Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To identify the effect of myocardial ischemia on systemic neurohormones and vascular resistance, 32 untreated, normotensive patients with coronary artery disease underwent incremental atrial pacing until angina. Arterial and coronary venous lactate and arterial values of catecholamines and angiotensin II were determined at control, at maximal pacing rates, and at 1, 2, 5 and 30 minutes after pacing. Based on pacing-induced ST-segment depression (greater than or equal to 0.1 mV) or myocardial lactate production, or both, patients were selected as ischemic (n = 25) or nonischemic (n = 7). Baseline clinical and hemodynamic data were comparable. During pacing, chest pain was similar (20 ischemic vs 7 nonischemic patients). Also, hemodynamic measurements were comparable, except for contractility, which did not improve, and left ventricular end-diastolic pressure, which significantly increased in ischemic patients. Moreover, during ischemia arterial pressures increased significantly (13%) and systemic resistance increased from 1,470 +/- 60 (control) to 1,632 +/- 76 dynes.s.cm-5 5 minutes after pacing (p less than 0.05) in ischemic but not in nonischemic patients. Pacing did not affect neurohormones in nonischemic patients. In contrast, norepinephrine in ischemic patients increased significantly from 1.7 +/- 0.2 (control) to 2.6 +/- 0.3 (maximal pacing) and to 3.0 +/- 0.4 nmol/liter (1 minute after pacing), whereas angiotensin II levels increased from 6.2 +/- 1.4 (control) to 9.3 +/- 2.1 pmol/liter (1 minute after pacing, p less than 0.05). Epinephrine only increased during maximal rates (0.9 +/- 0.1 vs 0.6 +/- 0.1 nmol/liter at control, p less than 0.05). Thus, myocardial ischemia activates circulating catecholamines and angiotensin II, accompanied by systemic vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Systemic neurohumoral activation and vasoconstriction during pacing-induced acute myocardial ischemia in patients with stable angina pectoris. 206 79

Recovery of contractile function and of fatty acid oxidation may be delayed in viable postischemic myocardium. To determine whether a metabolic reserve is preserved after reperfusion of reversibly injured myocardium, we studied the effect of epinephrine on myocardial fatty acid oxidation in isolated rat hearts perfused retrogradely with erythrocyte enriched buffer containing albumin 0.4 mM, palmitate 0.4 mM, and glucose 11 mM. Hearts were subjected to 60 min of low-flow ischemia (5% of control flow) followed by 60 min of reperfusion. Five minutes following the onset of reperfusion, developed left ventricular pressure (DLVP) and oxidation of palmitate were reduced to 53% (p less than 0.01) and 46% (p less than 0.01), respectively, of values measured in nonischemic control hearts. Subsequently, DLVP and oxidation of palmitate gradually recovered to 78% (NS) and 91% (NS) by 60 min of reperfusion. Epinephrine 5.10(-1) M elicited an immediate stimulation of both contractile function and palmitate oxidation. Early after reperfusion stimulated DLVP and palmitate oxidation were still lower compared to values measured in control hearts exposed to the same concentration of epinephrine. Later than 15 min after the onset of reperfusion the response of DLVP and of palmitate oxidation to epinephrine no longer differed between control and reperfused hearts. These results indicate that viable postischemic myocardium exhibits a remarkable oxidative metabolic reserve. The observation provides further evidence for the view that impairment of myocardial energy production is not responsible for contractile dysfunction early after reperfusion.
 ...
PMID:Epinephrine-stimulated contractile and metabolic reserve in postischemic rat myocardium. 207 95

Sickle cell retinopathy in its advanced form is complicated by preretinal neovascularization, vitreous hemorrhage, and retinal detachment. Treatment of neovascularization can be performed with photocoagulation. Complications such as retinal breaks, retinal detachments, and choroidally fed neovascularization may result from such treatment. The risks vs. the benefits of various types of photocoagulation are currently being evaluated. Cryotherapy also may be used to treat neovascularization. It is currently being used in eyes with media that are too hazy to permit photocoagulation. It is used commonly during scleral buckling and vitrectomy procedures. In eyes with decreased visual acuity secondary to prolonged vitreous hemorrhage, pars plana vitrectomy can be utilized to produce optically clear media. Complications (including erythrocyte-induced glaucoma), however, may be severe. Retinal detachment can be treated by scleral buckling, but the markedly increased risk of anterior segment ischemia in patients with sickle cell hemoglobin necessitates preoperative, intraoperative, and postoperative prophylactic measures to minimize the risk of this potentially devastating complication. In eyes with retinal detachment with cloudy media and severe vitreous traction, combined scleral buckling and vitrectomy may be necessary. These eyes are extremely fragile, and a successful result is currently obtained in only about 50% of such cases. Hyphemas in patients with sickle cell hemoglobinopathies, whether traumatically or surgically induced, may have devastating effects on the eye. If elevated IOP results decreased vascular perfusion of the eye may cause irreversible damage to the retina and optic nerve. Most antiglaucoma medications, when used in the sickle cell patient, have a narrow margin of safety. Therefore, early surgical intervention for the treatment of sickle cell hyphemas is currently being evaluated.
 ...
PMID:Diagnosis and management of ocular complications of sickle hemoglobinopathies: Part V. 242 44

Opinions are still not unanimous about the mechanism behind circulation during external cardiac compression and this leads to uncertainty regarding the correct frequency, force of compression and its duration. Adrenaline and other alpha-stimulators increase blood flow during external cardiac compression and increase survival. Cardiac arrest results in anaerobic metabolism and combined metabolic and respiratory acidosis. On account of relatively low minute volume during external cardiac compression decrease in end-tidal carbon dioxide concentration is observed together with arterial alkalosis on account of hyperventilation and venous acidosis. No communications exist about the favourable effect of administration of bicarbonate during cardiac arrest. On the other hand, several conditions suggest that bicarbonate increases the intracellular acidosis with poorer possibilities for resuscitation with this form of treatment. Ischaemia results inter alia in intracellular accumulation of calcium which initiates potential cell destructive processes. No investigations are available which favour employment of calcium during cardiac arrest. Conversely animal experiments suggest the possibility of favourable effects from calcium-entry blockers. Ischaemia and, in particular, reperfusion release cell and vessel damaging free oxygen redicals. Intensive investigations are being conducted at present about the value of anti-oxidants for cerebral and myocardial protection.
 ...
PMID:[Treatment of cardiac arrest. Recent aspects of cardiopulmonary resuscitation]. 267 53

We have used radioligand binding techniques and subcellular fractionation to assess whether changes in expression of myocardial alpha 1- and beta-adrenergic receptors are mediated by a redistribution of receptors between various membrane fractions. Three fractions were prepared from the left ventricles of guinea pigs that underwent either 1 h of ischemia or injection of epinephrine (0.25 mg/kg ip): a crude membrane, a purified sarcolemma, and a light vesicle fraction. In control animals alpha 1-adrenergic receptors ([3H]prazosin binding) in light vesicles was only 25% of the total alpha 1-receptor density found in sarcolemmal and light vesicle fractions as compared with 50% for beta-adrenergic receptors ([125I]iodocyanopindolol binding sites). Although ischemia was associated with a 53% decrease in the number of light vesicle beta-adrenergic receptors and a 42% increase in the number of sarcolemma beta-receptors (P less than 0.05), there was no change in the number of light vesicle alpha 1-receptors, even though the number of sarcolemmal alpha 1-receptors increased 34%. Epinephrine treatment promoted internalization of beta-adrenergic receptors; sarcolemma beta-receptors decreased 37% and light vesicle beta-receptors increased 28% (P less than 0.025). For alpha 1-receptors, epinephrine treatment decreased the number of sarcolemmal receptors 41% (P less than 0.025) but failed to increase the number of receptors in the light vesicle fraction. The changes in receptor binding to beta-adrenergic receptors in sarcolemmal fractions were mirrored by parallel changes in isoproterenol-stimulated adenylate cyclase activity. These results indicate that alpha 1- and beta-adrenergic receptors may undergo a different cellular itinerary in guinea pig myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Ischemia- and agonist-induced changes in alpha- and beta-adrenergic receptor traffic in guinea pig hearts. 282 44

The management of the pulseless, nonbreathing pediatric patient continues to be a frustrating experience because mortality and morbidity are high. Improvement in outcome awaits a better understanding of the pathophysiology of organ ischemia and reperfusion injury. In the interim, early recognition and therapy of respiratory and circulatory failure are the only effective means to affect outcome. The approach to the pediatric cardiac arrest victim differs from the adult, because dysrhythmias rarely are the etiology of pediatric arrest. Instead, attention to securing the airway and provision of adequate ventilation are keys. Epinephrine is the most effective drug in this setting, and may be administered through an endotracheal tube as well as intravenously or intraosseously. The latter route provides a useful means of rapid vascular access in the pediatric victim less than 3 years of age. Sodium bicarbonate use has been discouraged and there are few indications for calcium, greatly simplifying the pharmacologic approach to the pediatric cardiac arrest patient. In those patients in whom a rhythm and pulse are restored, support of the circulation often is required. Dopamine or epinephrine are the catecholamines of choice in this setting. Ventricular arrhythmias are treated with defibrillation or cardioversion as appropriate. Infrequently, lidocaine or bretylium may be needed. Once the patient has been stabilized, further care is best delivered at a tertiary care center with a pediatric intensive care unit.
 ...
PMID:Cardiopulmonary resuscitation in children. 332 42

Lysophosphoglycerides accumulate in ischemic myocardium and induce electrophysiologic alterations in normoxic tissue in vitro closely resembling those seen with ischemia in vivo. Delayed afterdepolarizations and triggered activity may be particularly important in the pathogenesis of arrhythmias in the ischemic heart. The present study was performed to determine whether lysophosphatidylcholine (LPC), at concentrations comparable to those present in ischemic myocardium, can induce delayed afterdepolarizations and/or triggered activity in normoxic canine Purkinje fibers. In the present study, as little as 75 microM LPC was found to induce delayed afterdepolarizations and as little as 100 microM LPC was found to induce delayed afterdepolarizations and triggered activity even at low cycle lengths. The amplitude of the induced delayed afterdepolarizations was enhanced by augmentation of the extracellular concentration of calcium (7 mM) or by exogenous epinephrine (10(-9) to 10(-6) M). The amplitude was decreased by verapamil (1 mg/l) or Mn++ (2.5 mM). Epinephrine at a concentration of 10(-6) M also initiated triggered activity in Purkinje fibers exposed to LPC (75 microM), a response blocked by l-propranolol (2 X 10(-7) M and 10(-6) M) but not by the alpha 1-adrenergic blocking agent BE-2254 (10(-6) M). Delayed afterdepolarizations induced by LPC (75 microM) and epinephrine (10(-6) M) persisted even in the presence of acidosis (pH 6.7) and hyperkalemia ([K+]o = 7 mM). Thus, delayed afterdepolarizations and triggered activity induced by LPC may contribute to the induction and/or maintenance of arrhythmias early after the onset of myocardial ischemia. However, because of the reversal of these effects after superfusion with media devoid of LPC, they may occur with ischemia in vivo but not be seen in tissue isolated from ischemic regions and evaluated in vitro.
 ...
PMID:Induction of delayed afterdepolarizations and triggered activity in canine Purkinje fibers by lysophosphoglycerides. 379 82

Electro-encephalo-dynamographic investigations taken from 36 glaucoma patients showed that the autoregulative mechanism in the region of the anterior part of the optic nerve (apon) is disturbed and the ciliary perfusion pressure is altered in a characteristic manner. The results lead to the conclusion that glaucomatous ischemia occurring in the apon may mainly be due to the following causes and their combinations: high IOP; low blood pressure in the ciliary arterial circulation; insufficiency of autoregulation, and changes of the local conditions of diffusion of oxygen and nutrients.
 ...
PMID:Deficient autoregulation and lengthening of the diffusion distance in the anterior optic nerve circulation in glaucoma: an electro-encephalo-dynamographic investigation. 380 88

The normal rat spinal cord blood flow (SCBF) has been shown to increase after administration of nimodipine, a calcium channel blocker. The present study investigates the capability of nimodipine to improve SCBF, as measured by the hydrogen clearance technique, after a 53.0-gm clip compression injury to the T-1 segment of the rat spinal cord. The profound drop in mean systemic arterial blood pressure (MSAP) after cervical cord injury precluded any improvement in posttraumatic SCBF by nimodipine alone. Hence, in a randomized controlled study with five rats per group, pressor agents (whole blood, angiotensin, or adrenaline) were infused to maintain MSAP between 100 and 120 mm Hg after injury. Control animals received only a saline infusion. Nimodipine at the optimal dose found in normal animals (1.5 microgram/kg/min) was added to the pressor agents. The MSAP and other physiological parameters were measured in rats receiving the pressor agents only and in those receiving pressor agents combined with nimodipine. In rats receiving whole blood, angiotensin, or adrenaline the posttraumatic MSAP improved to between 100 and 120 mm Hg, but there was no improvement in SCBF compared to the saline group. The addition of nimodipine decreased MSAP and SCBF in all groups except those animals also receiving adrenaline, where the MSAP was maintained at 109 +/- 5 mm Hg. In these animals a significant increase in posttraumatic SCBF from 16.5 +/- 2.1 to 20.2 +/- 2.3 ml/100 gm/min (mean +/- standard error of the mean) occurred at the site of injury with the addition of nimodipine. The maintenance of an adequate MSAP by a pressor agent was crucial for nimodipine to improve posttraumatic SCBF by its ability to dilate the spinal vascular bed. Adrenaline was the only pressor agent that could fulfill the above criteria, although other pressor agents need to be investigated. Experiments are underway with the combination of adrenaline and nimodipine to further verify these encouraging results demonstrating an improvement in posttraumatic ischemia of the spinal cord.
 ...
PMID:Effect of a calcium channel blocker on posttraumatic spinal cord blood flow. 381 38

Attempts were made to define the effects of epinephrine and dobutamine on the myocardium during early reperfusion for 60 minutes following hypothermic global ischemia at a myocardial temperature of 28 degrees C for 60 minutes under cardiopulmonary bypass. Ischemia was induced by cross-clamping the dog aorta. Epinephrine (0.1 microgram/kg/min) and dobutamine (5 micrograms/kg/min) were given throughout the reperfusion period by intravenous drip infusion, a control group was treated with saline infusion. Comparison of hemodynamic parameters was made before cardiopulmonary bypass, and at 30 and 60 minutes of reperfusion. Epinephrine and dobutamine significantly increased stroke volume index, left ventricular stroke work index and tissue calcium content compared with saline, however, myocardial water content was only slightly higher in the group given saline, compared with the other two groups. Myocardial mitochondrial membranes and cristae were slightly damaged and creatine phosphate content was reduced. Ultrastructural integrity was related to myocardial tissue calcium content, with a significant negative correlation. These results suggest that epinephrine (0.1 microgram/kg/min) will improve stroke volume index and left ventricular stroke work index, as does dobutamine (5 micrograms/kg/min), however, both agents had a minimal effect on reducing myocardial morphological and biochemical integrity, although catecholamines have detrimental effects on the myocardium in early reperfusion following ischemia.
 ...
PMID:Effects of catecholamines on myocardial viability in early reperfusion following hypothermic global ischemia in dogs--comparison between epinephrine and dobutamine. 383 1


<< Previous 1 2 3 4 5 6 7 Next >>