary decrease in inspired minute ventilation (Vi) caused by sustained hypoxia. (+info)
Jaw reflexes evoked by mechanical stimulation of teeth in humans.
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Jaw reflexes evoked by mechanical stimulation of teeth in humans. The reflex response of jaw muscles to mechanical stimulation of an upper incisor tooth was investigated using the surface electromyogram (SEMG) of the masseter muscle and the bite force. With a slowly rising stimulus, the reflex response obtained on the masseter SEMG showed three different patterns of reflex responses; sole excitation, sole inhibition, and inhibition followed by excitation. Simultaneously recorded bite force, however, exhibited mainly one reflex response pattern, a decrease followed by an increase in the net closing force. A rapidly rising stimulus also induced several different patterns of reflex responses in the masseter SEMG. When the simultaneously recorded bite force was analyzed, however, there was only one reflex response pattern, a decrease in the net closing force. Therefore, the reflex change in the masseter muscle is not a good representative of the net reflex response of all jaw muscles to mechanical tooth stimulation. The net response is best expressed by the averaged bite force. The averaged bite force records showed that when the stimulus force was developing rapidly, the periodontal reflex could reduce the bite force and hence protect the teeth and supporting tissues from damaging forces. It also can increase the bite force; this might help keep food between the teeth if the change in force rate is slow, especially when the initial bite force is low. (+info)