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Effects of buphenin on the rat portal vein.

The vasodilator and tocolytic substance buphenin (10 mumol/l) stimulated the spontaneous phasic activity of some (8 out of 18) isolated rat portal vein preparations; 0,1-1 mmol/l buphenin diminished or abolished the activity in all preparations. The isotonic and isometric tonic contractions of portal vein in response to adrenaline, noradrenaline and phenylephrine (0,1-1 mumol/l) disappeared almost completely after addition of buphenin in equimolar concentrations, whereas acetylcholine contractions persisted. The beta-adrenergic blocking agents propranolol and dichloisoprenaline (10 mumol/l) only slightly antagonized the inhibitory effect of buphenin on the contractile responses to catecholamines. It is concluded that buphenin exerts dual action upon rat portal vein: the drug partially stimulates the beta-receptors and partially blocks the alpha-adrenergic receptors.

Acetylcholine↗
PubMed1994

Theory and observation of spontaneous oscillatory contractions in skeletal myofibrils.

At low levels of activation, an isometrically-held myofibrillar preparation on the descending limb may exhibit persistent oscillations of period 1-6 s in tension and sarcomere lengths. We propose a sarcomeric theory of spontaneous oscillatory contraction, based on the phenomena of force creep and delayed length activation. The time delay leads to oscillations and controls their period. A computer model using these ideas simulates spontaneous oscillatory contraction for fixed-end fibres only if isometric tension capacity varies slightly along the fibre. The form of this inhomogeneity controls a diversity of spontaneous oscillatory contraction behaviour: the tension waveform can vary from large and sinusoidal to small-amplitude pulses or chaotic behaviour, and these variations are observed in slow-twitch soleus fibres from the same animal (rat). The model predicts that oscillatory and quiescent regions coexist in the fibre, with large-amplitude sawtooth waveforms in sarcomere length in the former as observed. It can also generate travelling-wave structures, similar to those found by the Tokyo group, in oscillating regions when there is a spatial gradient in isometric tension capacity. Phase discontinuities in sarcomere length occur near the oscillatory-quiescent boundary. Predictions for the Ca2+ concentrations and sarcomere lengths in which spontaneous oscillatory contraction occurs and for differences in the spontaneous oscillatory contraction frequencies of fast- and slow-twitch fibres compare well with experiment. Spontaneous oscillatory contraction is also predicted under isotonic conditions.

Animals↗
PubMed1994

Relaxation of smooth muscle.

We have demonstrated that in dogs antigen sensitization results in alterations of contractile properties. These changes could account for the hyperresponsiveness reported in asthma. The failure of the muscle to relax could be another important factor responsible for maintaining high airway resistance. We therefore developed an index of isotonic relaxation, t1/2, CE (half time for relaxation that is independent of muscle load and initial contractile element length), for evaluation of the relaxation process. Because the maximum shortening velocity at 2 s but not at 10 s was greater in sensitized bronchial smooth muscle than that in controls, studies of relaxation were also undertaken at these two times. The mean half-relaxation time indicated by t1/2,CE showed no difference between sensitized and control muscles after 10 s of stimulation (8.38 +/- 0.92 vs. 7.78 +/- 0.93 s, means +/- SE); however, it was prolonged significantly in the sensitized muscle only stimulated for 1 s (12.74 +/- 2.5 s, mean +/- SE) compared with the control (6.98 +/- 1.01 s). During the late phase of isotonic relaxation, both groups showed an unexpected spontaneous increase in zero-load shortening velocity, which is an index of cross-bridge cycling rate. We conclude that (i) both contraction and relaxation properties of early normally cycling cross bridges are altered after sensitization and these changes may account for the hyperresponsiveness observed in asthmatics and (ii) the cross-bridge cycling rate increases spontaneously during isotonic relaxation, probably as a result of reactivation of the contractile mechanism.

Allergens↗
PubMed1991

Fatigue of mammalian skeletal muscle in situ during repetitive contractions.

When the gastrocnemius-plantaris muscle group of the dog is stimulated to contract repetitively for 30 min at frequencies high enough to generate VO2 levels at or near VO2 max, VO2 and mechanical performance decline with time. This decline with time is fatigue, and it occurs during twitch and tetanic contractions that are isometric or isotonic. There is oxidation of the mitochondrial electron transport system, and net lactic acid output is transient, ending after 20 min of contractions. Energy and substrate stores and intracellular pH are only moderately changed and do not appear to be well correlated with the development of fatigue. Blood flow through the muscle is well correlated with the development of fatigue and decreases as fatigue develops in a manner that keeps the blood arteriovenous O2 difference nearly constant. Changing the blood flow alters the rate of development of fatigue as an inverse relation, and this response does not appear to be related to changes in the availability of O2 in the mitochondria. Nerve-muscle transmission of excitation does not seem to be involved in the development of fatigue. Excitation-contraction coupling is well accepted to be at least part of the genesis of the development of fatigue. Metabolic limitations and control may affect excitation-contraction coupling by one or more changes in the internal environment. Blood flow affects this system by an unknown mechanism. The role of blood flow in fatigue deserves further consideration.

Animals↗
PubMed1993

Use of a new index to study relaxation in a vascular model of anaphylactic shock.

We have reported increased smooth muscle shortening ability in ragweed pollen-sensitized saphenous vein (SSV). This may account for the vascular hyperreactivity of anaphylactic shock. We have now investigated relaxation in SSV. Because isotonic relaxation is load and initial contractile element length dependent, we developed an adjusted half-relaxation time index, which was independent of these variables. Muscle activation state was monitored by measuring maximum unloaded velocity. The relaxation index showed no difference between SSV and control saphenous vein after 2.5, 10, and 15 s of electrical stimulation; however, after 1 s of stimulation it was prolonged significantly in SSV. We concluded that the cross bridges activating early in contraction demonstrated prolonged relaxation. Activation state during muscle relaxation spontaneously increased toward the end of relaxation, coincident with a slowing in isotonic re-elongation rate. This was seen only in muscles relaxing from 15 s of stimulation. Our results indicate that 1) the relaxation properties of early cycling (1 s) cross bridges are altered after sensitization; and 2) toward the end of isotonic relaxation, cross-bridge cycling rate increases spontaneously, a phenomenon not previously reported. We speculate that the rapid re-elongation in late relaxation may reactivate muscle.

Allergens↗
PubMed1973

Influence of previous mechanical events on the contractility of isolated cat papillary muscle.

1. The influence of previous mechanical events on myocardial contractility has been investigated in the cat papillary muscle preparation.2. When a muscle that had been producing a stable response under isometric conditions was allowed to shorten isotonically, its ability to do so increased in successive beats until it reached a steady level, which represented a potentiated state compared with that seen in the first isotonic beat and in the preceding stable isometric contractions.3. The increase in tension development in the first isometric beat after a period of isotonic beating was used as an index of the degree of potentiation. It was found to be well correlated with the changes in other parameters that could have been used for this purpose.4. The main determinants of the degree of potentiation produced by a period of isotonic beating were:(a) the amount by which the muscle shortened. This was inversely related to the force opposing shortening (i.e. the isotonic load);(b) the number of isotonic beats. There was some potentiation (about 10%) after a single isotonic beat, but the number of beats required for maximal potentiation (up to 25%) depended on the frequency of stimulation; about 8 beats were required at 24 min(-1).5. An isotonic release during the rise of tension in an isometric response was even more effective in potentiating the next isometric beat than an afterloaded contraction against the same load. Isotonic releases at later times had a diminishing influence on tension development in the next isometric beat.6. In the absence of stimulation, the potentiated state produced by a period of isotonic beating decayed with a half-time of about 50 sec. When the muscle was stimulated it disappeared sooner, and its rate of decay depended on the frequency of stimulation; at 24 min(-1) about 8 beats were required to restore contractility to its previous steady level.7. The characteristics of the decay of the potentiated state were closely similar to those of the potentiated states that can be produced by various electrical interventions, and the possibility that all of these might have the same underlying mechanism is discussed.8. Attention is drawn to the practical implications of this phenomenon in the design of experiments in which the muscle contracts under changing mechanical conditions.

Animals↗
PubMed1990

Negative inotropy of halogenated anesthetics in ferret ventricular myocardium.

The effects of the volatile anesthetics halothane, enflurane, and isoflurane on amplitude and time variables of contraction and relaxation in isometric, isotonic, and zero-load clamped twitches of isolated right ventricular ferret papillary muscles (n = 24) were compared with those of changing extracellular Ca2+ concentration [( Ca2+]o). Contraction and relaxation variables were compared at equal contraction amplitudes to determine whether the studied anesthetics exert specific effects on contraction and relaxation other than those that may exist as a consequence of their negative inotropic effect. Both changes in [Ca2+]o and anesthetic concentrations had quantitatively and qualitatively similar effects on the following variables of contraction amplitude: peak isometric developed force (DF), maximal extent of shortening (DL), and maximal unloaded velocity of shortening (MUVS). Analysis of anesthetic concentration-effect curves normalized for effects to changes in [Ca2+]o demonstrated that anesthetic effects relative to those of changes in [Ca2+]o were greater on DF greater than DL greater than MUVS. When compared with twitches of equal amplitude in low [Ca2+]o, halothane, enflurane, and isoflurane accelerated isometric and isotonic relaxation. These data are consistent with the hypothesis that the negative inotropic effects of halothane, enflurane, and isoflurane are mostly a consequence of a reduction of intracellular Ca2+ availability and that anesthetic-induced decreases in myofibrillar Ca2+ responsiveness play only a minor role.

Animals↗
PubMed1996

Comparison of metabolic, ventilatory, and neurohumoral responses during light forearm isometric exercise and isotonic exercise in congestive heart failure.

Maximal treadmill exercise responses were compared with light forearm isometric exercise responses in patients with chronic, stable heart failure (n = 14), and normal sedentary controls (n = 11). Isometric exercise was performed to exhaustion with 25% of maximal voluntary contraction. Gas-exchange analysis was used to determine oxygen consumption (VO2), carbon dioxide production (VCO2), and minute ventilation (VE) during exercise. Significant correlations were observed in normal controls, but not in patients with heart failure, between peak isotonic exercise and peak isometric exercise for VO2 (r = 0.75, p = 0.001) and VCO2 (r = 0.67, p <0.03), and between submaximal isotonic exercise (50% of peak) and peak isometric exercise for VO2 (r = 0.75, p = 0.007), VCO2 (r = 0.67, p = 0.02), and VE (r = 0.71, p = 0.01). At 90 seconds after isometric exercise in both groups, significant correlations (p <0.05) were observed with peak isotonic exercise for VE (r = 0.62 normals, and r = 0.63 heart failure). Plasma norepinephrine increased significantly (p <0.01) after both isotonic and isometric exercise in patients with heart failure, although peak values were greater with isotonic than with isometric exercise (p = 0.01). Plasma atrial natriuretic peptide and renin activity did not change with either isotonic or isometric exercise. In conclusion, maximal isotonic exercise responses are not predictive of peak isometric VO2 or VCO2 in patients with heart failure. However, VE during maximal isotonic exercise predicts postisometric exercise ventilation in both normals and patients with heart failure; this may determine the extent of dyspnea that patients with heart failure experience with isometric activities of daily living.

Adult↗
PubMed1980

Joint position sense: the effects of muscle contraction.

The effects of isometric and isotonic force production on perceived static joint position were investigated in 12 adult subjects. The joint examined was the proximal interphalangeal joint of one index finger, and its perceived position was determined from matching movements of the equivalent joint on the other hand. When the perturbed joint was free to move, even when supporting substantial loads, the position was accurately estimated; however, when the subject was required to exert substantial isometric force against the device imposing the joint movement, significant errors occurred: these errors were in the direction of the increasing force. Similar effects were evident during increasing isometric flexion force in anaesthetized fingers. It is suggested that force-related afferent discharge from muscle, presumably originating in tendon organ receptors, contributes to static joint position sense. This force-feedback may allow the nervous system to accommodate for the effects of changing fusimotor bias, but it also appears to induce errors when afferent information of force and length provide potentially conflicting information.

Adult↗
PubMed1987

Changes in contractile dynamics during the course of a twitch of a frog muscle fibre.

Single skeletal muscle fibres from the frog were stimulated to produce isometric twitches and released after a delay to shorten isotonically unloaded or against a finite load (P). When varying the delay, the velocity of the initial shortening (V) against a given non-zero load reached its maximum value earlier than the peak of the isometric tension. The velocity of unloaded shortening (V0, slack test, range: 3.7-5.6 nm ms-1 per half-sarcomere) was independent of the delay of the release. For any given delay, V was hyperbolically related to P, except for the high-load end of the P-V curve at which the velocity took lower values than extrapolated from the hyperbolic relation. The relation between V and the load in units of P1 (corresponding to V = 1 nm ms-1 per half-sarcomere) coincided in the hyperbolic range with the relations obtained at other delays of the release. P1 was basically proportional to the maximum power which also had its peak value during the rising phase of the twitch. The quick releases required to reach the non-hyperbolic range of the P-V curves were estimated to be less than 9 nm per half-sarcomere irrespective of the delay of the release. At load levels in the non-hyperbolic range V could be increased if the quick release was followed by a brief (2 ms) extra reduction in the load preceding the shortening at isotonic load. The results can be explained if the kinetic properties of the individual strongly bound crossbridges are unaffected by the changing level of activation during the course of the contraction. The time-dependence of the non-hyperbolic range of the P-V relation can be accounted for if crossbridges attached before the release remain attached after the release thus constituting an internal load. The difference in time course of isometric tension as compared to velocity of initial shortening against a given load, P1, and maximum power may arise as the result of a reduction in the level of activation caused by the release to the isotonic load level.

Animals↗
PubMed1986

Contribution of Na+ and membrane depolarization to contraction induced by adrenaline in the guinea pig vas deferens.

The contribution of Na+ and membrane depolarization to biphasic contractions induced by adrenaline were investigated in the smooth muscle of guinea pig vas deferens. Adrenaline (5 X 10(-6) M) produced an initial small contraction (first contraction) followed by a large tonic contraction (second contraction) with subsequent rhythmic activity. The entire response to adrenaline was largely inhibited by phentolamine (5 X 10(-6) M). By adding an appropriate concentration of Mn2+ (2 X 10(-4) M) or nifedipine (3 X 10(-7) M), a Ca2+ blocker, the second contraction was strongly reduced, accompanied by abolishment of the rhythmic contraction, whereas the first contraction was virtually unaffected. However, the first contraction was markedly suppressed by a higher concentration of Mn2+. All contractions produced by adrenaline were greatly reduced in Ca2+-free solution containing 0.5 mM EGTA. By lowering external Na+ concentration, the first contraction was markedly increased without greatly affecting the second contraction. By exposure to Na+-free isotonic high K+ solution, which elicited a greater depolarization of the membrane, the first contraction produced by adrenaline was also greatly potentiated, while the second and rhythmic contractions were eliminated. These results suggest that the adrenaline-evoked first contraction may be due to an influx of membrane bound Ca2+ which is independent of membrane depolarization, while the second (rhythmic) contraction is due to an influx of extracellular Ca2+ which is dependent upon depolarization.

Animals↗
PubMed2003

A new view of K+ -induced contraction in rat aorta: the role of Ca2+ binding.

Strong, K+ -induced contractions of rat aorta in Ca-free, Mg-free media were not accompanied by increased intracellular calcium concentration, [Ca2+](i), whereas such contractions in the presence of the divalent cations were correlated with rising [Ca2+](i) as assessed by fura-2. At the same time, calcium channel blockers, a modulator of Ca2+-binding proteins, and a modulator of actin polymerization, inhibited all types of K+ -induced contractions. Increasing the K+ in isotonic medium evoked a rise of (45)Ca2+ binding to the plasma membrane of freshly isolated aortic cells. Although Ca2+ -dependent events underlie the mechanism of K+ -induced vascular contractions in both the presence and absence of Ca2+, in contrast to the view that [Ca2+](i) is a key regulator of excitation-contraction coupling in smooth muscle, we suggest that the modulation of Mg2+ -dependent Ca2+ binding, probably within/at the L-type calcium channel by K+, is a trigger for aortic contraction. This Ca2+ binding may then activate actin-myosin interaction.

Actins↗
PubMed1987

Mechanical determinants of maximum isotonic lengthening rate in rat left ventricular myocardium.

The effects of changing loading conditions and inotropic state on maximum isotonic lengthening rate (+dL/dt, muscle lengths/sec) were examined in isolated rat myocardium. Physiologically sequenced contractions were studied in 18 left ventricular papillary muscle preparations (stimulation rate, 12/min). To study the effects of changing loading conditions, only one loading variable (preload, total load, or late load) was changed during each contraction, while the others were held constant. To study the effects of isoproterenol (10(-6) M) and temperature (28 vs. 33 degrees C) on maximum isotonic lengthening rate, preload and late load were held constant and +dL/dt was examined at a common total load. When preload was increased from 0.7 +/- 0.1 to 1.4 +/- 0.1 g/mm2, muscle length increased from 0.98 +/- 0.003 to 1.01 +/- 0.002 muscle lengths, the extent of shortening increased from 0.05 +/- 0.003 to 0.08 +/- 0.003 muscle lengths, but minimum length (0.93 +/- 0.01 muscle lengths) and +dL/dt (1.1 +/- 0.1 muscle lengths/sec) were unchanged. When total load was increased from 1.5 to 4.5 g/mm2, minimum length increased from 0.91 +/- 0.05 to 0.97 +/- 0.05 muscle lengths and +dL/dt fell from 1.4 +/- 0.1 to 0.5 +/- 0.1 muscle lengths/sec. Late load (the load borne by or applied to the muscle during isotonic lengthening) was altered by changing its magnitude (g/mm2) or time (milliseconds after stimulation) of application. As late load was increased from 1.4 +/- 0.02 to 2.1 +/- 0.3 g/mm2, +dL/dt increased from 1.3 +/- 0.2 to 2.1 +/- 0.3 muscle lengths/sec.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Effects of phasic and tonic activation on contraction dynamics in smooth muscle.

Responses to isotonic quick releases of rabbit urinary bladder strips and rat portal veins activated by AC-stimulation and K+-high medium were studied. The AC stimulation was adjusted to give the same tension as th K+-contractures. Releases were performed at peak of the contractions (which was attained after 1.5-4.5 s AC-stimulation or 2-3 min in K+-high solution). The length response consisted of 3 parts: (1) elastic recoil, (2) isotonic transient, (3) steady shortening. Shortening velocity was determined at 100 ms after the release, as phase (2) had subsided by then. Characteristics of the initial elastic response was virtually unaffected by the mode of stimulation for both preparations. Vmax was significantly higher for the AC-stimulations than for the K+-contractures (bladder: 0.37 l/s vs. 0.26 l/s, portal vein: 0.46 l/s vs. 0.33 l/s). By means of computer analysis a fast exponential shortening component comprising the larger part of phase (2) could be separated from the subsequent slower shortening (see further in Hellstrand & Johansson 1979). In each preparation the amplitude of this exponential was the same for both modes of activation. The time constant was, however, smaller for the AC-stimulation preparations. Our results thus indicate that in response to a sudden decrease in force the initial elastic recoil is the same whereas the rate of transition to steady shortening, and the steady shortening velocity itself, are lower for preparations activated by K+-high medium compared to AC-stimulation.

Animals↗
PubMed1992

Positive inotropic effects of RP 62719, a new pure class III antiarrhythmic agent, on guinea pig myocardium.

The mechanical effects of RP 62719 [(-)1-[-2-(3,4-dihydro-2H-1- benzopyran-4-yl)ethyl]-4-(3,4-dimethoxyphenyl)-piperidine] were tested in vitro on guinea pig left ventricular papillary muscle. RP 62719 is a novel pure class III antiarrhythmic agent known to prolong the cardiac action potential duration by selectively blocking the inward rectifying K+ current. Mechanical parameters were determined from contraction and relaxation phases under isotonic and isometric conditions. At a concentration of 0.02 microM, RP 62719 did not produce significant effects on inotropy or lusitropy. At 0.2 and 2 microM, the drug improved contraction under both heavy and low loading conditions, as evidenced by a 30% increase in maximum unloaded shortening velocity (Vmax, P < .001), peak amplitude of shortening (delta L, P < .001), peak isometric active force normalized per cross-sectional area (AF/s, P < .001) and positive peak of the force derivative per mm2 (+dF/s, P < .001). At the same concentrations, positive lusitropic effects were evidenced by an increase in maximum lengthening velocity (maxVr) and negative peak of force derivative per mm2 (-dF/s, P < .001). At a higher concentration (20 microM), effects of RP 62719 on inotropy and lusitropy were less marked, thus accounting for the bell-shaped form of the dose-response curve. An increase in the extracellular Ca++ concentration from 2.5 to 3.75 mM improved inotropy to a similar extent (+30-50%) as did 2 microM RP 62719. However, lusitropy and mechanical coupling between contraction and relaxation were not modified in the same proportion under RP 62719 and under 3.75 mM Ca++.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

The control mechanisms of gastric emptying are not overridden by motor stimulants.

We wanted to determine if an acceleration of the normal emptying rate by motor stimulants interfers with control mechanisms limiting gastric emptying. Therefore, we studied the effects of 5-hydroxytryptophane (5-HTP) and cisapride on canine gastrointestinal motility and gastric emptying after ingestion of viscous acaloric and nutritive meals. Prolonged contractions and relaxations that change lumen size (isotonic component) and wall tension (isometric component) are defined as "basal contractions" and "basal relaxations", respectively. The nutrient meal emptied much slower than the acaloric meal due to several alterations of gastric, pyloric, and duodenal motility. Both drugs stimulated antral motility but failed to accelerate gastric emptying of the nutrient meal. The main causes for the failure were a basal relaxation of the proximal antrum and a basal contraction of the duodenum. In conclusion, basal contractions of the proximal antrum and duodenum play an important role in the process of gastric emptying, and under physiological conditions the control mechanisms of gastric emptying provide an optimal emptying rate that cannot be markedly accelerated by 5-HTP and cisapride.

5-Hydroxytryptophan↗
PubMed1993

Mechanical determinants of isotonic relaxation in isolated diaphragm muscle.

Determinants of lengthening velocity have not been investigated in the diaphragm muscle. This study was undertaken to define the mechanical determinants of isotonic relaxation rate over the entire load continuum in isolated rat diaphragm (n = 30). We tested the hypothesis that the determinants of lengthening could include loading conditions, namely, preload and afterload; abrupt changes of load during the contraction phase; end-shortening muscle length (ESL); extent of shortening (delta L); time; stimulation mode; and stimulation frequency. In afterloaded contractions preloaded at optimal initial length and stimulated in tetanus at 30 Hz, peak lengthening velocity (+dL/dtmax) was linearly related to delta L, ESL, and/or total load. Varying initial muscle length, ESL, afterload, or the load imposed on the muscle during the isotonic lengthening process did not modify +dL/dtmax vs. delta L relationship, whereas +dL/dtmax vs. load and +dL/dtmax vs. ESL relationships were modified by these procedures. For a given delta L, +dL/dtmax could be modified when lengthening was delayed by reversing the relaxation sequence and when twitch and tetanus modes were compared. In conclusion, our results demonstrate that in isolated diaphragm muscle, delta L is the main determinant of +dL/dtmax over a wide range of loads and under various experimental conditions, independent of ESL and initial muscle length and independent of the load imposed on the muscle during the lengthening process. Time and stimulation mode were also shown to modulate the lengthening rate in diaphragm muscle.

Animals↗
PubMed1983

[Caerulein-induced contraction of the ileal longitudinal smooth muscle isolated from various animal species].

An effect of caerulein was studied on a contractile response of the ileal longitudinal smooth muscle isolated from seven animal species, monkey, dog, rabbit, guinea-pig, rat, vole and mouse. In isotonic recording, caerulein induced a contraction in the muscle isolated from all animal species. Sensitivities of ileal strips to caerulein in the contractile response was divided into three groups. That is, a high sensitive group; dog and guinea-pig, a middle sensitive group; rabbit and vole, a low sensitive group; monkey, rat and mouse. In another series of experiment, effect of several antagonists was examined on the caerulein-induced contraction in ileal muscle of dog, rabbit or guinea-pig. TTX inhibited the contractions in all the ilea. As the contraction was inhibited by atropine and scopolamine in dog ileum but not in rabbit one, the contraction may be due to an excitation of the cholinergic neuron or an excitation of non-cholinergic excitatory neuron, respectively. On the other hand, it is supposed that the contraction in guinea-pig ileum is involved to both the neurons because the contraction was inhibited partially by scopolamine and not by atropine. In conclusion, the ilea isolated from seven animal species showed species differences in sensitivity to caerulein in contractile response, and caerulein seems induces the contractions involving to different nervous systems in dog, rabbit or guinea-pig ileum, respectively.

Animals↗