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At least 325 records · Page 18Linked to original sources
PubMed1992

Cerebral and spinal cord blood flow in awake and fentanyl-N2O anesthetized rats: evidence for preservation of blood flow autoregulation during anesthesia.

Blood flow responses to alterations in mean arterial blood pressure (MABP) were measured in the cerebral cortex, subcortex, midbrain, and spinal cord of awake rats. Data were compared with those of rats anesthetized with an i.v. fentanyl infusion and inspired nitrous oxide (N2O). Regional cerebral blood flow was measured using radioactive microspheres in the following blood pressure ranges: (a) <40 mm Hg; (b) 40-60; (c) 60-80; (d) 80-100; (e) 100-120; (f) 120-140; (g) 140-160; and (h) >160. Blood pressure was increased with phenylephrine or decreased with trimethaphan combined with blood withdrawal. Cerebral blood flow was not measured when MABP was less than 60 mm Hg in awake rats. Autoregulation was seen in all brain areas between 60 and 140 mm Hg in both treatment groups. Although regional cerebral blood flow was not different between the two treatment groups, PaCO2 was 2-4 mm Hg lower in awake rats. This suggests that PaCO2-corrected cerebral blood flow may be 10-20% lower with fentanyl-N2O anesthesia.

Journal Article↗
PubMed1995

Blood pressure control during surgical operations.

In order to reduce intraoperative blood loss and spare blood transfusion, we developed a blood pressure control system using a state-predictive controller. Using adult mongrel dogs, the mean arterial pressure (MAP) was recorded from a femoral artery while trimethaphan camsilate was infused at constant rates. A pure delay plus a first-order delay model was then derived from the dose-response curves and the values of plant parameters (gain, time-constant, dead-time, and so on) were estimated based on the experimental data. For this model, a state-predictive servo system was designed to cope with the pure delay existing in the model, and simulated. In order to evaluate the accuracy and reliability of this system, we experimented on dogs. With a reference MAP set at 60 mmHg, the MAP reached the reference level in 5.8 to 26.5 min. The duration of error from the reference MAP (+/- 10%) was 2.3 +/- 3.9 min/h (n = 7). These results indicated the safety and stability of our system.

Animals↗
PubMed1996

Cerebral autoregulation is impaired in patients resuscitated after cardiac arrest.

BACKGROUND: Cerebral autoregulation is important to maintain a constant perfusion in the face of changes in blood pressure. It is reported to be impaired in pathologic states, including hypertension, cerebral infarction, and head injury. However, it is not clear whether cerebral autoregulation is impaired in resuscitated patients after cardiac arrest. METHODS: Cerebral autoregulation in comatose patients after cardiac arrest was assessed by using an indirect method of cerebral blood flow (CBF). Eight patients who had cardiac arrest outside of the hospital and were successfully resuscitated in the emergency room were included in this study. A catheter was inserted percutaneously into the right internal jugular vein and positioned so that the tip was in the jugular bulb. Mean arterial pressure (MAP) was changed to a value of 30% lower or higher than baseline MAP by infusing trimethaphan or methoxamine, respectively. At each MAP level, arterial and jugular bulb venous blood gases were measured, and arterial-jugular bulb venous oxygen content difference (AVDO2) was calculated. RESULTS: The 1/AVDO2 (CBFI) and oxygen saturation of jugular bulb venous blood (SjvO2) significantly decreased at the lower MAP level, and significantly increased at the higher MAP level. The ratio of the CBFI at the lower MAP level to the CBFI at baseline (CBFI-L/CBFI-B) inversely correlated with the SjvO2 at baseline. CONCLUSIONS: Assuming that the cerebral metabolic rate of oxygen does not change during the interventions in MAP, the changes of CBFI and SjvO2 seen after the decrease or increase in MAP indicate that cerebral autoregulation was impaired in these resuscitated patients. The degree of the impairment of cerebral autoregulation may be secondary to the degree of brain injury caused by the cerebral ischemia accompanying cardiac arrest.

Aged↗
PubMed1993

Blood pressure effects of thromboxane A2 blockade in spontaneously hypertensive rats.

1. The effects of CGS 22652, a thromboxane (Tx) A2 synthase inhibitor and TxA2/prostaglandin (PG) H2 receptor antagonist, on blood pressure (BP) were studied in conscious freely moving spontaneously hypertensive rats (SHR). 2. Three groups of 13 male SHR were subcutaneously infused from 5 to 11 weeks of age via osmotic minipumps with CGS 22652 at doses of 5 (SHRa) or 10 (SHRb) mg/kg per 24 h or with the vehicle only (SHRc). A fourth group (SHRd, n = 13) was orally treated from 3 to 11 weeks of age with CGS 22652 (30 mg/kg) given by gavage once a day. 3. CGS 22652 dose-dependently reduced the age-related increase in systolic BP. The pressor response to noradrenaline (200 ng/kg, i.v.) but not to angiotensin I or II was slightly (P < 0.05) diminished in 11 week old SHRb and SHRd compared to SHRc. Acute ganglionic blockade by trimethaphan (10 mg/kg, i.v.), as well as angiotensin converting enzyme inhibition by perindopril (2 mg/kg, i.v.) decreased BP to a similar extent in the four groups. After combined blockade of vasopressin receptors and of the autonomic nervous system and the administration of a direct vasodilator (hydralazine, 3 mg/kg, i.v.), the residual mean BP was identical in the four groups of rats. 4. Chronic treatment with CGS 22652 dose-dependent antagonized the TxA2/PGH2 receptors but did not modify the TxA2 synthesis. The urinary sodium excretion did not differ between groups. 5. In conclusion, at the doses used, CGS 22652 given either orally or subcutaneously exhibited only TxA2/PGH2 receptor blocking properties in SHR.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1985

Characterization of cholinoreceptors in the rat urinary bladder by the use of agonists and antagonists of the cholinergic system.

The effects of stimulatory and inhibitory compounds acting on both nicotinic and muscarinic receptors have been evaluated in the isolated urinary bladder from adult and immature (14-18 days old) rats. Acetylcholine and bethanechol were found to induce concentration-dependent contractions which were inhibited by atropine and pirenzepine; compound McN-A-343 had a negligible contractile activity whereas DMPP had no effect at all. Responses to electrical field stimulation were abolished by tetrodotoxin (3 X 10(-8) M), enhanced by eserine (10(-8) M) and scarcely affected by hexamethonium (10(-3) M), trimethaphan (10(-3) M) and d-tubocurarine (10(-3) M). Atropine, pirenzepine and DMPP induced only a partial inhibition (50%) of the twitch response, whereas compound McN-A-343 caused a concentration-dependent inhibitory effect which was maximum (100% inhibition) at 10(-2) M. No significant differences were found between results obtained in immature and adult animals as regards either the stimulatory or the inhibitory compounds tested. It was concluded that postjunctional muscarinic receptors were responsible for the stimulatory responses observed, whereas an additional involvement of unknown mechanisms, probably not related to the cholinergic system, was suggested by the peculiar results obtained with DMPP and compound McN-A-343 on electrically-stimulated urinary bladder. Whatever the mechanisms involved, however, they are already present at the first stage of postnatal development.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1986

Impaired autoregulation of cerebral blood flow in long-term type I (insulin-dependent) diabetic patients with nephropathy and retinopathy.

Autoregulation of cerebral blood flow, i.e., the maintenance of cerebral blood flow within narrow limits during changes in arterial perfusion pressure, was studied in nine healthy control subjects and in 12 long-term Type I (insulin-dependent) diabetic patients with clinical microangiopathy. Cerebral blood flow was measured by the intravenous 133Xenon method. Mean arterial blood pressure was elevated approximately 30 mmHg by intravenous infusion of angiotensin amide II and lowered about 10 mmHg by intravenous infusion of trimethaphan camsylate. In the control subjects the flow/pressure curve was horizontal indicating perfect autoregulation. In the diabetic patients the flow/pressure curve showed a significant slope with a 1.9% change in CBF per 10 mmHg change in mean arterial blood pressure as compared to a slope value of -0.4% in the control subjects (P less than 0.05). Our results confirm the previous findings suggesting that autoregulation of cerebral blood flow is impaired in some long-term Type I diabetic patients with clinical microangiopathy (arteriolar hyalinosis).

Adult↗
PubMed1984

Models for studying long-term recovery following forebrain ischemia in the rat. 2. A 2-vessel occlusion model.

A model is described in which transient ischemia is induced in rats anaesthetized with N2O:O2 (70:30) by bilateral carotid artery clamping combined with a lowering of mean arterial blood pressure to 50 mm Hg, the latter being achieved by bleeding, or by bleeding supplemented with administration of trimetaphan or phentolamine. By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long-term recovery studies. Autoradiographic measurements of local CBF showed that the procedure reduced CBF in neocortical areas, hippocampus, and caudoputamen to near-zero values, flow rates in a number of subcortical areas being variable. Administration of trimethaphane or phentolamine did not affect ischemic and postischemic flow rates, nor did they alter recovery of EEG and sensory-evoked responses, but trimetaphan blunted the changes in plasma concentrations of adrenaline and noradrenaline. Recovery experiments showed that 10 min of ischemia gave rise to clear signs of permanent brain damage, with a small number of animals developing postischemic seizures that led to the death of the animals in status epilepticus. After 15 min of ischemia, such alterations were more pronounced, and the majority of animals died. It is concluded that the short revival times noted are explained by the fact that the model induces near-complete ischemia, and that recovery following forebrain ischemia is critically dependent on residual flow rates during the period of ischemia.

Animals↗
PubMed1992

Reflex changes in post- and preganglionic sympathetic adrenal nerve activity and postganglionic sympathetic renal nerve activity upon arterial baroreceptor activation and during severe haemorrhage in the rat.

The aim of the study was to compare pre- (pre-aSNA) and postganglionic adrenal sympathetic nerve activity (post-aSNA) and postganglionic renal sympathetic nerve activity (rSNA) in rats during arterial baroreceptor activation and haemorrhage. Adrenal multifibre nerve activity was recorded in chloralose-anaesthetized Wistar rats. To test for pre-aSNA or post-aSNA in adrenal nerves, a ganglionic blocker, trimethaphan (10 mg kg-1), was administered i.v. If the nerve activity in the adrenal nerve decreased or increased the nerve was considered to contain predominantly post- or preganglionic fibres, respectively. In contrast, the renal nerves exhibit an almost pure postganglionic activity. Baroreceptor activity was tested by activation of baroreceptors, with an alpha-receptor agonist, phenylephrine, which was slowly infused (0.5-2 micrograms kg-1 min-1), and to deactivate the baroreceptors the rats were bled down to 50 mmHg for 8 min. The experiments showed that all tested nerve types were baroreceptor dependent. There were no significant differences between the slopes relating nerve activity inhibition to increase in blood pressure (infusion of phenylephrine). During maximal inhibition there was a difference between the rSNA and pre-aSNA, 87 +/- 4%, n = 6, and 68 +/- 6%, n = 10 (P less than 0.01) of the control value, respectively. The maximal inhibition of post-aSNA was 80 +/- 3%, n = 7, of the control value. During haemorrhage there was a difference between the nerve populations. Pre-aSNA responded with a marked increase within 1.5 min (159 +/- 29% of control, n = 7) and was then maintained at that level until retransfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1992

Differential responses in post- and pre-ganglionic adrenal sympathetic nerve activity and renal sympathetic nerve activity after injection of 2-deoxy-D-glucose and insulin in rats.

The aim of the study was to compare pre-ganglionic adrenal nerve activity (pre-aSNA) to post-ganglionic adrenal nerve activity (post-aSNA) in rats after administration of 2-deoxy-D-glucose (2-DG, 500 mg kg-1, i.v.), which mimicks a central hypoglycaemia or to the response in pre-aSNA and post-aSNA to hypoglycaemia after injection of insulin (5U). Renal postganglionic sympathetic nerve recordings (rSNA) in a separate group was used as a reference. Adrenal or renal multifibre nerve activity was recorded in chloralose-anaesthetized Wistar-rats. Trimethaphan, a short-lasting ganglionic blocker, was administered i.v. (10 mg kg-1) in order to test for pre- or post-aSNA in the adrenal nerves. The adrenal nerves was considered to contain predominantly post or preganglionic fibres, respectively if the nerve activity in the adrenal nerve decreased (post-aSNA) or increased (pre-aSNA). In contrast, all renal nerves showed almost a pure postganglionic activity. Post-aSNA responded with a tendency to increase after the 2-DG injection. The highest value (percentage change from control) 5 min after injection was 12 +/- 9%. The pre-aSNA increased with values of 99 +/- 52% at 3 min and 86 +/- 31% at 5 min (percentage change from control). The activity in the rSNA was only slightly decreased after the injection of 2-DG when compared to pre-drug control activity. There was a significant difference between the pre-aSNA vs. post-aSNA at 1 min (P less than 0.05), 3 min (P less than 0.01) and 5 min (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1993

Nicotinic agonists antagonize quantal size increases and evoked release at frog neuromuscular junction.

1. Previous studies at the frog neuromuscular junction showed that quantal size can be increased two- to fourfold by a variety of treatments, including prior exposure to hypertonic solution (which activates protein kinase A) and insulin (which acts via an unknown pathway). Size increases largely because quanta contain more acetylcholine (ACh). 2. Now the effects of cholinergic agonists on the increases in quantal size have been studied. One muscle from a frog was kept for 2 h in hypertonic sodium gluconate solution. The miniature endplate potential (MEPP) sizes were measured in saline: they had increased about fourfold. The paired muscle went through the same experimental sequence, except that an agonist was added to the hypertonic gluconate solution. Again MEPP sizes were measured in saline. The increase in quantal size was significantly depressed by 0.2 microM 1,1-dimethyl-4-phenyl- piperazinium (DMPP). The sequence of effectiveness of agonists was: DMPP > carbachol > or = ACh = cytisine > oxytremorine. This sequence suggests that the receptor belongs in the nicotinic class. 3. Quantal size is doubled after 1 h in insulin. One micromolar carbachol largely blocked the size increase. 4. The effects of cholinergic antagonists were tested by keeping the experimental muscle in hypertonic gluconate solution containing 1 microM carbachol plus an antagonist. The controls were paired muscles kept in hypertonic gluconate solution (without carbachol or antagonist). MEPP sizes were measured in saline. The depressing action of carbachol on the increase in MEPP size was blocked by 0.2 microM neuronal-bungarotoxin (nBTX). The sequence of effectiveness of antagonists was: nBTX > trimethaphan > d-tubocurarine (dTC). Ten micromolar atropine (without carbachol) depressed the increase in quantal size. Therefore, the antagonist potency of atropine could not be adequately tested. Carbachol action was not blocked by 10 microM hexamethonium or 10 microM mecamylamine. 5. Once quanta are made large they can be converted back to normal size by cholinergic agonists. Muscles in which quantal size had been enlarged were exposed to hypertonic solutions containing the agonist. Quantal size was reduced to a fraction of its former value when the hypertonic solution contained 1 microM carbachol- or 1 microM DMPP. One micromolar oxytremorine had no effect. Carbachol still reduced quantal size when applied in low-Ca2+ solutions, so it does not appear to act by elevating intracellular [Ca2+]. 6. Previous work suggested that the treatments produce a subpopulation of large quanta that are positioned for release.(ABSTRACT TRUNCATED AT 400 WORDS)

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1988

Sites of action of mu-, kappa- and sigma-opiate receptor agonists at the feline ileocecal sphincter.

The sites of action of several opiate agonists at the feline ileocecal sphincter (ICS) were studied. Dose-response curves for the relatively specific ligands for the mu-, kappa-, and sigma-receptors were determined using morphine (mu-receptors), dynorphin-(1-13) (kappa-receptors), and N-allylnormetazocine (sigma-receptors). Each agonist results in a contractile ICS response. The ICS responded stereospecifically to the levo-isomer of N-allylnormetazocine. Atropine (30 micrograms/kg) or naloxone (100 micrograms/kg) antagonized the ICS response to morphine and to (-)-N-allylnormetazocine. Higher doses of naloxone were required to inhibit the ICS response to dynorphin. Neither atropine nor tetrodotoxin inhibited the ICS response to dynorphin. The ICS response to dynorphin was enhanced after tetrodotoxin. Morphine tachyphylaxis inhibited the ICS response to (-)-N-allylnormetazocine and vice versa. The ICS response to morphine was unaffected by vagotomy but inhibited by trimethaphan camsylate. This study suggests that dynorphin (kappa-receptor) acts at a smooth muscle receptor to mediate contraction and a neural receptor to mediate relaxation, while (-)-N-allylnormetazocine acts at the ICS via a mu-receptor. mu-Receptor activation causes ICS contraction via a cholinergic pathway.

Animals↗
PubMed1989

Substance P: mechanism of action and receptor distribution at the feline ileocecal sphincter region.

The purpose of this study was to determine the mechanism of action of substance P at the distal ileum, ileocecal sphincter (ICS), and proximal colon in the cat and to determine the localization of substance P receptors at these sites by autoradiography. Intraluminal pressures and myoelectric activity were recorded at the feline distal ileum, ICS, and colon. Substance P caused a tonic and phasic spike-dependent contractile response at all three sites. The antagonists propranolol, phentolamine, and naloxone did not affect the contractile response to substance P at the ileum, ICS, or colon. The ganglionic blocker trimethaphan camsylate potentiated the response to substance P at all three sites, P less than 0.05. Both atropine and tetrodotoxin reduced the response of substance P at the ileal site. At the ICS, atropine or tetrodotoxin reduced, but did not obliterate, the effect of substance P. Neither atropine nor tetrodotoxin reduced substance P-induced colonic contractions. By use of autoradiography, specific binding for substance P was determined to be present at all three sites with the greatest concentration of substance P receptors in the circular muscle layer. In conclusion, these studies suggest multiple sites of action of substance P. At the ileum, substance P causes contraction via a cholinergic pathway. At the ICS, substance P has an excitatory action through a cholinergic pathway and also at smooth muscle receptors. In the proximal colon, the excitatory action of substance P is via smooth muscle receptors. An inhibitory ganglionic pathway also exists at all three sites. Substance P receptors exist predominantly in the circular muscle region of the ileum, ICS, and the proximal colon.

Animals↗
PubMed1977

Brain blood flow autoregulation and metabolism during halothane anesthesia in monkeys.

Past studies suggest that halothane causes cerebrovascular dilatation and increased cerebral blood flow (CBF); these properties may be relevant to its use for neurosurgical procedures. We studied CBF autoregulation in monkeys during anesthesia with 66% N2O/33% O2 and with 0.5%, 1.0%, and 2.0% inspired halothane at various cerebral perfusion pressures (CPP) achieved by infusion of trimethaphan camsylate or phenylephrine. CBF was measured by monitoring brain xenon-133 clearance after intra-arterial injection of the isotope in saline. CBF autoregulation was intact during N2O/O2 and during 0.5% halothane/N2O/O2 anesthesia at CPPs ranging from 50 to 100 mmHg, but began to fail at 1.0% halothane. Complete loss of autoregulation occurred during 2% halothane/N2O/O2 anesthesia. Estimated brain O2 consumption fell by 30%, 40%, and 50% during 0.5%, 1.0%, and 2.0% halothane anesthesia, respectively, compared to O2 consumption during N2O/O2 anesthesia (100%).

Anesthesia↗
PubMed1980

Adrenal contribution to cardiac responses elicited by acute hypoxia in piglets.

The adrenal contribution to cardiac responses elicited by acute hypoxia was assessed in 16 piglets, 1-12 wks old, anesthetized with pentobarbital (30 mg/kg). External cardiac work was held constant and parasympathetic blockade was produced in each animal with atropine (1 mg). Hypoxia was produced by addition of N2 to the respirator. In a sham-adrenalectomy group (n = 6) left ventricular (LV) dP/dtmax increased significantly during hypoxia (PaO2 approximately 30 mmHg) to 3,680 +/- 414 mmHg/s from control values of 2,686 +/- 317 mmHg/s (P < 0.01). Heart rate rose from 171 +/- 6 to 186 +/- 7 beats/min (P < 0.02). These responses were not significantly altered by ganglionic blockade with trimethaphan camsylate (0.5 mg x kg-1 x min-1). Equally large increases of LV dP/dtmax appeared when heart rate was held constant by pacing. beta-Adrenoreceptor blockade with practolol (4 mg/kg) sharply reduced but did not eliminate the response. In contrast, no changes in LV dP/dtmax or heart rate were observed during hypoxia in adrenalectomized piglets (n = 6). These findings indicate that the increased cardiac contractility during acute hypoxia in piglets is dependent on the integrity of the adrenal glands and that there is minimal contribution from cardiac sympathetic nerves.

Acute Disease↗
PubMed1987

Control of cardiac function and venous return in thyrotoxic calves.

The mechanisms responsible for maintenance of the high-output state associated with thyrotoxicosis have been investigated by measurement of cardiac-function curves and venous compliance during ganglionic blockade with trimethaphan. Thirteen calves were injected daily with L-thyroxine (200 micrograms/kg) for 12-14 days. Thyroxine treatment increased heart rate (70%), left ventricular systolic pressure (22%), cardiac output (120%), left ventricular maximum rate of pressure development (dP/dt) (56%), and total blood volume (18%) and decreased systemic vascular resistance (39%). These hemodynamic changes persisted during ganglionic blockade or autonomic blockade with atropine and propranolol. Cardiac-function curves in conscious thyrotoxic calves were displaced upward and to the left. Mean circulatory filling pressure (MCFP), measured during anesthesia, was increased from 8 +/- 1 to 12 +/- 1 mmHg. During autonomic and ganglionic blockade MCFP remained elevated after treatment with thyroxine. Venous compliance decreased from 2.1 +/- 0.2 to 1.3 +/- 0.1 ml X mmHg-1 X kg-1 after thyroxine. Unstressed vascular volume was increased from 52.3 +/- 1.1 to 67.1 +/- 0.9 ml/kg. Thus the elevated cardiac output and new cardiac-function curve in thyrotoxicosis are associated with a combination of increased inotropic state, increased blood volume, and decreased venous compliance. These effects are not the result of autonomic influences and may represent direct actions of thyroid hormone on the heart and peripheral venous circulation.

Animals↗
PubMed1987

Renal pressor reflex: involvement of sympathetic vasoconstrictor mechanisms.

We examined whether vasopressin and/or sympathetic vasoconstrictor mechanisms constitute the efferent limb of an afferent renal nerve (ARN)-dependent renal pressor "reflex" produced by acute unilateral renal artery stenosis (RST). Rats that had received sinoaortic denervation (SAD) were implanted with right renal artery occluders and flow probes. After recovery, conscious rats received captopril. Acute RST increased arterial pressure (AP) by 25% and mesenteric and hindquarters resistances by 35 and 51%, respectively. Vasopressin receptor antagonism was without effect on the reflex. Ganglionic blockade (chlorisondamine or trimethaphan) abolished the reflex, as did alfaxalone/alfadolone or urethan-chloralose anesthesia. In an additional study, SAD animals were prepared with chronic T6 spinal cord transection. Increases in AP during RST were unaffected by spinal transection (27 +/- 4 mmHg). However, the increase in hindquarter resistance in the sham-transected animals (57 +/- 12%) was markedly attenuated (19 +/- 4%) in the spinal-transected group. The data suggest that in animals with depressed baroreflexes and renin-angiotensin system responsiveness, acute RST initiates an ARN-dependent pressor reflex with vasoconstrictor nerves comprising the efferent limb of the reflex. The reflex can be integrated at the spinal level and is highly sensitive to anesthesia.

Animals↗
PubMed2001

Mechanisms of respiratory sinus arrhythmia in patients with mild heart failure.

The high-frequency (HF) component of the heart rate variability (HRV) is regarded as an index of cardiac vagal responsiveness. However, when vagal tone is decreased, nonneural mechanisms could account for a significant proportion of the HF component. To test this hypothesis, we examined the HRV spectral power in 20 patients with mild chronic heart failure (CHF) and 11 controls before and during ganglion blockade with trimethaphan camsylate (3-6 mg/min iv). A small HF component was still present during ganglion blockade, and its amplitude did not differ between CHF patients and controls. The average contribution of nonneural oscillations to the HF component was 15% (range 1-77%) in patients with CHF and 3% (range 0. 7-30%) in healthy controls (P < 0.005). During controlled breathing at 0.16 Hz, however, it decreased to 1% (range 0.2-13%) in healthy controls and 5% (range 1-44%) in CHF patients. Our results indicate that the HF component can significantly overestimate cardiac vagal responsiveness in patients with mild CHF. This bias is improved by controlled breathing, since this maneuver increases the vagal contribution to HF without affecting its nonneural component.

Arrhythmia, Sinus↗
PubMed2002

Synergistic interactions between airway afferent nerve subtypes mediating reflex bronchospasm in guinea pigs.

The hypothesis that airway afferent nerve subtypes act synergistically to initiate reflex bronchospasm in guinea pigs was addressed. Laryngeal mucosal application of capsaicin or bradykinin or the epithelial lipoxygenase metabolite 15(S)-hydroxyeicosatetraenoic acid evoked slowly developing but pronounced and sustained increases in tracheal cholinergic tone in situ. These reflexes were reversed by atropine and prevented by vagotomy, trimethaphan, or laryngeal denervation. Central nervous system-acting neurokinin receptor antagonists also abolished the reflexes without altering baseline cholinergic tone. Baseline tone was, however, reversed by disrupting pulmonary afferent innervation while preserving the innervation of the trachea and larynx. Surprisingly, selective pulmonary denervation also prevented the laryngeal capsaicin-induced tracheal reflexes, suggesting that laryngeal C-fibers act synergistically with continuously active intrapulmonary mechanoreceptors to initiate reflex bronchospasm. Indeed, reflex bronchospasm evoked by histamine was markedly potentiated by bradykinin, an effect mimicked by intracerebroventricular, but not intravenous, substance P. These data, as well as anatomic evidence for afferent nerve subtype convergence in the commissural nucleus of the solitary tract, suggest that airway nociceptors and mechanoreceptors may act synergistically to regulate airway tone.

Administration, Topical↗