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PubMed2004

Treatment of inoperable coronary disease and refractory angina: spinal stimulators, epidurals, gene therapy, transmyocardial laser, and counterpulsation.

Intractable angina from refractory coronary disease is a severe form of myocardial ischemia for which revascularization provides no prognostic benefit. Inoperable coronary disease is also accompanied by a "vicious cycle" of myocardial dystrophy from a chronic alteration of the cardiac sympathetic tone and sensitization of damaged cardiac tissues. Several adjunctive treatments have demonstrated efficacy when revascularization is either unsuccessful or contraindicated. Spinal cord stimulation modifies the neurologic input and output of the heart by delivering a very low dose of electrical current to the dorsal columns of the high thoracic spinal cord. Neural fibers then release CGRP and other endogenous peptides to the coronary circulation reducing myocardial oxygen demand and enhancing vasodilation of collaterals to improve the myocardial blood flow of the most diseased regions of the heart. Randomized study has shown the survival data at five years is comparable to bypass for high-risk patients. Transmyocardial laser revascularization creates small channels into ischemic myocardium in an effort to enhance flow though studies have shown no improvement in prognosis over medical therapy alone. Enhanced external counterpulsation uses noninvasive pneumatic compression of the legs to improve diastolic filling of the coronary vessels and promote development of collateral flow. The compressor regimen requires thirty-five hours of therapy over a seven-week treatment period. Therapeutic angiogenesis requires injection of cytokines to promote neovascularization and improve myocardial perfusion into the regions affected by chronic ischemia. Phase 3 trials are pending. High thoracic epidural blockade produces a rapid and potent sympatholysis, coronary vasodilation and reduced myocardial oxygen demand in refractory coronary disease. This technique can be used as an adjunct to bypass surgery or medical therapy in chronic or acute unstable angina. Epidurals are easy to perform and often available for outpatient or inpatient use. The rapid anti-ischemic effect may complement therapeutic angiogenesis or other interventions with delayed onset to clinical benefit. A new era for interventional and implant cardiology is beginning to emerge as more clinicians, including cardiologists, gradually learn new procedures to safely provide more therapeutic options for patients suffering refractory angina.

Anesthesia, Epidural↗
PubMed1992

Calcifications in the portal venous system: comparison of plain films, sonography, and CT.

We describe 10 patients with long-standing portal hypertension and calcifications in the splenoportal and mesenteric venous systems or collateral vessels. The patients were examined with abdominal plain films (n = 10), sonography (n = 10), and CT (n = 9). Calcium was seen on CT scans in nine cases, on sonograms in seven, and on abdominal plain films in five. Calcifications appeared to be located in the wall of the vein in all cases. Sites of detection included the main portal, splenic, superior mesenteric, coronary, and peripancreatic veins. CT was more sensitive than sonography, and both were more sensitive than plain films, in showing portal venous calcification. Detection of such calcifications may influence surgical or percutaneous therapy of portal hypertension.

Aged↗
PubMed1991

[Coronary disease in patient following heart transplantation].

Coronary artery disease is a common and particularly severe complication of cardiac transplantation because it may cause progressive destruction of the graft by acute or chronic ischemia. The ischemia is usually silent because of cardiac denervation. Cardiac failure related to graft dysfunction, asymptomatic infarction on the ECG, or sudden death, are sometimes the only signs of severe coronary disease. The prevalence of coronary lesions has been evaluated by coronary angiography at nearly 25% at 2 years and 50% at 5 years. The distribution and morphology of the lesions are characteristic: diffuse concentric, irregular and occlusive, predominantly distal stenoses, without a distal and usually without a collateral circulation. The histological features are variable: the association of medial necrosis, severe endothelial lesions and intense parietal inflammation are suggestive of acute arteriolitis, often present during acute rejection, may be related to a common pathological process. Diffuse obliterative arteriolar lesions with concentric proliferation of medial smooth muscle are the usual appearances in transplant patients who have died or been retransplanted. There is no non-invasive diagnostic method sufficiently sensitive of specific which justifies the practice of many groups of systematic annual coronary angiography in transplanted patients. The pathogenesis is poorly understood and probably multifactorial: disorders of lipid metabolism, immunological factors, the atherogenic role of Cytomegalovirus infection. The absence of an identifiable risk factor makes preventive measures difficult. The evolutive risk justifies retransplantation in selected patients, the results of which are less satisfactory but which reduces the risk of acute coronary events and sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Angiography↗
PubMed1988

Resting and hypercapnic rCBF in patients with unilateral occlusive disease of the internal carotid artery.

Regional cerebral blood flow was measured by the 133Xe inhalation technique in 15 patients with severe unilateral internal carotid artery stenosis (75%) or occlusion, and in the absence of evidence of any sign of occlusive disease in other main afferent cerebral arteries. A comparison with normal subjects showed that lowered resting flow in both hemispheres was a common finding in all patients. Interhemispheric asymmetry was present only in patients with occlusion and the precentral, posterior temporal, and occipital regions were the most seriously affected. The CO2 reactivity was substantially reduced in both hemispheres of all stenotic and occluded patients, but occluded patients showed an increased reduction of CO2 reactivity only in the ipsilateral hemisphere. In addition to an hypothetical age effect, the atherosclerotic involvement of the cerebral vascular system leads to a reduction of flow and loss of CO2 reactivity in both hemispheres. In this context, the collateral supply capacity is not overloaded in case of a unilateral severe stenosis but fails in case of a unilateral occlusion of the internal carotid artery. A suitable estimate of the blood flow reduction as a result of occlusion is made by the hemispheric and regional laterality indices applied in resting and hypercapnia conditions. These indices could be used as indicators for endarterectomy or bypass surgery as well as a sensitive means for appreciating cerebral blood flow response to treatment.

Adult↗
PubMed2000

QRS prolongation: a sensitive marker of ischemia during percutaneous transluminal coronary angioplasty.

The purpose of this study is to measure QRS duration changes in the human model of ischemia during percutaneous transluminal coronary angioplasty (PTCA) and compare these results to the commonly used ischemia markers, chest pain, and classical ST-T changes. Using a computerized method, QRS duration was measured in 51 patients undergoing elective PTCA. Three milliseconds (msec) or more prolongation of the QRS at peak inflation was considered to be an ischemic response. The results were compared to chest pain and ST-T changes and were analyzed for inflation site within individual coronary arteries. Forty-two patients had a pathological prolongation of the QRS during PTCA. Thirty-two patients developed chest pain, while 19 had ischemic ST-T changes. QRS duration was more prolonged in PTCA to proximal or middle segments of major arteries or their large branches, while it was less prolonged in distal segments or smaller branches. Using our method, QRS prolongation was an ischemia marker in most patients during PTCA and was more sensitive than chest pain or ST-T changes. QRS duration was more prolonged with occlusion of proximal and middle segments of major arteries. Cathet. Cardiovasc. Intervent. 50:177-183, 2000.

Adult↗
PubMed2002

End-to-side neurorrhaphy.

End-to-side neurorrhaphy, a possible strategy for treating nerve lesions without useable proximal nerve stumps, has been experimentally and clinically investigated. In end-to-side neurorrhaphy, three main elements should be considered: 1) the induction of axonal collateral sprouting in the donor nerve; 2) the ability of the collateral axons to pierce the different conjunctival layers, including the ability the donor nerve basal laminae, to reinnervate the recipient nerve; and 3) the functional plasticity and behavioral readjustment of single motoneurons that have eventually adopted new motor units. This article reviews the following areas of research and clinical investigation: animal models, axonal collateral sprouting from end-to-side neurorrhaphy, effect of epineurotomy and perineurotomy on axon regeneration, motor reinnervation, and clinical trials.

Anastomosis, Surgical↗
PubMed2003

Dobutamine stress echocardiography in the evaluation of young patients with Kawasaki disease.

There has been no consistent approach to the follow-up of Kawasaki disease patients for remote coronary perfusion abnormalities. Dobutamine stress echocardiography (DSE) has become a standard method for evaluation of perfusion abnormalities in adults with coronary artery disease. In addition, DSE has been used with success in some pediatric patients. The purposes of this study were to evaluate safety and accuracy of DSE in the follow-up of patients with Kawasaki disease, to evaluate whether DSE adds any additional value to the resting echocardiogram, and to determine the association of DSE results with American Heart Association (AHA) risk level categories. DSE was performed 1 month to 13 years after acute Kawasaki disease in 47 patients (range, 3.8-22.6 years; 33 males and 16 females). Patients were stratified according to AHA risk level categories (I-V). Ischemia was defined as a new or worsening regional wall motion abnormality or >1 mm ST segment depression on the electrocardiogram during DSE. In 45/47 patients, DSE was completed successfully (i.e., achievement of target heart rate or development of ischemia). No patients in risk levels lower than V (i.e., patients without coronary artery stenoses) had positive DSE, whereas 2/4 (50%) in the risk level V category had positive DSE, both of whom had coronary occlusion >50% confirmed by angiography. Of the 2 AHA risk level V patients with negative DSE, 1 had extensive collateralization and the other had coronary obstruction <50%. DSE is a safe and feasible method for the evaluation of children with Kawasaki disease. DSE provides a confirmatory benefit and may be a useful screening alternative to cardiac catheterization during follow-up. Patients in AHA risk levels I-IV are unlikely to have dobutamine-induced coronary perfusion abnormalities. Patients in the risk level V category may or may not have positive DSE depending on the degree of both coronary obstruction and collateralization.

Adolescent↗
PubMed1991

Stump pressure, the contralateral carotid artery, and electroencephalographic changes.

Electroencephalographic (EEG) monitoring and measurement of stump pressure are the most widely employed methods of assessing the risk of cerebral ischemia during carotid endarterectomy. The status of the contralateral carotid artery has also been thought to influence the need for placing a shunt. The relationship of EEG monitoring, stump pressure, and the contralateral carotid artery has not been completely delineated. We retrospectively reviewed these three variables in 113 patients undergoing 124 carotid endarterectomies. The contralateral artery was classified as occluded, stenotic (greater than 50% decrease in diameter), or nonstenotic. There was a 48% incidence of EEG changes with contralateral occlusion, 18% with stenosis, and 21% with nonstenotic arteries (p = 0.014). There was a 73% incidence of EEG changes when the stump pressure was less than 25 mm Hg, 32% when the stump pressure was 25 to 50 mm Hg, and 2% when the stump pressure was greater than 50 mm Hg (p less than 0.001). There was no significant difference in the mean stump pressure for patients with occlusion (43.8 mm Hg), stenosis (44.7 mm Hg), or nonstenotic contralateral arteries (51.3 mm Hg). All patients with contralateral occlusion and a stump pressure less than 25 mm Hg had EEG changes. No patient with a stump pressure greater than 50 mm Hg and a patent contralateral artery had EEG changes. Although the incidence of EEG changes in the majority of patients was not accurately predicted by the stump pressure and the status of the contralateral carotid artery, stump pressure less than or equal to 50 mm Hg was sensitive, identifying 97% of patients with EEG changes.

Aged↗
PubMed2002

Assessment of myocardium at risk with computerized vectorcardiography and technetium-99m-sestamibi-single photon emission computed tomography during coronary angioplasty.

OBJECTIVE: To compare the myocardium at risk (MAR) as estimated by computerized vectorcardiography (cVCG) with MAR determined by Tc-99m-sestamibi-SPECT using coronary angioplasty as the model for transient transmural ischemia in humans. METHODS AND RESULTS: In 37 patients with stable angina pectoris, cVCG was recorded continuously during coronary angioplasty. The scintigraphic defect was quantified using an automated software program (CEqual). The ST vector magnitude (ST-VM) and the ST change vector magnitude (STC-VM) correlated well with MAR estimated by scintigraphy, ST-VM (r = 0.71, p < 0.001) and STC-VM (r = 0.84, p < 0.001). All patients with STC-VM <50 microV during occlusion had defects of less than 10% of the left ventricle. CONCLUSION: 1) ST-VM and STC-VM give a reasonable useful estimate of MAR size during transient coronary occlusion. 2) STC-VM <50 microV is a reliable limit to identify patients with MAR size less than 10%. 3) ST-VM does not add information to STC-VM with respect to detection of ischemia. 4) The existence of collateral vessels has great impact on both ST-vector changes and scintigraphic imaging of myocardial ischemia.

Adult↗
PubMed1982

Atropine-sensitive gastric excitation by stimulation of thoracic dorsal roots--antidromic activation of afferents?

In chloralosed cats, usually with ligated adrenals and paralysed with gallamine, the thoracic dorsal roots were electrically stimulated and gastric motor responses were recorded. Thoracic dorsal root stimulation regularly elicited gastric contractions after pretreatment with guanethidine and/or hexamethonium which were readily blocked by atropine. It was established that these gastric motor responses were due to peripheral stimulation of the dorsal root and not to spread to the ventral roots. Together with other results (Delbro & Lisander 1980) the findings suggest an antidromic activation of thin afferent fibres with excitatory collaterals to intramural cholinergic neurons which convey the gastric contractions.

Animals↗
PubMed1986

Functional plasticity in the sympathetic nervous system of the neonatal rat.

The age-dependent effects of sympathetic superior cervical ganglionectomy on smooth muscle alpha-adrenoceptor contractile responses were investigated in Müller's muscle in the superior eyelid of the Sprague-Dawley rat. Ganglionectomies in juvenile (32 days) and adult (70 days) rats produced sustained sympathetic denervation, determined by absence of contractile responses to electrical stimulation of ipsilateral and contralateral sympathetic chains and reduced responses to indirect release of nerve terminal norepinephrine by tyramine. Denervation was associated with diminished contractile responses and postjunctional supersensitivity to alpha-adrenoceptor stimulation by methoxamine. In contrast, contractile responses in rats ganglionectomized as neonates (day 3) were greater than those of other groups and sensitivity to methoxamine was comparable to control values. Responses to tyramine suggested that noradrenergic reinnervation had occurred. Electrical stimulation of the ipsilateral chain did not elicit contractions; however, stimulation of the contralateral chain evoked contractions in all neonatally ganglionectomized preparations and responses were present by 20 days of age. Contralateral reinnervation was derived from postganglionic sympathetic neurons with axons in the internal carotid nerve. This pathway is probably not formed by collateral sprouting of neurons with bilateral projections at the time of surgery for contralateral stimulation did not evoke contractions in the neonate. It is concluded that Müller's muscle is reinnervated by sympathetic neurons in the contralateral chain after denervation in neonates but not in older animals, and it is suggested that the higher potential for plasticity is attributable to the immaturity of the neonatal sympathetic nervous system.

Animals↗
PubMed2006

Regulation of nitric oxide-induced apoptosis by sensitive to apoptosis gene protein.

Sensitive to apoptosis gene (SAG) protein, a novel zinc RING finger protein that protects mammalian cells from apoptosis by redox reagents, is a metal chelator and a potential reactive oxygen species (ROS) scavenger, but its antioxidant properties have not been completely defined. Nitric oxide (NO), a radical species produced by many types of cells, is known to play a critical role in many regulatory processes, yet it may also participate in collateral reactions at higher concentrations, leading to cellular oxidative stress. In this report, we demonstrate that modulation of SAG expression in U937 cells regulates NO-induced apoptosis. When we examined the protective role of SAG against NO-induced apoptosis with U937 cells transfected with the cDNA for SAG, a clear inverse relationship was observed between the amount of SAG expressed in target cells and their susceptibility to apoptosis. We also observed the significant decrease in the endogenous production of ROS and oxidative DNA damage in SAG-overexpressed cells compared to control cells upon exposure to NO. These results suggest that SAG plays an important protective role in NO-induced apoptosis, presumably, through regulating the cellular redox status.

Apoptosis↗
PubMed1996

MR angiography for mapping potential central venous access sites in patients with advanced venous occlusive disease.

OBJECTIVE: Patients who depend on long-term central venous catheter support frequently develop thrombi in central veins. An accurate, noninvasive technique is needed to find patent central veins for future access. We evaluated the suitability of MR angiography for this use. SUBJECTS AND METHODS: Using five healthy volunteers and 19 patients who had malfunctioning central venous catheters and a history of central venous occlusive disease, we tested the ability of MR angiography to assess central vein status. Three radiologists experienced in MR angiography blindly interpreted both source images and three-dimensional reconstructed images. RESULTS: In the volunteers, MR angiography provided diagnostic-quality images of the internal and external jugular, innominate, subclavian, axillary, femoral, and iliac veins, and of the superior and inferior venae cavae. Interobserver interpretations did not vary. In the patients, MR angiography of venous patency was confirmed by venography in 27 segments, by sonography n 32 segments, and by attempted line placement in 21 placements. Images were diagnostically adequate in 206 of 216 segments (95%). For detection of occlusion, sensitivity was 97% and specificity was 94%. MR angiography predicted 100% of successful line placements and 80% of failures. Interobserver interpretations varied by 44%. MR angiography directly influenced therapy in 19 of 21 studies. CONCLUSION: We conclude that MR angiography provides risk-free, thorough, relatively accurate, and clinically useful assessment of most available central venous access sites, although interpretation may prove difficult in patients with extensive occlusions because of complex collateral drainage patterns.

Adolescent↗
PubMed1991

Selective and divided attention during visual discriminations of shape, color, and speed: functional anatomy by positron emission tomography.

Positron emission tomography (PET) was used to identify the neural systems involved in discriminating the shape, color, and speed of a visual stimulus under conditions of selective and divided attention. Psychophysical evidence indicated that the sensitivity for discriminating subtle stimulus changes in a same-different matching task was higher when subjects selectively attended to one attribute than when they divided attention among the attributes. PET measurements of brain activity indicated that modulations of extrastriate visual activity were primarily produced by task conditions of selective attention. Attention to speed activated a region in the left inferior parietal lobule. Attention to color activated a region in the collateral sulcus and dorsolateral occipital cortex, while attention to shape activated collateral sulcus (similarly to color), fusiform and parahippocampal gyri, and temporal cortex along the superior temporal sulcus. Outside the visual system, selective and divided attention activated nonoverlapping sets of brain regions. Selective conditions activated globus pallidus, caudate nucleus, lateral orbitofrontal cortex, posterior thalamus/colliculus, and insular-premotor regions, while the divided condition activated the anterior cingulate and dorsolateral prefrontal cortex. The results in the visual system demonstrate that selective attention to different features modulates activity in distinct regions of extrastriate cortex that appear to be specialized for processing the selected feature. The disjoint pattern of activations in extravisual brain regions during selective- and divided-attention conditions also suggests that preceptual judgements involve different neural systems, depending on attentional strategies.

Adult↗
PubMed1992

Evidence for nitric oxide synthase inhibitor-sensitive and insensitive hippocampal synaptic potentiation.

1. Nitric oxide (NO) has been proposed as a retrograde messenger, mediating the postsynaptic to presynaptic transfer of the effects of conditioning stimulation, responsible for the initiation of hippocampal long-term potentiation (LTP). To further test this hypothesis, we inhibited nitric oxide synthase (NOS) to determine whether synaptic potentiation produced by different conditioning stimulus patterns and intensities was differentially affected by reduction of stimulation-dependent NO production. 2. Synaptic potentiation was produced in hippocampal slices from young F-344 rats by two different conditioning stimulation protocols. Conditioning stimuli were delivered to the Schaffer-collateral commissural system, and moderate levels of potentiation of the population excitatory postsynaptic potential (EPSP) in area CA1 were produced by a single 100 Hz, 1-s conditioning train delivered at half-maximal stimulus intensity. Higher levels of potentiation of the population EPSP were obtained by delivering two 100 Hz, 1-s conditioning stimulus trains, with a 60-s intertrain interval, at high stimulus currents. 3. Application of the nitric oxide synthase inhibitors NG-nitro-L-arginine (NOARG; 0.1-200 microM) and NG-monomethyl-L-arginine (NMMA; 100 microM) produced no significant direct effects on synaptic responses. 4. In slices that received a single conditioning stimulus train, both NOARG and NMMA were ineffective in blocking or reducing potentiation at concentrations between 0.1 and 200 microM. In slices receiving the more intense pair of conditioning stimulus trains, levels of potentiation in control slices were higher, and there was a very significant reduction by both NOARG (50 and 100 microM) and NMMA (100 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1973

The membrane effects, and sensitivity to strychnine, of neural inhibition of the Mauthner cell, and its inhibition by glycine and GABA.

1. Anionic conductance changes in Mauthner neurones of goldfish were measured during synaptically evoked inhibition and inhibition caused by iontophoretic application of the putative inhibitory transmitters glycine and gamma-aminobutyric acid (GABA).2. The effects of either amino acid were indistinguishable from those of the neural inhibitory transmitter(s). The membrane permeability during the neural or drug response was increased to Br(-), Cl(-), I(-), SCN(-), NO(3) (-), ClO(3) (-), and formate (HCOO(-)), but not to HCO(3) (-), BrO(3) (-), IO(3) (-), SO(4) (-), HPO(4) (-), H(2)PO(4) (-), acetate and citrate.3. Strychnine was injected intramuscularly, iontophoretically, or applied topically to the exposed brain in order to compare quantitatively its ability to prevent inhibition evoked by synaptic activation and by pharmacological means. Inhibitions were measured by the increase in membrane conductance.4. Strychnine, at concentrations just adequate to block completely the late collateral inhibition (LCI) and crossed VIII nerve inhibition, had little effect on the pharmacological inhibition caused by glycine, and sometimes there was no detectable effect at all. In one experiment even a local iontophoretic application of strychnine in a sufficient dose to diffuse over the cell and block the LCI almost completely, merely halved the effect of a small dose of glycine applied to the same localized region of the membrane.5. Higher concentrations of strychnine than those necessary to block synaptically evoked inhibition would reduce the effect of glycine but not that of GABA. The evidence indicated that any apparent effect of strychnine upon GABA could be explained by displacement of the GABA-containing iontophoretic pipette.6. The glycine-blocking action of iontophoretic pulses of strychnine was of relatively very slow onset and long duration compared to the effects of pulses of glycine and GABA.7. These findings can be interpreted as either (1) strychnine has a presynaptic action, preventing the release of inhibitory neurotransmitter, in addition to its less potent post-synaptic one in blocking pharmacological inhibition, or (2) strychnine acts entirely post-synaptically, but the physiological transmitter action differs from that of glycine and GABA in being considerably more sensitive to strychnine antagonism. In either case, the use of strychnine as evidence for the claim that glycine is an inhibitory neurotransmitter at the Mauthner cell is questionable.

Aminobutyrates↗
PubMed1991

Activity of hippocampal extract on development of [3H]5-HT high-affinity uptake in dissociated microcultures.

Specific and localized lesions of the 5-HT fibers in the hippocampus induce homotypic collateral sprouting and enhance serotonergic fiber outgrowth from adult neurons and transplanted fetal tissue. In this study, hippocampal extracts were prepared and applied to primary cultures of fetal serotonergic neurons. The effects of plating density and serum additives were examined. The growth of the serotonergic neurons in the rostral brainstem dissociated cultures were estimated by measuring the specific uptake of [3H]5-HT. The results indicate the presence of a trypsin-sensitive factor which is active when prepared fresh at dilutions up to 1/10,000. The factor is higher in hippocampus than cerebellum. Young male tissue contained more activity than either female or aged hippocampus. Although both positive and negative effects are described, higher dilutions of factor (1/1,000) were generally stimulatory in high density cultures while lower dilutions (1/10) were inhibitory in low density cultures. Specific removal of 5-HT hippocampal afferents with fornix-fimbria microinjections of 5,7-dihydroxytryptamine resulted in an initial loss of activity (2 days and 2 weeks) followed by an enhanced activity (2 months) compared to normal hippocampal extract. Several possibilities are discussed as to the identity of the serotonergic growth factor from hippocampal supernatant.

5,7-Dihydroxytryptamine↗
PubMed2003

Effects of prolonged exposure to darkness on circadian photic responsiveness in the mouse.

Circadian rhythms in mammals are generated by an endogenous pacemaker but are modulated by environmental cycles, principally the alternation of light and darkness. Although much is known about nonparametric effects of light on the circadian system, little is known about other effects of photic stimulation. In the present study, which consists of a series of five experiments in mice, various manipulations of photic stimulation were used to dissect the mechanisms responsible for a variation in the magnitude of light-induced phase-shifts that results from prolonged exposure to darkness. The results confirmed previous observations that prolonged exposure to darkness causes an increase in the magnitude of phase shifts (both phase advances and phase delays) evoked by discrete light pulses. The results also indicated that the increase in responsiveness results from the lack of exposure to light per se and not from collateral effects of exposure to constant darkness such as the lack of previous entrainment. The lack of exposure to light causes the circadian system to undergo a process of dark adaptation similar to dark adaptation in the visual system but with a much slower temporal course. The results suggest that circadian dark adaptation may take place at the retinal level, but it is not clear whether it involves a change in the sensitivity or maximal responsiveness of the system.

Animals↗