Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normal plasma thyroid hormones with elevation of thyrotrophin levels in asymptomatic patients is known as subclinical hypothyroidism. Radionuclide angiography was used to study left ventricular function in 10 such patients before and after establishment of normal thyrotrophin levels with thyroxine. Resting left ventricular ejection fraction was similar in both states but exercise left ventricular ejection fraction was less in the subclinical hypothyroid (61 +/- 3 per cent) compared with the euthyroid (68 +/- 3 per cent; p less than 0.025) state. Sodium nitroprusside caused similar increases in resting cardiac output but in subclinical hypothyroidism this resulted from a large increase in heart rate (26 +/- 4 beats/min) and reduction in stroke volume (11 +/- 4 per cent) whereas in the euthyroid state, the heart rate increment was less (14 +/- beats/min) and stroke volume was unchanged. Analysis of left ventricular pressure-volume relationships at end-systole during exercise showed a steeper pressure-volume slope in the euthyroid compared with the subclinical hypothyroid state (p less than 0.05). Subtle impairment of left ventricular function is detectable in subclinical hypothyroidism and may justify use of hormone replacement.
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PMID:Left ventricular performance in subclinical hypothyroidism. 409 55

The anti-hypertensive properties of sodium nitroprusside have been tested in 20 patients undergoing coronary arterial surgery. Were measured the arterial pressure, heart rate, mean right atrial pressure and mean left atrial pressure. The cardiac output, systemic vascular resistance and left ventricular stroke work index were deduced. A dose of 0.8 to 3 micrograms . kg-1 . min-1 sodium nitroprusside was given at the start of surgery, and immediately afterwards. The results showed a decrease of the systemic vascular resistance, a significant drop of arterial pressure, and a significant increase of heart rate as well as a tendency for the cardiac output to fall, probably because of insufficient vascular filing. When the mean left atrial pressure was kept at 14.8 +/- 3 mmHg (1.97 +/- 0.40 kPa), and left ventricular stroke work index fell, whilst cardiac output increased. Sodium nitroprusside seemed to be useful in coronary arterial surgery if used with care.
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PMID:[Sodium nitroprusside and coronary surgery]. 662 45

Although hypertension is the greatest risk factor for stroke, its control with antihypertensive drugs improves survival and decreases the incidence of stroke. If a stroke should occur, careful antihypertensive therapy has not been harmful. Sodium nitroprusside is the initial drug of choice in acute crises.
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PMID:Hypertension and cerebrovascular disease. 690 Nov 85

Sodium nitroprusside (SNP) is used to control proximal hypertension during cross-clamping of the descending thoracic aorta (XC). To assess the haemodynamic effects of SNP on cardiac output (CO) during XC, 21 pigs were anaesthetized with ketamine and fentanyl. In the control group (n = 11), no vasodilating therapy was given. In the investigation group (SNP group), 2 animals died during the surgical preparation and were excluded, leaving 8 animals in the group (n = 8). In these animals, SNP was infused in order to keep the mean arterial pressure (MAP) at about 100 mm Hg during cross-clamping. In both groups, aorta was cross-clamped for 30 min, and cardiac output (CO) was measured by the thermodilution technique. Following cross-clamping, CO increased 107% in the control group and 96% in the SNP group. There was an increase in heart rate (HR) of 77% in the control group and of 110% in the SNP group, and a reduction in systemic vascular resistance of 41% in the SNP group. Stroke volume (SV) was unchanged in both groups. MAP increased 83% in the control-group. No differences were observed between the two groups regarding central venous pressure or pulmonary artery pressure. Four animals in the SNP group died 5-10 min after release of the aortic clamp. In conclusion, we found equal increase in CO in both groups. The increase in CO was related predominantly to increased HR, whereas SV was largely unaltered. Vasodilation with SNP increased the mortality following clamp removal in this experimental model.
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PMID:Effect of sodium nitroprusside on cardiac output during cross-clamping of the descending thoracic aorta in pigs. 758 4

Diastolic blood pressure of 120 mm Hg or more is often cited as identifying a hypertensive crisis. However, the absolute level of blood pressure may not be as important as the rate of increase. One important feature that distinguishes hypertensive emergency from hypertensive "urgency" is the ongoing vascular damage that occurs with hypertensive emergency. When this is present, therapy should be initiated as soon as possible. The initial goal is to reduce mean arterial pressure about 15% to 25% within the first 48 hours. Overzealous or uncontrolled reduction in blood pressure may result in coma, stroke, myocardial infarction, acute renal failure, or death. Thus, a drug with titratable dosing (eg, intravenous nitroprusside sodium [Nipride, Nitropress]) is preferred in most situations. Patients with hypertensive urgency do not have evidence of vascular damage. Usually, they are asymptomatic, have no retinal lesions, and have a marked elevation in diastolic blood pressure. Hypertensive urgency does not require immediate normalization of blood pressure, but initiation of therapy and careful follow-up are critical.
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PMID:Treating hypertensive emergencies. Controlled reduction of blood pressure and protection of target organs. 843 61

Acute ischaemic stroke is characterised by reductions in local cerebral blood flow (CBF) and activation of circulating platelets and leucocytes. Nitric oxide is a vasodilator and can inhibit these circulating cells. The aim of this study was to assess the effect of nitric oxide on platelet function and regional CBF in patients with acute ischaemic stroke. Sodium nitroprusside (SNP), a spontaneous nitric oxide donor, was administered at a dose which caused a 10 mm Hg fall in mean arterial blood pressure (MABP) in a pathophysiological study to 22 patients with acute ischaemic stroke and 12 matched control subjects. Platelet function (whole blood aggregation and flow cytometry) was assessed before and during SNP administration. Changes in regional CBF were measured using single photon emission computerised tomography (SPECT) scanning. SNP significantly reduced platelet aggregation in both the patient and control subject groups. Equally, the expression of platelet adhesion molecules P-selectin (CD62) and glycoprotein (GP) GP IIIa (CD61) were significantly reduced in both groups. GP Ia (CDw49b) expression was significantly attenuated in the patient but not in the control group. Four patients underwent SPECT scanning and improvements in local CBF corresponding to the penumbral area of the clinical stroke site were seen in 3 of these patients. A total of 24 regions of asymmetrical perfusion were examined, pre-SNP (median (SQR)), 0.68 (0.14) vs. peri-SNP 0.78 (0.17), 2p = 0.065. SNP, given at a dose which reduced MABP by 10 mm Hg, significantly inhibited platelet aggregation and adhesion molecule expression. Improved regional CBF was seen in some patients. SNP is a candidate therapeutic agent for patients with acute ischaemic stroke and warrants further study.
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PMID:Pathophysiological assessment of nitric oxide (given as sodium nitroprusside) in acute ischaemic stroke. 961 99

The objective of this research was to determine the amount and timing of nitric oxide (NO, nitrogen monoxide) gas produced by the lungs, intestinal mucosa, and organ surfaces facing the peritoneal cavity after iv injection of a bacterial toxin, lipopolysaccharide (LPS). Some of the deleterious effects of LPS on organ function have been attributed to NO or strong oxidants formed locally from NO. Medical-grade air was used as an inspiratory air source (50 strokes/min x 3 ml/stroke) or was pumped through the ileal lumen or peritoneal cavity (20 strokes/min x 3 ml/stroke). The air was collected at intervals of 15-30 min for 3 h after LPS and analyzed for authentic NO gas by chemiluminescence. LPS (5 mg/kg) or saline was injected iv. Sodium nitroprusside (SNP) was injected to determine the appearance of its NO released into the perfused compartments. Blood pressure, plasma nitrate plus nitrite (NO(x)), and total plasma leukocytes were measured as other manifestations of LPS effects. NO began to increase in the pulmonary expired air 90 min after LPS and continued to increase for the remainder of the experiment. The final pulmonary post-LPS [NO] was about 20-fold greater than the [NO] before LPS. LPS had no effect on intraluminal or intraperitoneal [NO]. The saline injection had no effect on [NO] in any compartment. SNP injection increased NO entry into all three air-perfused compartments. Thus, NO from an exogenous tissue source was not prevented from being detected. Blood pressure was decreased by LPS only during the pulmonary perfusion. There were no significant effects of LPS on leukocytes or plasma NO(x). LPS decreased blood pressure and leukocytes and increased plasma NO(x) when air perfusion was not done. It was concluded that different organs can produce LPS-induced NO at markedly different rates and times. However, some aspect of the experimental technique of air perfusion could alter the effects of LPS.
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PMID:Organ sites of lipopolysaccharide-induced nitric oxide production in the anesthetized rat. 1138 97

Excessive hypertension can challenge the brain's capacity to autoregulate cerebral blood flow, and can aggravate increased intracranial pressure (ICP) and cerebral edema. Hypotension may worsen ischemic damage in marginally perfused tissue, and in some cases can trigger cerebral vasodilation and ICP plateau waves. There is a lack of high-quality data regarding optimal BP management in these conditions. Existing guidelines for target BP levels are based largely on class III evidence. Class I data only exist for enteral candesartan and nimodipine use in acute ischemic stroke and aneurismal subarachnoid hemorrhage (SAH), respectively, and for parenteral magnesium use in eclampsia. Class II data exist for reducing BP to <180/105 mmHg in patients with ischemic stroke who are treated with intravenous tissue plasminogen activator, for elevating systolic BP to 180-220 mmHg in SAH patients with symptomatic vasospasm, and for maintaining cerebral perfusion pressure (CPP)>60 mmHg in traumatic brain injury. Short-acting continuous-infusion agents with a reliable dose-response relationship and favorable safety profile are desirable. To reduce BP, labetalol, esmolol, and nicardipine best meet these criteria. Sodium nitroprusside should be avoided in most neurological emergencies because of its tendency to raise ICP and cause toxicity with prolonged infusion. To elevate BP, the preferred agents are phenylephrine, dopamine, and norepinephrine.
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PMID:Optimizing blood pressure in neurological emergencies. 2751 96

Acute cerebrovascular diseases (ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage) affect 780,000 Americans each year. Physicians who care for patients with these conditions must be able to recognize when acute hypertension requires treatment and should understand the principles of cerebral autoregulation and perfusion. Physicians should also be familiar with the various pharmacologic agents used in the treatment of cerebrovascular emergencies. Acute ischemic stroke frequently presents with hypertension, but the systemic blood pressure should not be treated unless the systolic pressure exceeds 220 mm Hg or the diastolic pressure exceeds 120 mm Hg. Overly aggressive treatment of hypertension can compromise collateral perfusion of the ischemic penumbra. Hypertension associated with intracerebral hemorrhage can be treated more aggressively to minimize hematoma expansion during the first 3 to 6 hours of illness. Subarachnoid hemorrhage is usually due to aneurysmal rupture; systolic blood pressure should be kept <150 mm Hg to prevent re-rupture of the aneurysm. Nicardipine and labetalol are recommended for rapidly treating hypertension during cerebrovascular emergencies. Sodium nitroprusside is not recommended due to its adverse effects on cerebral autoregulation and intracranial pressure. Hypoperfusion of the injured brain should be avoided at all costs.
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PMID:Blood pressure control in acute cerebrovascular disease. 2136 52

Constriction and dilation of large arteries of brain regulates cerebral vascular resistance and cerebral microvascular pressure, which play key roles in regulation of cerebral circulation. We investigated the effect of ischemic stroke on vascular reactivity of middle cerebral artery (MCA) using a rat transient focal cerebral ischemia model. Focal cerebral ischemia was induced by 1 hour MCA occlusion followed by reperfusion. MCAs were dissected from ischemic or contralateral hemisphere at 2 days or 2 weeks post reperfusion and mounted on 2 glass micropipettes for assessment of vascular reactivity. MCAs from brains of sham surgeries were used as control. At 2 days post reperfusion, a significant alteration of myogenic reactivity was found in MCAs dissected from both ischemic and non-ischemic hemispheres, which could still be identified at 2 weeks after reperfusion. Phenylephrine (PE) induced remarkable vasoconstriction in MCAs from animals that underwent sham surgery. No significant alteration of vasoconstrictive response to PE was found in MCAs isolated from either ischemic or contralateral hemisphere at 2 days or 2 weeks after ischemic stroke, as compared with MCAs from sham animals. Acetylcholine (ACh) induced mild dilation in normal MCAs, which was reversed in MCAs from both ischemic and non-ischemic hemispheres at 2 weeks after ischemic stroke. Sodium nitroprusside (SNP) induced vasodilation in MCAs from animals with sham operation, which was diminished in MCAs from both ischemic and non-ischemic hemisphere at 2 days and 2 weeks after ischemic stroke. These results demonstrated that focal cerebral ischemia could induce long-term global cerebral vasculature dysfunction.
Transl Stroke Res 2012 Jun
PMID:Transient focal cerebral ischemia induces long-term cerebral vasculature dysfunction in a rodent experimental stroke model. 2289 69


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