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PubMed1978

[Short-term and long-term therapy with slow-release ISDN. Echographic, vector cardiographic and ergometric findings (author's transl)].

The effect of slow-release isosorbide dinitrate (Maycor retard) on the myocard was investigated in a short-term study (single dose of 20 mg slow-release ISDN) and in a long-term study (2 X 20 mg slow-release ISDN daily) in 10 patients with coronary heart disease. The parameters assessed were heart rate, blood pressure and skin temperature at rest, load ECG, orthogonal ECG and VCG by computer and UCG echocardiography. The reductions of diastolic and systolic ventricular diameter are statistically significant in the short-term and long-term trials. The ejection time decreases. The velocity of circumferential fiber shortening as a measure of myocardial contractility increases highly significantly. R peak and T wave amplitude in the Y lead change significantly. These findings can be interpreted as an expression of improved myocardial tension and a normalization of the contraction and relaxation.

Blood Pressure↗
PubMed1997

Endothelial dysfunction of conduit arteries in insulin-dependent diabetes mellitus without microalbuminuria.

OBJECTIVE: Previous studies have shown that endothelial dysfunction, an early sign of atherosclerosis, occurs in animal models of diabetes mellitus and in resistance vessels of patients with insulin-dependent diabetes. In the present study we examined whether young patients with insulin-dependent diabetes without microalbuminuria present abnormal endothelial function of large peripheral arteries. METHODS: Twenty-six patients with insulin-dependent diabetes without microalbuminuria were compared with 26 normal controls and 5 patients with insulin-dependent diabetes with microalbuminuria. Brachial artery diameter was measured at rest, during reactive hyperaemic flow (endothelium-dependent dilatation) and after sublingual isosorbide dinitrate (endothelium-independent dilatation). RESULTS: Baseline artery diameter and flow as well as the degree of reactive hyperaemia were similar in all groups compared to controls. Flow-mediated dilatation was lower in patients with diabetes without microalbuminuria (5.8 +/- 7 vs 11 +/- 7%. P = 0.01) as well as in patients with diabetes without microalbuminuria (0.75 +/- 2.5 vs 11 +/- 7%, P = 0.003); nitrate-induced dilatation was normal in patients without microalbuminuria and attenuated in patients with microalbuminuria. In the group of diabetes patients without microalbuminuria, those with disease duration > 10 years and HbAlc > 6% had the worse endothelial function. CONCLUSIONS: Our results demonstrate that endothelial dysfunction of conduit arteries can be detected in patients with insulin-dependent diabetes mellitus without microalbuminuria, probably contributing to the high prevalence of atherosclerosis in these patients.

Adolescent↗
PubMedDate not supplied

Action of vasodilating drugs on small and large arteries of hypertensive patients.

We studied blood pressure, arterial diameter, and blood flow of the brachial artery in patients with sustained essential hypertension before and after administration of the vasodilating drugs nitroglycerin, captopril, dihydralazine, diltiazem, and isosorbide dinitrate (ISDN). The diameter and the blood flow of the brachial artery were measured with a pulsed Doppler device which allowed the angle between the ultrasound beam and the vessel axis to be determined with a precision better than 2%. Nitroglycerin and captopril decreased blood pressure slightly but increased arterial diameter markedly. Dihydralazine, diltiazem, and ISDN decreased blood pressure similarly and significantly and also reduced forearm vascular resistance. Dihydralazine reduced arterial diameter (p less than 0.001), but did not change brachial blood flow. Diltiazem and ISDN increased the arterial diameter markedly (p less than 0.001 and p less than 0.01, respectively), but only the former increased brachial blood flow. We conclude that antihypertensive drugs that dilate small arteries can either reduce (dihydralazine) or increase (nitroglycerin, captopril, diltiazem, ISDN) the caliber of large peripheral arteries and thus have different effects on peripheral blood flow.

Adult↗
PubMed1999

Dissociation of vascular tolerance and plasma norepinephrine adjustment during long-term nitrate therapy in human coronary arteries.

OBJECTIVE: We examined whether changes in plasma norepinephrine (NE) concentration contribute to the development of nitrate tolerance in human coronary arteries. METHODS: Patients with stable angina were randomized to receiving nitrate (isosorbide dinitrate: ISDN or nitroglycerin: TNG) infusion for 30 minutes (group A), 48 hours (group B), or 78 hours (group C). Coronary diameters were measured angiographically at baseline (CT), during maximum dilation by ISDN (N1), at the end of nitrate infusion (N2) and after additional ISDN (1 mg) injection (N3). RESULTS: In groups A and B, N1, N2, and N3 were greater than CT, and there was no significant difference between N1, N2, and N3 for each group. In group C, N1 and N3 were greater than CT, but there was no difference between CT and N2, in the development of nitrate tolerance. In group A, NE increased significantly during nitrate infusion (304+/-163 vs. 418+/-273 pg/ml). NE did not change in groups B and C. CONCLUSION: The change in NE concentration is not a primary contribution to the development of nitrate tolerance.

Aged↗
PubMed1995

Relationship between ventilatory threshold and onset of ischaemia in ECG during stress testing.

UNLABELLED: The study was carried out to determine the relationship between ventilatory threshold and the onset of ischaemia, as shown on the ECG (horizontal and/or descending ST depression of 0.05 mV, on average). Twenty-seven male patients (aged 58 +/- 7 years) with angiographically documented coronary artery disease (CAD) were assessed by cardiopulmonary exercise testing without medication. Oxygen uptake (VO2), heart rate (HR), rate-pressure-product (RPP) and blood lactate were measured and/or calculated every 30 s during exercise. In addition, 10 patients, comparable with the above group, were examined to find out the acute effects of isosorbide dinitrate (ISDN) at ventilatory threshold in relation to ischaemic threshold. The first cardiopulmonary exercise test was carried out without medication, the second 1 h later with 5 mg ISDN, taken sublingually 30 min before the test. RESULTS: (means, SD): (1) The mean ventilatory threshold preceded the ischaemic threshold in relation to exercise capacity (48 +/- 14 vs 55 +/- 20 watts; P < 0.05), VO2.kg-1 (10.0 +/- 2.2 vs 12.0 +/- 2.9 ml.kg-1.min; P < 0.05), HR (93 +/- 15 vs 100 +/- 16.min-1; P < 0.01), RPP (15095 +/- 4424 vs 17166 +/- 5245; P < 0.01) and blood lactate (1.28 +/- 0.53 vs 1.44 +/- 0.60 mmol.l-1; P < 0.05). (2) This relationship was observed more often in the subgroup of patients with angina during cardiopulmonary exercise testing or with myocardial infarction or with three-vessel disease than in patients without angina or infarction or with one- and two-vessel disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1996

[Clinical observation of wenxin decoction in treating 82 patients with spontaneous angina pectoris].

One hundred twenty-two patients with spontaneous angina pectoris (SAP) were randomly divided into treated group (82 cases) and control group (40 cases), and treated with Wenxin decoction and isosorbide dinitrate respectively. Results showed that in treated group the total effective rate of SAP was 95.12% and that of electrocardiographic findings were 74.39%. These results were all superior to those of control group (P < 0.01). Moreover, results of extracorporeal thrombosis test showed after Wenxin decoction treatment, the length of thrombus decreased from 23.56 +/- 5.47 mm to 20.04 +/- 5.17 mm, the wet weight of it decreased from 92.65 +/- 18.45 mg to 76.94 +/- 15.08 mg and the dry weight from 21.76 +/- 7.30 mg to 16.90 +/- 5.35 mg. The submaximal exercise test revealed an increase of exercise time from 474.66 +/- 96.33 seconds to 548.83 +/- 99.93 seconds, increase of acting quantity from 104.16 +/- 19.65 W to 123.61 +/- 24.96 W and a decrease of ST segment depression from 0.183 +/- 0.041 mV to 0.139 +/- 0.038 mV. These results suggested that Wenxin decoction is valuable in treating SAP.

Adult↗
PubMed2004

Oral nitric oxide donors: a new pharmacological approach to detrusor-sphincter dyssynergia in spinal cord injured patients?

PURPOSE: Detrusor-sphincter dyssynergia is a common cause of bladder outlet obstruction in spinal cord injured patients and leads to poor bladder emptying and high bladder pressures, which if left untreated might cause renal failure. In this study, we tested the recently published hypothesis that oral administration of a nitric oxide donor could be a new pharmacological approach to treat detrusor-sphincter dyssynergia in humans with spinal cord injury. METHODS: 12 male spinal cord injured patients presenting with neurogenic detrusor overactivity and detrusor-sphincter dyssynergia were studied. 6 performed clean intermittent catheterisation and 6 used suprapubic tapping for bladder emptying. During cystometry the bladder was filled until the first overactive bladder contraction accompanied by detrusor-sphincter dyssynergia occurred while bladder and external urethral sphincter pressures were continuously recorded. Then the bladder was emptied and the patients received 10 mg of isosorbide dinitrate sublingually. Resting pressures were recorded and cystometry was repeated starting 15 min after drug administration. Maximal and mean values for bladder and external urethral sphincter pressures were calculated in both fillings and statistically compared by analysis of variance for repeated measurements (level of significance p < 0.05). RESULTS: Nitric oxide significantly reduced external urethral sphincter pressures at rest (p < 0.05) and during dyssynergic contraction (p < 0.05) while bladder pressures at rest and during contraction as well as the reflex volume remained unchanged. In the patients who used suprapubic tapping for bladder emptying the mean post triggering residual volume was significantly reduced (p < 0.05). CONCLUSIONS: Oral administration of nitric oxide donors significantly reduced bladder outlet obstruction due to detrusor-sphincter dyssynergia suggesting a role for nitric oxide in inhibitory neurotransmission to the urethral sphincter. This new approach could offer a potential pharmacological option to treat detrusor-sphincter dyssynergia in spinal cord injured patients.

Administration, Oral↗
PubMed2001

[Tolerance to nitrates in patients with angina and effect of plasmapheresis].

AIM: To evaluate tolerance to isosorbide dinitrate (ID) in patients with angina pectoris functional class II-III and effect of plasmapheresis in this tolerance management. MATERIAL AND METHODS: 85 patients with angina pectoris functional class II-III taking long-acting ID. RESULTS: As shown by repeat transesophageal left atrial pacing, 24.7% patients have developed tolerance to nitrate while taking prolonged ID. Two methods of this tolerance elimination were compared: plasmapheresis + withdrawal of long-acting nitrate and withdrawal of the nitrates only. The former has shown some advantages: use of plasmapheresis reestablished ID efficiency in 4 days (two sessions) in 81.8% and in 7 days (3 sessions) in 100% patients without withdrawal syndrome. The latter method reestablished a marked antiischemic effect of ID in 7 days and 20% patients exhibited a variant of withdrawal syndrome--early negative aftereffect. CONCLUSION: When withdrawal of long-acting nitrates is combined with plasmapheresis in anginal patients to eliminate tolerance to nitrates, the effect is better.

Angina Pectoris↗
PubMed1993

The effect of nitric oxide-donating vasodilators on monocyte chemotaxis and intracellular cGMP concentrations in vitro.

The effects of sodium nitroprusside (SNP) and 3-morpholino sydnonimine (SIN-1), isosorbide dinitrate (ISDN) and glyceryl trinitrate (GTN), and molsidomine (the inactive precursur of SIN-1) on monocyte chemotaxis and cyclic GMP (cGMP) concentration were studied. SNP and SIN-1 inhibited monocyte N-formyl-methionyl-leucyl-phenylalanine-stimulated migration and increased cGMP concentrations in a dose-dependent (> 10(-5) mol.l-1) and time-dependent manner. Furthermore, 8-bromo cGMP inhibited monocyte chemotaxis in a dose-dependent fashion. In contrast, ISDN, GTN and molsidomine did not alter monocyte migration or cGMP concentration. These results support earlier observations that nitric oxide inhibits monocyte function in vitro via a cGMP-mediated mechanism. The differential effects of the spontaneous and thiol-dependent NO-donating nitrovasodilators on monocyte function suggests that monocytes, like platelets, are not able to directly metabolise ISDN and GTN. If similar observations can be made in vivo, it is possible that certain nitrovasodilators might be used therapeutically to inhibit monocyte function, for example during atherogenesis.

Cell Migration Inhibition↗
PubMed1993

Lack of effect of nitrates on exercise tolerance in patients with mild to moderate heart failure caused by coronary disease already treated with captopril.

OBJECTIVE: To test the hypothesis that the addition of nitrates improves exercise tolerance in patients with heart failure caused by coronary artery disease already treated with an angiotensin converting enzyme inhibitor and diuretics. DESIGN: Randomised, double blind, placebo controlled, 16 week treatment periods. SETTING: Outpatient clinic at a university hospital. PATIENTS: 54 patients with previous myocardial infarction, symptoms of mild to moderate heart failure, left ventricular ejection fraction below 40%, no exercise-induced angina or electrocardiographic signs of ischaemia. Four patients in the nitrate group (n = 24) and one patient of the placebo group (n = 25) were withdrawn from the study. INTERVENTION: After the patients had been on constant doses of captopril and diuretics for at least 2 weeks, they were randomised to receive a target dose of 40 mg isosorbide dinitrate twice daily or placebo in addition to the continuation of captopril and diuretics. MEASUREMENTS: Bicycle exercise tests with measurement of gas exchange were carried out before randomisation and after 1, 6, 12, and 16 weeks of the double blind treatment. The change in peak oxygen uptake from control to week 16 was prospectively defined as the main outcome measure. RESULTS: The increase in peak oxygen uptake from before randomisation tended to be greater in the placebo group (before randomisation 17.4 (3.4) ml/min/kg) than in the nitrate group (before randomisation 17.1 (3.5) ml/min/kg) after 12 weeks (mean increase 1.1 (2.7) v 0.0 (2.7) ml/min/kg, p < 0.12) and 16 weeks (1.7 (3.0) v 0.3 (2.6) ml/min/kg, p < 0.14) of treatment. CONCLUSION: The addition of nitrates to a baseline treatment consisting of captopril and diuretics did not improve exercise tolerance.

Adult↗
PubMed1985

[Comparative evaluation of the effectiveness of various peripheral vasodilators in the treatment of cardiac insufficiency].

The efficacy of peripheral vasodilators with different action mechanisms was studied and compared in 96 patients with chronic circulatory failure, stages IIB-III, of different genesis (rheumatic fever, congestive cardiomyopathy, postinfarction cardiosclerosis). Isosorbide dinitrate was used in 16 patients, nitroglycerin in 36, pratsiol in 24, and captopryl in 20 patients. Monitoring of the ECG, heart rate, respiratory rate and arterial blood pressure as well as catheterization of the right heart and tetrapolar impedance plethysmography were performed. The parameters of the heart pre- and afterload, pulmonary hemodynamics as well as those characterizing myocardial contractility were measured. It was established that the successful use of the different vasodilators rests on an adequate determinations of the indications for use. Captopryl is particularly effective in grave circulatory failure associated with a dramatic activation of the renin-angiotensin system. Pratsiol is effective in all the cases of chronic CF, since the tone of the sympathoadrenal system is virtually always high in patients with grave decompensation. Pratsiol was particularly efficacious in chronic CF with mitral or aortal regurgitation.

Administration, Oral↗
PubMed1989

Inhibition of rat mesangial cell mitogenesis by nitric oxide-generating vasodilators.

Recent studies indicate that endothelium-derived relaxing factor (EDRF) may be identical with nitric oxide (NO). The purpose of this study was to investigate the antimitogenic effect of NO-generating drugs in cultured mesangial cells. S-nitroso-N-acetylpenicillamine, sodium nitroprusside, and isosorbide dinitrate, which generate NO, dose dependently inhibited serum-stimulated DNA synthesis. All three drugs also inhibited the rate of cell proliferation, whereas sodium nitroprusside and S-nitroso-N-acetylpenicillamine decreased cell density at confluence. The antimitogenic activity of S-nitroso-N-acetylpenicillamine was labile in culture medium and could be inhibited by hemoglobin, supporting the view that NO, in free or bound form, was the ultimate effector. All three vasodilators increased cellular guanosine 3',5'-cyclic monophosphate (cGMP) levels dose dependently; moreover, 8-bromo-cGMP mimicked the effects of the NO-generating drugs, suggesting that cGMP may be an intracellular mediator of antimitogenesis. The growth-inhibitory effect of S-nitroso-N-acetylpenicillamine was reversible and was not due to cell toxicity as shown by several criteria of cell viability. The results raise the possibility that EDRF/NO may be a modulator of mesangial cell growth in vivo.

Animals↗
PubMed2001

Reversal of the gastric effects of nicotine by nitric oxide donor treatment.

Nicotine intensifies experimental gastric ulceration by reducing gastric mucosal blood flow (GMBF) and mucus. As both these parameters can be improved by nitric oxide (NO), we evaluated the impact of a NO donor in ethanol-induced gastric mucosal injury in rats administered nicotine. A nicotine solution or water was administered for 20 days to Sprague-Dawley rats. NO donor (isosorbide dinitrate) was given 60 and 10 min before preparation of ex vivo gastric chambers and exposure to ethanol. Chronic nicotine intake significantly reduced GMBF and gastric mucus content. Nicotine intensifies ethanol-induced gastric injury and short-term administration of NO donor failed to antagonize the ulcerogenic action from either nicotine or alcohol. In another study, rats drank nicotine solution for 20 days, after which the nicotine was withdrawn and replaced by water for 10 additional days. NO donor was provided during these last 10 days. The gastric effects of nicotine persisted for at least 10 days after nicotine was withdrawn but then these effects could be abolished by prolonged NO treatment. Nicotine reduces plasma nitrite level, but gastric mucosal MPO activity remained unchanged. Our data suggest that nicotine cessation plus a longer period of NO donor administration can completely abolish the gastric effects of nicotine.

Analysis of Variance↗
PubMed1999

Exogenous nitric oxide inhibits platelet activation in whole blood.

We examined the effect of NO on collagen-induced whole blood aggregation and platelet activation in whole blood by using impedance aggregometry and flow cytometry. For the extracellular generation of NO, we chose sodium nitroprusside dihydrate (SNP), and as intracellular generators of NO, L-arginine and isosorbide dinitrate (ISDN). The latter two significantly inhibited whole blood aggregation, whereas SNP had no such effect. The inhibitory effect of ISDN was diminished by addition of methylene blue (MB) or 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-l-oxyl 3-oxide (carboxyl-PTIO), and the inhibitory effect of L-arginine was diminished by addition of N(G)-monomethyl-L-arginine monoacetate (L-NMMA). Although the addition of ISDN increased the cyclic guanosine monophosphate (cGMP) level in whole blood and in the suspension of platelets and white blood cells (PLTs + WBCs), no increase was found in platelet-rich plasma (PRP). The P-selectin expression on the platelet surface in whole blood was reduced by ISDN and L-arginine. These findings suggest that the intracellular generation of NO inhibits whole blood aggregation, and this mechanism may play an important role in its antithrombotic effect in whole blood.

Arginine↗
PubMed1995

Nitric oxide regulates angiotensin II receptors in vascular smooth muscle cells.

The objective of this study was to determine whether an enhanced generation of nitric oxide (NO) causes regulation of angiotensin II receptors in vitro using rat vascular smooth muscle cells in culture. Chronic treatment of cells with a series of NO-generating drugs, sodium nitroprusside, S-nitroso-N-acetylpenicillamine and isosorbide dinitrate for 18h dose and time-dependently decreased [125I]-angiotensin II binding to cells without any significant change in affinity. Induction of nitric oxide synthase following lipopolysaccharide (10 and 100 ng/ml) treatment of cells for 18 h increased basal nitric oxide synthase activity with a concomitant increase of nitrite and cyclic cGMP levels in the conditioned media. LPS treatment significantly (P < 0.05) decreased [125I]-angiotensin II binding to these cells, an effect that was significantly (P < 0.05) attenuated in the presence of NG-nitro-L-arginine methyl ester. In contrast, treatment of cells with atrial natriuretic factor, dibutyryl cGMP, 8-bromo-cGMP, NaNO2 or NaNO3 failed to significantly alter the affinity or number of [125I]-angiotensin II binding sites. These results suggest that NO regulates angiotensin II receptors in vitro through a cGMP-independent mechanism.

Amino Acid Oxidoreductases↗
PubMed2002

The effects of vasodilators on the relaxation of guinea-pig aorta during acute recoil.

BACKGROUND: We have investigated the effects of various vasodilators on smooth muscle relaxation during acute recoil with guinea-pig aorta to find effective therapies to prevent acute recoil at percutaneous transluminal coronary angioplasty (PTCA). METHODS: Muscle strips from guinea-pig aorta without endothelium were placed in a bath filled with modified Krebs solution. The strip was isotonically stretched with a tension of 9 mN for 1 min, and then isometric tension was measured until the tension reached a steady state. Various vasodilators were applied during isometric tension measurement. RESULTS: When no drug was applied (control), isometric tension reached a steady state within 20 min. The steady state was approximately 10% lower (more relaxed) than the stretched level. When isosorbide dinitrate (ISDN, 1 mM) was applied during isometric measurement, 18.7+/-5.3% greater relaxation occurred than in control relaxation (P<0.05, n=5). When nicorandil (1 mM) was applied, the following relaxation was 18.6+/-5.7% greater than control (P<0.05, n=8). The simultaneous application of glibenclamide (1 mM) completely inhibited such additional relaxation by nicorandil. Application of nifedipine (10 microM) caused a 12.9+/-2.5% greater relaxation than control (P=0.066, n=4). The first metabolite of sarpogrelate (BP984, 10 microM) caused much greater relaxation than control (23.7+/-7.9%, P<0.05, n=6). Amlodipine (10 microM), phentolamine (10 microM), and sarpogrelate (10 microM) had no influence on the relaxation of the strip. CONCLUSIONS: ISDN, nicorandil and BP984 significantly increase relaxation of the muscle strips after stretching compared to the control. These vasodilators may reduce acute recoil of the smooth muscle after PTCA.

Adrenergic alpha-Antagonists↗
PubMed2003

Continuous administration of organic nitrate decreases hepatic cytochrome P450.

We previously reported that cytochrome P450 (P450) is a key enzyme of organic nitrate biotransformation and that P450 levels of the heart and its vessels markedly decreased at the development of nitrate tolerance. Although our attention was mainly focused on the circulatory organs, most organic nitrates, including nitroglycerin (NTG), are metabolized in the liver, where nitric oxide (NO) is concomitantly produced from the organic nitrates. NO reacts with various molecules such as superoxide, heme, thiols, and oxygen. This paper examined whether hepatic P450 levels are also affected after organic nitrate administration, since the liver is the major organ of P450 related metabolism. Male Wistar rats were intravenously administrated NTG or isosorbide dinitrate (ISDN) for 24-96 h. We observed the level of hemeoxygenase-1 (HO-1) as the functional marker of hepatic P450, since one of the acute phase target proteins of NO induction is an inducible type of HO-1. Hepatic P450 was drastically decreased after 48 or 72 h of continuous NTG or ISDN infusion, when nitrate tolerance was observed, but it recovered 48 h after cessation of the NTG administration. HO-1 was induced within 24 h of continuous NTG infusion, but it returned to normal levels 48 h after cessation of NTG. The administration of sodium nitroprusside, an agent to which the animals showed no tolerance, did not induce HO-1 or P450 depletion. Chronic administration of organic nitrates significantly decreased hepatic P450. These results suggest that P450-dependent drug metabolism may be drastically affected after continuous organic nitrate administration.

Animals↗
PubMed1987

Controlled study of the haemodynamic effects of isosorbide 5-mononitrate in acute myocardial infarction.

In view of the favourable results of the short-term therapy of acute myocardial infarction (AMI) with glyceryl-trinitrate (GTN) infusion, we undertook a randomized study to test the hypothesis whether the administration of a single dose of isosorbide 5-mononitrate (IS 5-MN) given orally would have the same favourable haemodynamic effect as observed with GTN infusion. For this purpose we evaluated the haemodynamic effects of IS 5-MN compared to isosorbide dinitrate (ISDN), observed in the same group of patients. 10 patients (8 males, 2 females) aged 50-76 years (mean 63) with AMI (7 anterior, 3 inferior) admitted to the coronary care unit within 48 h from onset of symptoms were entered into this single-blind randomized study; at the time of study entry, 8 patients were in Killip class I, and 2 patients in Killip class II. All drugs with haemodynamic effects were withdrawn 12 h before the study started. Both the haemodynamic profile and the clinical status were stable in all patients. Haemodynamic parameters were recorded with a Swan-Ganz thermodilution catheter, cardiac output was measured by the thermodilution method, and the left ventricular ejection time was calculated according to the Weissler method. The echo left ventricular end-diastolic diameter was measured by evaluation of the M-mode echocardiographic recording.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗