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Biomedical subjects

S A Mills

Publications and source records attributed to S A Mills.

At least 19 recordsLinked to original sources
PubMed1991

Effect of desmopressin on vein graft patency in a microvascular model.

Desmopressin acetate decreases blood loss after cardiac surgery by activating platelets. We studied whether this effect was detrimental to small-caliber vein grafts in rats. Thirty minutes before femoral artery grafting with 0.75-mm-diameter reverse autogenous saphenous vein grafts, 20 rats received desmopressin acetate intravenously at 1.0 micrograms/kg over 10 minutes, and 20 control rats received normal saline intravenously over 10 minutes. In each group, 10 rats received a 6-mm-long graft and 10 an 18-mm-long graft. Graft patency was evaluated at 20 minutes, 24 hours, and 30 days. Intimal thickening was assessed by light and scanning electron microscopy. At 30 days, 9 short grafts and 8 long grafts in the desmopressin-treated group were patent, whereas only 8 short control grafts and only 6 long control grafts were patent. Intimal thickening and platelet deposition were the same in both groups. These data show no detrimental effects of desmopressin acetate on saphenous vein graft patency.

Animals↗
PubMed1991

Improved lung preservation with cold air storage.

Conventional topical slush cooling limits lung transport to 4 to 6 hours. For this canine study of an alternate air cooling system, 37 canine lungs were removed: 24 were placed in plastic bags, and inserted in a Transplanthermm container at core air temperatures (n = 6 lungs each) of (A) 4 degrees C, (B) 8 degrees C, (C) 12 degrees C, and (D) 20 degrees C; 6 were stored conventionally in ice slush (E); and 7 were transplanted immediately (F). After 8 hours, the stored lungs were transplanted and the contralateral pulmonary artery was ligated. Survival, arterial oxygen tension, and extravascular lung water were monitored at 15 minutes and every hour for 4 hours. Four-hour survival was 100% in groups A, B, and F; 83% in group C, 50% in group D, and 17% in group E. The mean arterial oxygen tension at 1 hour was lower in group E (6.4 +/- 2.4 kPa) than in group A (39.8 +/- 13.2 kPa) (p = 0.0002) or in group F (42.0 +/- 16.2 kPa) (p = 0.0035). Extravascular lung water in group E was higher at 15 minutes (15.44 +/- 5.63 mL/kg) than in group A (3.76 +/- 0.63 mL/kg) (p = 0.0001) and group F (4.69 +/- 1.65 mL/kg) (p = 0.003). Cold air storage appears to provide better lung preservation than hypothermic immersion in ice slush.

Air↗
PubMed1991

Sodium nitroprusside infusion does not dilate cerebral resistance vessels during hypothermic cardiopulmonary bypass.

This study determined whether sodium nitroprusside (SNP) changes cerebral vascular resistance during stable, hypothermic cardiopulmonary bypass (CPB). Cerebral blood flow (CBF) was measured using Xenon clearance in 39 patients anesthetized with fentanyl. In 25 patients (group 1), CBF was measured before and during infusion of SNP at a rate sufficient to reduce mean arterial pressure (MAP) approximately 20%. In 14 other patients (group 2), CBF was measured before and during simultaneous infusion of SNP and phenylephrine; SNP was continued at a rate that had reduced MAP approximately 20% while phenylephrine was added in a dose sufficient to restore MAP to preinfusion levels. Patients within each group were randomized to maintenance of PaCO2 approximately 40 mmHg (groups 1a and 2a), uncorrected for body temperature, or to maintenance of PaCO2 approximately 50 mmHg (groups 1b and 2b). The following variables were maintained within a narrow range: nasopharyngeal temperature (26-29 degrees C), pump oxygenator flow (1.7-2.5 l.min-1.m-2), PaO2 (150-300 mmHg), and Hct (22-28 vol%). In each patient, controlled variables varied no more than +/- 5% between measurements. In group 1a (PaCO2 approximately 40 mmHg), MAP was 86 +/- 9 mmHg (mean +/- SD) before and 65 +/- 8 mmHg during SNP infusion (P less than 0.0001). CBF was 12 +/- 3 ml.100g-1.min-1 before and 10 +/- 2 ml.100(-1).min-1 during SNP infusion (P less than 0.01). In group 1b (PaCO2 approximately 55 mmHg), MAP was 86 +/- 11 mmHg before and 66 +/- 13 mmHg during SNP infusion (P less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1991

Neuropsychiatric complications following cardiac surgery.

Few patients are neurologically devastated following cardiac surgery. However, a substantial number of patients suffer sufficient deterioration in neurologic and neuropsychologic function that the quality of their recovery is limited. Intensive research is necessary to determine what surgical and pharmacologic techniques are suitable for use in this large at-risk population.

Cardiac Surgical Procedures↗
PubMed1990

Decrease in hippocampal [3H]vinylidene kainic acid binding in genetically epilepsy-prone rats.

Specific [3H]vinylidene kainic acid binding to the kainate-sensitive subtype of glutamate receptor was studied in brain of 31-day-old non-epileptic Sprague-Dawley control and two colonies of genetically epilepsy-prone rats using in vitro autoradiographic techniques. At 37.5 nM [3H]vinylidene kainic acid, specific [3H]vinylidene kainic acid binding was reduced significantly by 18 and 22% in dorsal and ventral hippocampal formation stratum lucidum of 31-day-old genetically epilepsy-prone-9 rats compared with non-epileptic controls. Hippocampal [3H]vinylidene kainic acid binding was reduced in genetically epilepsy-prone-3 rats by 15 and 18%, but these reductions were not statistically significant. Saturation of [3H]vinylidene kainic acid binding studies indicated that the total number of ventral hippocampal [3H]vinylidene kainic acid binding sites was decreased by 21% in genetically epilepsy-prone-3 rats and 28% in genetically epilepsy-prone-9 rats. The reduction in ventral hippocampal [3H]vinylidene kainic acid binding in genetically epilepsy-prone rats resembles the reduction in ventral hippocampal [3H]vinylidene kainic acid binding sites observed in perinatal hypothyroid rats. As genetically epilepsy-prone rats are hypothyroid during the neonatal period, the reduction in hippocampal [3H]vinylidene kainic acid binding in the genetically epilepsy-prone rats may be a consequence of a hypothyroid-induced defect in the development or maturation of the hippocampal mossy fiber projection in genetically epilepsy-prone rats. An alternative hypothesis is that the putative occurrence of spontaneous limbic seizures in genetically epilepsy-prone rats may lead secondarily to a reduction in hippocampal [3H]vinylidene kainic acid binding sites.

Animals↗
PubMed1990

Labetalol for the control of elevated blood pressure following coronary artery bypass grafting.

In a multicenter study, the efficacy and safety of intravenous (IV) labetalol for the control of elevated blood pressure were studied in the intensive care unit (ICU) in 65 patients within 4 hours following coronary artery bypass grafting (CABG). Patients with pre-existing ventricular dysfunction, bradycardia, bronchospastic disease, or postoperative complications were excluded. All patients were monitored with a thermodilution pulmonary artery catheter. Entry criteria were a systolic blood pressure (SBP) greater than 140 mm Hg or diastolic blood pressure (DBP) greater than 90 mm Hg for at least five minutes. Intravenous labetalol was loaded incrementally (5, 10, 20, and 40 mg at 10-minute intervals) to a maximum cumulative dose of 75 mg, until either SBP decreased 10% or DBP decreased 10% and was less than 90 mm Hg. Responders were entered into a 6-hour maintenance period, and received 5 to 40 mg of IV labetalol every 10 minutes as needed for blood pressure control. Hemodynamic data and temperature were recorded at baseline, just before each dose of labetalol during the loading period, and at the end of the maintenance period. Alternative therapy was given in the case of nonresponse or adverse events. Intravenous labetalol successfully controlled post-CABG hypertension in 55 of 65 patients (85%); of these, 46 responded to 35 mg or less. Although 28 patients required no further labetalol in the maintenance period, in the others dosage varied from 5 to 400 mg. Reductions in SBP and DBP were associated with moderate reductions in pulse pressure (SBP-DBP) and heart rate (HR). Cardiac index decreased by 18.5%, with a 12.5% decrease in stroke index and 8.1% decrease in HR. Systemic vascular resistance did not increase significantly. Four patients (6%) developed hypotension related to IV labetalol. There was one death due to perioperative myocardial infarction, which was unrelated to labetalol use. The mechanism of action of IV labetalol in controlling hypertension after CABG surgery seems to be moderate negative inotropy and chronotropy. Its alpha-blocking effects seem to be important in preventing reflex vasoconstriction. This is directly opposite to the primary vasodilator effect found when IV labetalol is used to control nonsurgical hypertension. Because of these actions, labetalol should be avoided or used with caution in patients with preoperative and postoperative cardiac dysfunction. In patients with normal left ventricular function, IV labetalol appears to be a safe, effective agent in controlling post-CABG hypertension, with the added potential benefit of enhanced myocardial oxygen balance.

Analysis of Variance↗
PubMed1990

Calcium attenuates epinephrine's beta-adrenergic effects in postoperative heart surgery patients.

Epinephrine and calcium possess both cardiac inotropic and vasopressor activity. In addition, epinephrine's cardiovascular effects are mediated via increases in intracellular calcium. As a result, many clinicians administer the two agents together in an attempt to augment their effects. Although this approach seems rational, it has never been proven effective. We evaluated the cardiovascular and hyperglycemic actions of epinephrine (10 and 30 ng/kg/min), with and without calcium chloride administration (10 mg/kg bolus followed by 2 mg/kg/hr infusion), in a prospective, randomized, blinded, crossover designed study. Twelve adult patients were studied 1 day after aortocoronary bypass surgery. Calcium chloride raised ionized calcium levels from 1.06 +/- 0.03 (mean +/- SEM) to 1.44 +/- 0.05 mM (p less than 0.05). Calcium raised mean arterial pressure from 85 +/- 1 to 94 +/- 2 mm Hg (p less than 0.05) but had no significant effect on cardiac index. Epinephrine alone at 10 and 30 ng/kg/min significantly raised cardiac index from 2.7 +/- 0.2 to 3.0 +/- 0.2 (p less than 0.05) and 3.6 +/- 0.3 (p less than 0.05) l/min/m2. After calcium, epinephrine failed to significantly increase cardiac index. Epinephrine at 30 ng/kg/min significantly increased mean arterial pressure from 87 +/- 1 to 95 +/- 2 mm Hg (p less than 0.05). After calcium, epinephrine had no significant effect on blood pressure. In addition, epinephrine's hyperglycemic effect was blunted by calcium. Plasma epinephrine levels were similar during control and calcium infusions. We conclude that calcium blunts epinephrine's beta-adrenergic actions in postoperative cardiac surgery patients.

Blood Glucose↗
PubMed1990

Hypercarbia depresses cerebral oxygen consumption during cardiopulmonary bypass.

No human studies have systematically examined the relations among PaCO2, cerebral blood flow, and the cerebral metabolic rate for oxygen during hypothermic cardiopulmonary bypass. We varied PaCO2 during hypothermic (26-28 degrees C) cardiopulmonary bypass and estimated the cerebral metabolic rate for oxygen by multiplying cerebral blood flow (measured using xenon-133 clearance) by the cerebral arteriovenous difference in oxygen contents. Patients were randomly assigned to either of two methods of managing PaCO2 (uncorrected for body temperature). In group 1 (PACO2 32-48 mm Hg, n = 13) the mean +/- SD cerebral metabolic rate for oxygen was 0.40 +/- 0.11 ml O2 X 100 g-1 X min-1 at a mean +/- SD PaCO2 of 36 +/- 2.0 mm Hg and 0.40 +/- 0.14 ml O2 X 100 g-1 X min-1 at a mean +/- SD PaCO2 of 45 +/- 2 mm Hg. and 49-72 mm Hg, n = 12) the mean +/- SD cerebral metabolic rate for oxygen was 0.31 +/- 0.09 ml O2 X 100 g-1 X min-1 at a mean +/- SD PaCO2 of 55 +/- 3 mm Hg and 0.21 +/- 0.07 ml O2 X 100 g-1 X min-1 at a mean +/- SD PaCO2 of 68 +/- 2 mm Hg. Group 2 values differed significantly from those in Group 1 (p less than 0.05). In both groups, cerebral blood flow increased as PaCO2 increased. During cardiopulmonary bypass, increasing PaCO2 increases cerebral blood flow and decreases the cerebral metabolic rate for oxygen.

Arteries↗
PubMed1990

Heparin dosing and monitoring for cardiopulmonary bypass. A comparison of techniques with measurement of subclinical plasma coagulation.

Subclinical plasma coagulation during cardiopulmonary bypass has been associated with marked platelet and clotting factor consumption in monkeys. To better define subclinical coagulation in man, we measured plasma fibrinopeptide A concentrations before, during, and after cardiopulmonary bypass. Patients were assigned to one of three groups of heparin management: group 1 (n = 10)--initial heparin dose 300 IU/kg, with supplemental heparin if the activated coagulation time fell below 400 seconds; group 2 (n = 6)--initial heparin dose 250 IU/kg, with supplemental heparin if activated coagulation time was less than 400 seconds; and group 3 (n = 5)--initial heparin dose 350 to 400 IU/kg, with supplemental heparin if whole blood heparin concentration was less than or equal to 4.1 IU/ml. Activated coagulation time and heparin concentration were measured every 30 minutes during cardiopulmonary bypass, and fibrinopeptide A was measured at hypothermia, normothermia, and whenever activated coagulation time was less than 400 seconds. Quantitative and qualitative blood clotting competence was assessed after cardiopulmonary bypass, including mediastinal drainage for the first 24 hours. Fibrinopeptide A values were markedly elevated during cardiopulmonary bypass but were well below the levels present before and after cardiopulmonary bypass. Fibrinopeptide A correlated inversely with heparin concentration during cardiopulmonary bypass (r = -0.46, p = 0.03), but higher fibrinopeptide A levels during cardiopulmonary bypass did not correlate with post-cardiopulmonary bypass coagulopathy. Group 3 patients received the highest heparin doses (p less than 0.05) and had the greatest postoperative blood loss (p less than 0.05). Protamine dose and heparin concentration during cardiopulmonary bypass correlated best with postoperative mediastinal drainage. Our findings support the following conclusions: (1) compensated subclinical plasma coagulation activity occurs during cardiopulmonary bypass despite activated coagulation time greater than 400 seconds or heparin concentration greater than or equal to 4.1 IU/ml; (2) post-cardiopulmonary bypass mediastinal drainage correlates strongly with increased heparin concentration during cardiopulmonary bypass (p less than 0.05) and protamine dose (p less than 0.05); and (3) during cardiopulmonary bypass at both normothermia and hypothermia, activated coagulation times greater than 350 seconds result in acceptable fibrinopeptide A levels and post-cardiopulmonary bypass blood clotting.

Blood Coagulation↗
PubMed1989

Cardiac transplantation in a patient with muscular dystrophy and cardiomyopathy.

A 17-year-old boy with muscular dystrophy developed a cardiomyopathy. His brother died of a cardiomyopathy, and muscle enzyme levels were elevated in asymptomatic family members. Examination revealed cardiomegaly, hepatomegaly, proximal muscle atrophy and weakness, and calf hypertrophy. Skeletal muscle and endomyocardial biopsy specimens were consistent with Becker's muscular dystrophy. Because of intractable heart failure, orthotopic cardiac transplantation was performed. Two years after transplantation, the patient has returned to work and regained previous exercise tolerance. Heart transplantation can be an acceptable treatment of patients who have muscular dystrophy, with preserved ambulation and favorable life expectancy, and also life-threatening cardiomyopathy refractory to medical management.

Adolescent↗
PubMed1989

Radial artery-to-aorta pressure difference after discontinuation of cardiopulmonary bypass.

To test whether the radial artery-to-aorta pressure gradient seen in some patients after cardiopulmonary bypass (CPB) is due to reduction in hand vascular resistance, the authors compared pressures in the ascending aorta with pressures in the radial artery before and after CPB in 12 patients. They increased hand vascular resistance by briefly occluding the radial and ulnar arteries at the wrist and recorded that effect on the radial artery-to-aorta pressure relationship. They also recorded the effect of wrist compression on radial artery pressures before and after CPB in 38 patients not having aortic pressure measurements. Before CPB in the first 12 patients, the radial systolic arterial pressure (SAP) was significantly higher (P less than 0.05) than the ascending aortic SAP, and wrist compression did not significantly affect that difference (P greater than 0.05). After CPB, the radial artery and aortic SAPs were not statistically different (P greater than 0.05), but wrist compression restored the higher radial artery SAP. The mean arterial pressure (MAP) was equal in four patients and 1-3 mmHg higher or lower in eight patients before CPB, and wrist compression did not alter those relationships. After CPB, MAP was equal in four patients; radial MAP was 1-3 mmHg higher or lower in six patients, and 7 and 10 mmHg lower in the last two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Cerebral blood flow does not change following sodium nitroprusside infusion during hypothermic cardiopulmonary bypass.

Changes in cerebral blood flow (CBF) associated with decreases in mean arterial pressure (MAP) produced by sodium nitroprusside (SNP) infusion were measured by intra-aortic injection of 133Xe in 17 patients during hypothermic cardiopulmonary bypass (CPB). In each patient, CBF was determined at baseline and then again following SNP-induced reduction of MAP. Two groups were studied. In Group I (n = 9), PaCO2 was maintained near 42 mm Hg uncorrected for nasopharyngeal temperature (NPT). In Group II (n = 8), PaCO2 was maintained near 60 mm Hg, uncorrected for NPT. Nasopharyngeal temperature, MAP, pump oxygenator flow, PaO2, and hematocrit were maintained within a narrow range in each patient during both studies. Since the baseline CBF determinations were conducted at the higher MAP in all subjects, we corrected post-SNP CBF data for the spontaneous decline that occurs over time during CPB. In Group I, a reduction in MAP from 76 +/- 9 mm Hg (mean +/- SD) to 50 +/- 6 mm Hg was associated with a reduction in CBF from 17 +/- 5 to 13 +/- 3 ml.100 g.min-1 (P less than 0.01), a decrease that became statistically insignificant once the time correction factor had been applied (16 +/- 4 ml.100 g-1.min-1). In Group II, MAP declined from 75 +/- 5 mm Hg to 54 +/- 5 mm Hg, and CBF declined from 25 +/- 10 to 17 +/- 7 ml.100 g.min-1 (P less than 0.01), but, again, after time correction, the CBF decline was statistically insignificant (22 +/- 8 ml.100 g-1.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Current treatment of traumatic aortic disruptions.

Eighteen patients with traumatic disruptions of the descending thoracic aorta were treated at the Wake Forest University Medical Center from 1979 through 1986. Their preoperative evaluation and operative management are presented, with emphasis being placed on methods for preventing complications related specifically to aortic cross-clamping. Two patients died, for an operative mortality of 11 per cent. One of the two patients had exsanguinating hemorrhage with profound shock on the way to the operating room; in the second patient, the aorta was occluded just beyond the disruption, and there had been no distal perfusion for several hours before operation. Four patients (22%), three of whom had not had a shunting procedure, had major neurologic complications relating to the spinal cord. Thus, shunting procedures during repair of descending aortic disruption appear to offer some protection from neurologic deficits.

Adult↗
PubMed1988

Elevation of naloxone-sensitive 3H-dihydromorphine binding in hippocampal formation of genetically epilepsy-prone rats.

3H-Dihydromorphine (DHM) binding sites were measured in the brain of non-epileptic control and GEPR rats using in vitro autoradiographic techniques. The number of naloxone-sensitive 3H-DHM binding sites was increased 38-57% in the pyramidal cell layer of ventral hippocampal CA3 and Ca1 of GEPR-3 and GEPR-9 rats compared to non-epileptic controls. No significant differences in 3H-DHM binding were observed in dorsal hippocampal formation, lateral entorhinal cortex, lateral geniculate or cerebellum. The results suggest that an increase in the number of opioid receptors in ventral hippocampus of GEPR rats may be one factor contributing to the enhanced sensitivity of GEPR-9 rats to the proconvulsant effects of morphine.

Acoustic Stimulation↗
PubMed1986

Response of cerebral blood flow to changes in carbon dioxide tension during hypothermic cardiopulmonary bypass.

Changes in cerebral blood flow (CBF) in response to changes in PaCO2 were measured by intraaortic injection of 133Xe in 12 patients during hypothermic (23-30 degrees C) cardiopulmonary bypass. In each patient, CBF was determined at two randomly ordered levels of PaCO2 obtained by varying the rate of gas inflow into the pump oxygenator (Group I, n = 6) or by varying the percentage of CO2 added to the gas inflow (Group II, n = 6). Nasopharyngeal temperature, mean arterial pressure, pump-oxygenator flow, and hematocrit were maintained within a narrow range. In group I, a PaCO2 (uncorrected for body temperature) of 36 +/- 4 mmHg (mean +/- SD) was associated with a CBF of 13 +/- 5 ml X 100 g-1 X min-1, while a PaCO2 of 42 +/- 4 mmHg was associated with a CBF of 19 +/- 10 ml X 100 g-1 X min-1. In group II, a PaCO2 of 47 +/- 3 mmHg was associated with a CBF of 20 +/- 8 ml X 100 g-1 X min-1, and a PaCO2 of 53 +/- 3 mmHg was associated with a CBF of 26 +/- 9 ml X 100 g-1 X min-1. Within group I, the difference in CBF was significant (P less than 0.05); within group II, the difference in CBF was significant at the P less than 0.002 level. All CBF measurements were lower than those reported for normothermic, unanesthetized subjects of similar age.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Immediate functional recovery and avoidance of reperfusion injury with surgical revascularization of short-term coronary occlusion.

Functional recovery with surgical revascularization of acutely ischemic myocardium has not been compared with its nonsurgical counterpart in experimental preparations of coronary occlusion. This study compares the functional and metabolic recovery of ischemic (1 hr coronary occlusion) segments revascularized either by restoration of coronary patency (simulating nonsurgical recanalization, e.g., angioplasty) or by surgical revascularization with multidose hypothermic potassium blood cardioplegic solution. Twenty-two anesthetized open-chest dogs were instrumented with Millar micromanometer-tip catheters to measure left ventricular and aortic pressures. Piezoelectric ultrasonic dimension gauges were implanted in the subendocardium supplied by the left anterior descending coronary artery to measure segmental contractile function. In five dogs, only biopsy samples were obtained for control measurements of ATP, creatine phosphate, and tissue water content. In the remaining 17 dogs, the left anterior descending artery and collaterals were ligated for 1 hr. The ligatures were removed in eight dogs and coronary perfusion continued for 2 hr, simulating nonsurgical reperfusion. The remaining nine dogs were placed on cardiopulmonary bypass and the hearts were arrested for 1 hr with multidose (every 20 min) blood cardioplegic solution enhanced with glutamate and aspartate, simulating surgical revascularization (coronary artery bypass grafting). The coronary ligatures were not released until the second cardioplegic infusion, simulating graft placement. One hour of coronary occlusion placed 39.4 +/- 2.5% of the left ventricle at risk, and converted active systolic shortening to persistent paradoxical bulging (25.2 +/- 2.2% to -5.8 +/- 1.2% systolic shortening).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1977

A fluorometric study of oxidative metabolism in the in vivo canine heart during acute ischemia and hypoxia.

Optical techniques for monitoring the fluorescence of intramitochondrial nicotinamide adenine dinucleotide (NADH) were employed to allow an on-line, non-invasive study of the metabolic state of healthy and ischemic cardiac tissue in the intact dog. Acute interruption of blood flow to the area of myocardium studied resulted in an immediate rise in NADH, indicating impairment of oxidative metabolism due to limitation of oxygen availability. Release of the coronary artery occlusion resulted in an oxidation of NADH to preocclusion baseline and signaled repayment of incurred O2 debt. Collateral flow produced a spontaneous fall in NADH levels towards preocclusion baseline. Hypoxic tissue was recognized by an oxidation of NADH on ventilation with 100 per cent O2, while in normal hearts no oxidation indicated the O2 was not rate limiting. Ischemic NADH increases preceded the onset of epicardial EKG changes, suggesting that an inability to rephosphorylate ADP to ATP is the primary cause of the EKG changes. Fluorometry of the in vivo heart provides a sensitive, continuous technique of monitoring cardiac cellular mitochondrial NAD;NADH redox levels and, therefore, the adequacy of high energy phosphate production and allows localization of cardiac tissue with marginal oxygen supply.

Animals↗