tetracycline and Myocardial-Infarction

The selective uptake of radiopharmaceuticals by acutely infarcted myocardium has emerged as an independent, noninvasive technique to aid in the detection, localization, and quantification of myocardial necrosis.

Topics: Diphosphates; Humans; Immunoglobulin Fab Fragments; Myocardial Infarction; Myocardium; Myosins; Radioisotopes; Radionuclide Imaging; Technetium; Tetracycline; Thallium

Topics: Bone and Bones; Citrates; Gallium Radioisotopes; Glucose; Humans; Indium; Iodine Radioisotopes; Leukocytes; Mercury Radioisotopes; Myocardial Infarction; Radioisotopes; Radionuclide Imaging; Technetium; Tetracycline

Detection of acute myocardial infarction as an area of increased activity has intrigued investigators for some time. Initial attempts with 203Hg-chlormerodrin and 203Hg-fluorescein analogues were successful in man. More recently, however, successful imaging of the acute myocardial infarct has been achieved with several 99mTc complexes. A large group of radiotracers localize in acutely damaged tissue in various models of experimental infarction. From these data, a number of specific structural properties associated with infarct avidity have been identified; these include the presence of mercury and the structural configuration of the organic carrier.

Topics: Animals; Diphosphates; Diphosphonates; Dogs; Fluoresceins; Humans; Mercury Radioisotopes; Myocardial Infarction; Organomercury Compounds; Radionuclide Imaging; Rats; Structure-Activity Relationship; Sugar Acids; Technetium; Tetracycline

Topics: Chlortetracycline; Humans; Microscopy; Microscopy, Fluorescence; Myocardial Infarction; Neoplasms; Tetracycline; Trichloroacetic Acid; Ultraviolet Rays; Vitamin B 12

Recent evidence suggests that antibiotic-induced changes in the composition of intestinal microflora, as well as the systemic immunoendocrine effects that result from them, can modulate myocardial tolerance to ischemia-reperfusion injury. The aim of this study was to investigate the effects of tetracycline (TTC) on myocardial infarct size in the isolated hearts obtained from obese rats with chemically-induced colitis (CIC). The association between TTC-induced changes in infarct size and intestinal microbiome composition as well as plasma levels of cytokines and short-chain fatty acids (SCFAs) was also studied.. Obesity was induced in Wistar rats by feeding them a high-fat, high-carbohydrate diet for five weeks. A single rectal administration of 3% acetic acid (2 mL) to the rats resulted in CIC. Healthy rats as well as obese rats with CIC received TTC (15 mg daily for 3 days) via gavage. The rats were euthanized, after which isolated heart perfusion with simulated global ischemia and reperfusion was performed. Infarct size was determined histochemically. Lipopolysaccharide (LPS) and cytokine levels in plasma were measured by enzyme-linked immunosorbent assay, whereas SCFA levels in plasma were measured by gas chromatography/mass spectrometry. The intestinal microbiome was analyzed using reverse transcription polymerase chain reaction.. The treatment with TTC resulted in significant infarct size limitation (50 ± 7 vs. 62 ± 4% for the control mice, p < 0.05) in the hearts from intact animals. However, infarct size was not different between the control rats and the obese rats with CIC. Furthermore, infarct size was significantly larger in TTC-treated obese rats with CIC than it was in the control animals (77 ± 5%, p < 0.05). The concentrations of proinflammatory cytokines and LPS in serum were elevated in the obese rats with CIC. Compared to the control rats, the rats with both obesity and CIC had lower counts of Lactobacillus and Bifidobacterium spp. but higher counts of Escherichia coli. The effects of TTC on infarct size were not associated with specific changes in SCFA levels.. TTC reduced infarct size in the healthy rats. However, this effect was reversed in the obese animals with CIC. Additionally, it was associated with specific changes in gut microbiota and significantly elevated levels of cytokines and LPS.

Topics: Animals; Biomarkers; Body Weight; Colitis; Disease Models, Animal; Fatty Acids, Volatile; Gastrointestinal Microbiome; Heart Function Tests; Male; Myocardial Infarction; Obesity; Rats; Tetracycline

Mice expressing the tetracycline transactivator (tTA) transcription factor driven by the rat α-myosin heavy chain promoter (α-MHC-tTA) are widely used to dissect the molecular mechanisms involved in cardiac development and disease. However, these α-MHC-tTA mice exhibit a gain-of-function phenotype consisting of robust protection against ischemia/reperfusion injury in both in vitro and in vivo models in the absence of associated cardiac hypertrophy or remodeling. Cardiac function, as assessed by echocardiography, did not differ between α-MHC-tTA and control animals, and there were no noticeable differences observed between the two groups in HW/TL ratio or LV end-diastolic and end-systolic dimensions. Protection against ischemia/reperfusion injury was assessed using isolated perfused hearts where α-MHC-tTA mice had robust protection against ischemia/reperfusion injury which was not blocked by pharmacological inhibition of PI3Ks with LY294002. Furthermore, α-MHC-tTA mice subjected to coronary artery ligation exhibited significantly reduced infarct size compared to control animals. Our findings reveal that α-MHC-tTA transgenic mice exhibit a gain-of-function phenotype consisting of robust protection against ischemia/reperfusion injury similar to cardiac pre- and post-conditioning effects. However, in contrast to classical pre- and post-conditioning, the α-MHC-tTA phenotype is not inhibited by the classic preconditioning inhibitor LY294002 suggesting involvement of a non-PI3K-AKT signaling pathway in this phenotype. Thus, further study of the α-MHC-tTA model may reveal novel molecular targets for therapeutic intervention during ischemic injury.

Topics: Animals; Chromones; Creatine Kinase; Echocardiography; Female; Gene Expression; Heart; In Vitro Techniques; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Morpholines; Myocardial Infarction; Myocardium; Myosin Heavy Chains; Organ Size; Phosphoinositide-3 Kinase Inhibitors; Promoter Regions, Genetic; Rats; Reperfusion Injury; Tetracycline; Trans-Activators; Ventricular Myosins

Fibroblast growth factor 9 (FGF9) is secreted from bone marrow cells, which have been shown to improve systolic function after myocardial infarction (MI) in a clinical trial. FGF9 promotes cardiac vascularization during embryonic development but is only weakly expressed in the adult heart.. We used a tetracycline-responsive binary transgene system based on the α-myosin heavy chain promoter to test whether conditional expression of FGF9 in the adult myocardium supports adaptation after MI. In sham-operated mice, transgenic FGF9 stimulated left ventricular hypertrophy with microvessel expansion and preserved systolic and diastolic function. After coronary artery ligation, transgenic FGF9 enhanced hypertrophy of the noninfarcted left ventricular myocardium with increased microvessel density, reduced interstitial fibrosis, attenuated fetal gene expression, and improved systolic function. Heart failure mortality after MI was markedly reduced by transgenic FGF9, whereas rupture rates were not affected. Adenoviral FGF9 gene transfer after MI similarly promoted left ventricular hypertrophy with improved systolic function and reduced heart failure mortality. Mechanistically, FGF9 stimulated proliferation and network formation of endothelial cells but induced no direct hypertrophic effects in neonatal or adult rat cardiomyocytes in vitro. FGF9-stimulated endothelial cell supernatants, however, induced cardiomyocyte hypertrophy via paracrine release of bone morphogenetic protein 6. In accord with this observation, expression of bone morphogenetic protein 6 and phosphorylation of its downstream targets SMAD1/5 were increased in the myocardium of FGF9 transgenic mice.. Conditional expression of FGF9 promotes myocardial vascularization and hypertrophy with enhanced systolic function and reduced heart failure mortality after MI. These observations suggest a previously unrecognized therapeutic potential for FGF9 after MI.

Topics: Animals; Bone Morphogenetic Protein 6; Fibroblast Growth Factor 9; Gene Expression; Heart; Heart Failure; Hypertrophy, Left Ventricular; Mice; Mice, Transgenic; Myocardial Infarction; Neovascularization, Pathologic; Phosphorylation; Rats; Tetracycline

Soluble stem cell factor (SCF) has been shown to mobilize bone marrow stem cells and improve cardiac repair after myocardial infarction (MI). However, the effect of membrane-associated SCF on cardiac remodeling after MI is not known. The present study investigated the effects of cardiomyocyte-specific overexpression of the membrane-associated isoform of human SCF (hSCF) on cardiac function after MI.. A novel mouse model with tetracycline-inducible and cardiac-specific overexpression of membrane-associated hSCF was generated. MI was induced by left coronary artery ligation. Thirty-day mortality after MI was decreased in hSCF/tetracycline transactivator (tTA) compared with wild-type mice. In vivo cardiac function was significantly improved in hSCF/tTA mice at 5 and 30 days after MI compared with wild-type mice. Endothelial progenitor cell recruitment and capillary density were increased and myocardial apoptosis was decreased in the peri-infarct area of hSCF/tTA mice. Myocyte size was decreased in hSCF/tTA mice 30 days after MI compared with WT mice. Furthermore, hSCF overexpression promoted de novo angiogenesis as assessed by matrigel implantation into the left ventricular myocardium.. Cardiomyocyte-specific overexpression of hSCF improves myocardial function and survival after MI. These beneficial effects of hSCF may result from increases in endothelial progenitor cell recruitment and neovascularization and decreases in myocardial apoptosis and cardiac remodeling.

Topics: Animals; Apoptosis; Doxycycline; Humans; Hypertrophy, Left Ventricular; Mice; Mice, Transgenic; Myocardial Infarction; Myocytes, Cardiac; Neovascularization, Physiologic; Proto-Oncogene Proteins c-kit; Stem Cell Factor; Stem Cells; Tetracycline; Vascular Endothelial Growth Factor Receptor-2; Ventricular Function, Left

A population-based case-control study of patients enrolled at Group Health Cooperative of Puget Sound was conducted to evaluate whether past use of antibiotics active against Chlamydia pneumoniae is associated with a decrease in the risk of first myocardial infarction (MI). Cases with incident fatal and nonfatal MI from mid-1986 through 1995 (n=1796) were compared with randomly sampled controls frequency-matched to cases for age, sex, and year (n=4882). Use of erythromycin, tetracycline, or doxycycline during the previous 5 years was not associated with an alteration in the risk of first MI. In an adjusted logistic regression model, the odds ratios and 95% confidence intervals for categories of cumulative duration of therapy with any of the three agents combined for 0, 1-14, 15-28, and >/=29 days were 1.0 (reference), 0.93 (0.81-1.07), 0.99 (0.81-1.20), and 1.03 (0.84-1.26), respectively. These results suggest little or no association between past use of erythromycin or tetracycline antibiotics and the risk of first MI among this population.

Topics: Aged; Anti-Bacterial Agents; Case-Control Studies; Chlamydia Infections; Chlamydophila pneumoniae; Doxycycline; Drug Therapy, Combination; Erythromycin; Female; Humans; Incidence; Male; Myocardial Infarction; Risk Factors; Tetracycline

Topics: Angina, Unstable; Anti-Bacterial Agents; Chlamydia Infections; Chlamydophila pneumoniae; Humans; Myocardial Infarction; Norway; Roxithromycin; Tetracycline

Myocardial infarction was produced in rats by ligation of the left coronary artery. Rats were injected with 3H-tetracycline (50 muCi/kg) i.p., 10 minutes prior to ligation. The rats were killed at various time periods after ligation and the myocardial accumulation of 3H-tetracycline determined in the left ventricle or in whole heart homogenates. CPK was also determined in the myocardium or serum. Myocardial 3H-tetracycline was not significantly elevated in the whole heart homogenates. However, there was a significant increase in 3H-tetracycline in the digests of the left ventricle 6 h post-infarct. This increase correlated very well with serum CPK activity. This suggest that this method could be a useful tool in the estimation of infarct size.

Topics: Animals; Coronary Vessels; Creatine Kinase; Male; Myocardial Infarction; Myocardium; Rats; Rats, Inbred Strains; Tetracycline; Tritium

There is an increasing importance of scintigraphy for the assessment of microcirculation in the myocardium. In animal experiments advantages and disadvantages of negative and positive representation of ischemic myocardiac areas were tried, after experimental infarction in particular. The results by computer scintigraphy prove that positive representation reveals an information on site and extent of an infarction.

Topics: Coronary Circulation; Humans; Microcirculation; Myocardial Infarction; Myocardium; Radionuclide Imaging; Technetium; Tetracycline

The gross and subcellular localizations of 99mTc-labeled pyrophosphate and tetracycline in myocardial infarcts were studied in a rabbit model. Experiments utilizing double-nuclide labeling were carried out using a useful mapping technique. Concentration of the various chelates decreases in an expected manner from the center of the infarcted area toward its periphery, but it is higher near the epicardial surface than toward the endocardium. Technetium-99m-pyrophosphate is concentrated in the same infarcted areas as 45Ca ion or 32P-pyrophosphate, but to a much greater degree. The uptake is dependent on both the degree of necrosis and residual blood flow. Gel filtration experiments with rabbit serum indicate that 99mTc-tagged pyrophosphate, tetracycline, and diphosphonate are mainly protein-bound, whereas 32P-pyrophosphate is not. Subcellular localization studies show that 99mTc-tetracycline and 99mTc-pyrophosphate are bound primarily to soluble protein, and only a small fraction is associated with nuclei, mitochondria, and microsomes. The uptake of technetium chelates in myocardial infarcts may be due to the formation of polynuclear complexes with denatured macromolecules rather than to the deposition of calcium in mitochrondria.

Topics: Animals; Diphosphates; Myocardial Infarction; Rabbits; Radionuclide Imaging; Technetium; Tetracycline

The accuracy of the scintigraphic diagnosis of acute myocardial infarction with 99mTc-pyrophosphate, 99mTc-tetracycline and 99mTc-glucoheptonate was assessed in 63 patients, 43 of whom had clinical evidence of acute myocardial infarction. In 15, studies with both 99mTc-tetracycline and 99mTc-pyrophosphate were performed. Accuracy was greatest with 99mTc-pyrophosphate (17/17 true positives, 8/10 true negatives) contrasted with 99mTc-tetracycline (12/25 true positives, 6/11 true negatives) and 99mTc-glucoheptonate (3/13 true positives, 2/2 true negatives). 99mTc-pyrophosphate was the most sensitive tracer for the detection of acute myocardial infarction. The diagnostic accuracy with 99mTc-glucoheptonate was poor.

Topics: Acute Disease; Diagnostic Errors; Diphosphates; Evaluation Studies as Topic; Heptoses; Humans; Myocardial Infarction; Radioisotopes; Radionuclide Imaging; Sugar Acids; Technetium; Tetracycline

The feasibility of acute infarct scintigraphy for the clinical evaluation of patients with known or suspected acute myocardial infarction is established. Further development of this methodologic approach may result in even better agents for the visualization of infarcts. Radiotracers with high affinity for the infarct, rapid blood clearance, and low concentrations in surrounding organs, such as liver and bone, would be more suitable than available radiopharmaceuticals for acute myocardial infarct scintigraphy. Ultimately, labeling these tracers and ultra-short-lived radionuclides will enable rapid sequential imaging to assess changes in the extent of infarction and to determine the efficacy of therapies aimed at limiting infarct size.

Topics: Acute Disease; Diphosphates; Humans; Mercury Radioisotopes; Myocardial Infarction; Myocardium; Radionuclide Imaging; Technetium; Tetracycline; Time Factors

The effects of the dimethyl quarternary analog of propranolol, UM-272, on myocardial infarct volume were studied in the canine heart. Myocardial infarction was produced by occlusion of the left circumflex coronary artery for 60 minutes followed by reperfusion and quantitation of infarct volume 24 hours later. Groups of dogs were either untreated or pretreated with UM-272 with an initial loading dose of 5.0 mg/kg (group A) or 2.5 mg/kg (group B) 30 minutes before occlusion of the left circumflex coronary artery. Both group A and group B animals received additional doses of 2.5 mg/kg of UM-272 every 90 minutes for a period of 6 hours so that the total respective doses were 15 and 12.5 mg/kg. Control animals received comparable volumes of 0.9% sodium chloride solution. All animals were followed throughout the 6-hour procedure with continuous electrocardiographic recordings which were used to assess the effects of acute myocardial ischemia upon disturbances in cardiac rhythm and the effects of drug treatment. Dogs which survived the procedure were given tetracycline i.v. the next day and sacrificed 1 hour later by an overdose of pentobarbital sodium. The hearts were removed and the left ventricle was sliced and examined first under ultraviolet light to localize the ischemic zone by noting the tetracycline fluorescence. The ventricular slices were next incubated in nitro blue tetrazolium which stains normal myocardial tissue, thus allowing one to quantitate the volume of infarcted myocardium by excising and weighing the nonstained and stained muscle separately. The untreated control group had an infarct volume of 23.8 +/- 3.2 g/100 g of left ventricle. The treated animals in groups A and B had respective infarct volumes of 2.3 +/- 0.8 g/100 g (P less than .001) and 7.0 +/- 3.3 g/100 g (P less than .025) of left ventricle. During the acute phase of ischemia and reperfusion, arrhythmias and alterations in the ST-segment, R-wave amplituted and development of pathologic Q-waves were more prominent in the untreated animals and almost totally absent in the treated animals. UM-272 produced a dose-dependent decrease in heart rate as well as a decrease in developed isometric tension. Pretreatment with UM-272 did not prevent the derangement of function in the ischemic zone nor did it permit a return of function upon reperfusion, even though it reduced the degree of cellular damage resulting from 60 minutes of regional ischemia. A possible mechanism for the protective ef

Topics: Animals; Blood Pressure; Cardiac Output; Coronary Circulation; Coronary Disease; Disease Models, Animal; Dogs; Electrocardiography; Heart Rate; Myocardial Contraction; Myocardial Infarction; Myocardium; Nitroblue Tetrazolium; Oxidoreductases; Propranolol; Tetracycline; Time Factors

Considering the diagnostic significance of a few 99mTc-chelates in the diagnosis of myocardial infarct, we have recently developed a necrosis model in tissue culture obtained from mammalian cells, where the dead cells showed enhanced binding of 99mTc-tetracycline like the necrotic cells of infarcted myocardium. Technical details of the principles of labeling, fixing, washing and drying, dipping in emulsion, exposure, development and staining of mammalian cells have been described. Considering the short half-life of 99mTc-radioisotope, the recently available techniques have been modified to make autoradiography possible in a reasonably short period of time. Technetium-99m in different physical and chemical states is playing a very important role in a variety of diagnostic procedures. The autoradiography of 99mTc-labeled cells and tissue will shed further light on the mechanism of cellular uptake and subcellular distribution in normal and pathologic states. Presently no information is available regarding autoradiography with 99mTc-chelates of mammalian cells obtained from tissue culture.

Topics: Autoradiography; Myocardial Infarction; Necrosis; Technetium; Tetracycline

Topics: Animals; Disease Models, Animal; Female; Isotope Labeling; Muscles; Myocardial Infarction; Radionuclide Imaging; Rats; Technetium; Tetracycline

The single intramuscular injection of 275 mg Rolitetracyclin (Reverin) led to a rise in serum creatine phosphokinase in 11 out of 20 heart healthy patients, 7 cases with values over 100 mU/ml. In sane cases the initial values had still not been reached 72 hours after injection. With Rolitetracyclin given intravenously the creatine phosphokinase values do not alter, as with an isotonic Na-Cl solution given intramuscularly. A rise in the serum creatine phosphokinase was seen in 2 out of 6 cases after an intramuscular injection of Oxytetracyclin (Terramycin -Depot). One is not dealing with a reaction which is typical only to Rolitetracyclin. The cause is thought to be the setting free of enzymes through the musclelesions. The results underline the sensitivity of and problems involved with creatine phosphokinase in the diagnosis of heart-infarction.

Topics: Adult; Aspartate Aminotransferases; Creatine Kinase; Diagnostic Errors; False Positive Reactions; Female; Humans; L-Lactate Dehydrogenase; Male; Middle Aged; Myocardial Infarction; Oxytetracycline; Rolitetracycline; Sodium Chloride; Tetracycline; Time Factors

The relative concentration of 99mTc(Sn)-tetracycline in infarcted myocardium was determined as a function of time after coronary artery occlusion in mongrel dogs. The concentration ratio (infarct-to-normal myocardium) was highest within the first 2 days after occlusion (6.7 +/- 0.5 at 1 day and 8.0 +/- 1.6 at 2 days). By 1 week after occlusion the ratio had fallen to 1.9 +/- 0.2. In the region of infarction, the concentration of 99mTc(Sn)-tetracycline was homogeneously distributed across the inner three-quraters of the myocardial wall; the outer quarter of the wall had substantially lower concentrations during the first 5 days after infarction. The present study confirms the observation suggested in initial investigations in man that scintigraphy performed with 99mTc(Sn)-tetracycline will distinguish between acute and chronic myocardial infarctions.

Topics: Acute Disease; Animals; Chronic Disease; Dogs; Myocardial Infarction; Radionuclide Imaging; Technetium; Tetracycline; Time Factors; Tin

After acute coronary occlusion in primates, the time period during which reperfusion results in significant salvage of reversibly injured myocardium was investigated. In 23 monkeys, the left anterior descending coronary artery was occluded from 1 to 6 h; and in 5 others, occlusion was maintained for the 1-wk study. Unipolar epicardial electrocardiograms were monitored from mapping points on the anterior and lateral left venticle. S-T segment elevation (S-T upward arrow) and R + S wave amplitude (RS) were measured before occlusion and at regular intervals during occlusion and reperfusion. Summated S-T upward arrow (SigmaS-T upward arrow) and summated RS (SigmaRS), computed for mapping points demonstrating greater than 2 mV S-T upward arrow, were used as serial measures of electrical injury. SigmaS-T upward arrow peaked within 2-h postocclusion and then gradually declined throughout the period of occlusion suggesting the progress of infarction within the area of injury. After reperfusion SigmaS-T upward arrow rapidly declined to near cnotrol values indicating the extent of reversible injury. During the period of occlusion, the magnitude of voltage loss in SigmaS-T upward arrow as a percent of maximum SigmaS-T upward arrow was proportional to the duration of occlusion, though the rate of loss decreased with increasing time of occlusion. Reperfusion after 6 h of occlusion resulted in reversal of only a small remaining component of the maximum current of injury. The voltage decrease in SigmaRS (from control values) was proportional to the duration of occlusion, though the decrease was accelerated during the first 2-h postocclusion. Whereas reperfusion interrupted the decline in SigmaRS, a consistent increase in SigmaRS postreperfusion was observed only after occlusion of 1 h. With respect to reperfusion groups, significance in SigmaS-T upward arrow voltage loss as a percent of maximum SigmaS-T upward arrow was demonstrated between 2-h and 4-h, 4- and 6-h, and 6-h and chronically ligated animals. Significance in SigmaRS voltage loss as a percent of control SigmaRS was demonstrated between 2- and 4-h, and 4- and 6-h reperfusion groups. Hearts were excised at 7 days for histological assessment of infarct size. Planimetric determination of left ventricular areas and areas of necrosis using slides made from 10 serial cross sections were used in estimating the percent of left ventricle infarcted. A significant reduction in infarct size was demonstrated between reper

Topics: Animals; Coronary Circulation; Coronary Disease; Coronary Vessels; Electric Injuries; Electrocardiography; Fluorescence; Heart Ventricles; Ligation; Macaca fascicularis; Models, Biological; Myocardial Infarction; Necrosis; Tetracycline; Time Factors; Tourniquets

Topics: Aspartate Aminotransferases; Chelating Agents; Clinical Enzyme Tests; Creatine Kinase; Electrocardiography; Humans; L-Lactate Dehydrogenase; Liver; Myocardial Infarction; Myocardium; Radionuclide Imaging; Technetium; Tetracycline; Time Factors; Tin

Topics: Humans; Myocardial Infarction; Myocardium; Radionuclide Imaging; Technetium; Tetracycline; Time Factors

Shock must be treated by correcting the cause, for any treatment of hypotension or shock, as such, is only an adjunctive measure; but the hemodynamic manifestations also need treatment. Vasopressors are helpful and effective under the right circumstances. Unless the blood volume is normal, the use of drugs that block the sympathetic nervous system (e.g., phenoxybenxamine) can be extremely hazardous and hasten death. However, the effect of adrenergic blocking drugs in endotoxic shock and other types of toxic shock is still to be determined; use of such drugs should be considered experimental until the results have been studied more extensively. Clinically, the most common forms of vascular shock are associated with blood loss, myocardial infarction, and endotoxemia. Characteristic hemodynamics of each situation are presented tabularly, and the physicians need to understand the differences is emphasized. The pharmacology of vasopressors, relating primarily to hemodynamic considerations and the response to vasopressors when severe reduction in blood pressure is associated with the shock syndrome is discussed. Drugs that stimulate the adrenergic receptors in the heart and blood vessels, with the exception of isoproteronol, are commonly referred to as vasopressors. The adrenergic stimulators may be classified into 3 groups: alpha (phenylephrine hydrochloride), beta (epinephrine), and alpha-beta (l-norepinephrine). Because alpha stimulators do not usually increase cardiac output, alpha-beta and beta-adrenergic stimulators are generally the most useful for treating shock. Routine use of adrenergic stimulators with the exclusion of other therapies, however, is generally unwarranted.

Topics: Bacteria; Chloramphenicol; Epinephrine; Humans; Isoproterenol; Metaraminol; Methoxamine; Morphine; Myocardial Infarction; Nalorphine; Norepinephrine; Phenoxybenzamine; Phenylephrine; Shock; Shock, Septic; Streptomycin; Tetracycline; Vasoconstrictor Agents

Topics: Animals; Cardiac Catheterization; Coronary Artery Bypass; Coronary Vessels; Dogs; Electrocardiography; Emergencies; Fluoresceins; Injections, Intravenous; Ligation; Myocardial Infarction; Myocardial Revascularization; Tetracycline

Topics: Animals; Electrocardiography; Haplorhini; Heart Function Tests; Myocardial Infarction; Myocardium; Perfusion; Primates; Stress, Mechanical; Tetracycline; Time Factors; Vectorcardiography

Topics: Acetates; Animals; Carcinoma 256, Walker; Mercury; Muscles; Myocardial Infarction; Organomercury Compounds; Radionuclide Imaging; Rats; Tetracycline; Time Factors

Topics: Angiocardiography; Animals; Dogs; Myocardial Infarction; Radionuclide Imaging; Technetium; Tetracycline

Topics: Animals; Coronary Vessels; Fluorescence; Injections, Intraperitoneal; Injections, Intravenous; Ligation; Methods; Microscopy, Electron; Myocardial Infarction; Rabbits; Staining and Labeling; Tetracycline; Time Factors; Ultraviolet Rays

Topics: Adult; Drug Hypersensitivity; Female; Humans; Myocardial Infarction; Myocarditis; Tetracycline

Topics: Animals; Coronary Vessels; Female; Fluorescence; Heart Diseases; Hydrocortisone; Ligation; Myocardial Infarction; Myocardium; Necrosis; Oils; Rats; Tetracycline

Topics: Animals; Cats; Fluorescent Dyes; Humans; Ischemia; Methods; Myocardial Infarction; Tetracycline; Ultraviolet Rays

Topics: Alanine Transaminase; Animals; Anti-Bacterial Agents; Aspartate Aminotransferases; Chlortetracycline; Clinical Enzyme Tests; D-Alanine Transaminase; Diagnosis; Dogs; Electrocardiography; Fluorescence; Microscopy; Microscopy, Fluorescence; Myocardial Infarction; Myocardium; Pharmacology; Research; Tetracycline

Topics: Anti-Bacterial Agents; Cardiovascular Diseases; Chlortetracycline; Fluorescence; Myocardial Infarction; Oxytetracycline; Protein Synthesis Inhibitors; Tetracycline

Topics: Anti-Bacterial Agents; Burns; Fluorescence; Humans; Inflammation; Ischemia; Myocardial Infarction; Necrosis; Neoplasms; Tetracycline

Bacteremic shock is second in frequency only to myocardial infarction as a cause of hypotension and death in hospitalized medical patients. The clinical course is marked by fever, usually with chills, and hypotension with a full pulse and warm extremities, followed by shock, often resistant to treatment. Anticipation of this complication in patients with certain predisposing diseases or factors facilitates early recognition of the symptoms and signs of bacteremic shock and prompt treatment. Early and effective treatment of the offending infection often prevents progression of hypotension to the stage of frank vascular collapse.

Topics: Anti-Bacterial Agents; Antibiotics, Antitubercular; Emergencies; Humans; Hypotension; Metaraminol; Methicillin; Myocardial Infarction; Norepinephrine; Phenoxybenzamine; Sepsis; Shock; Shock, Septic; Streptomycin; Tetracycline

Topics: Humans; Inflammation; Myocardial Infarction; Pancreatitis; Shock; Tetracycline

Topics: Anti-Bacterial Agents; Cardiovascular Diseases; Humans; Myocardial Infarction; Tetracycline