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Biomedical subjects

G A Porter

Publications and source records attributed to G A Porter.

At least 55 records · Page 3Linked to original sources
PubMed1990

Angiotensin converting enzyme inhibitors and the allergist.

Angiotensin converting enzyme inhibitors (ACEI) are used widely in the treatment of both hypertension and congestive heart failure. Although usually well tolerated, these medications may produce side effects that may be encountered by the allergist, including cough, angioedema, and rhinitis symptoms. The severity of ACEI-induced cough may vary, and is associated with increased bronchial hyperreactivity in some (but not all) patients as judged by methacholine sensitivity. Angiotensin converting enzyme inhibitor-induced cough may have its onset from one day to 12 months after initiation of therapy, and is not dose dependent. Angioedema caused by ACEI is usually mild and clears with discontinuation of the drug, however cases requiring intubation and tracheostomy have been reported. The mechanism of ACEI-induced cough remains unclear, but could be in part due to accumulation of substances whose degradation may also be impeded by ACEI, such as substance P, bradykinins, and/or prostaglandins. Knowledge of the side effects produced by this class of medication may help patients avoid unnecessary, costly, and often invasive diagnostic evaluations.

Angioedema↗
PubMed1990

Differential binding of the lectins Griffonia simplicifolia I and Lycopersicon esculentum to microvascular endothelium: organ-specific localization and partial glycoprotein characterization.

The lectins Griffonia simplicifolia I and Lycopersicon esculentum were used to assess the presence of endothelium-specific glycoproteins in the microvasculature of the rat myocardium, diaphragm and superficial cerebral cortex. Organs fixed by intravascular perfusion were processed to obtain semithin (0.5 micron) and thin (less than 0.1 micron) frozen sections that were reacted with biotinylated lectin followed by streptavidin conjugated to Texas Red, for semithin sections, or by streptavidin conjugated to 5-nm colloidal gold particles, for thin sections. Lycopersicon esculentum lectin exclusively labeled the endothelium of all small vessels in all three microvascular beds; it did not bind to components of either the parenchyma or the extracellular matrix. Griffonia simplicifolia I lectin exclusively labeled the endothelium of the entire microvasculature in the myocardium and diaphragm, but marked primarily pericytes in the cerebral microvasculature. It did not label any parenchymal or interstitial organ component. At the electron microscope level, the lectin Griffonia simplicifolia I labeling was associated with the plasmalemma proper and especially with plasmalemmal vesicles and their introits, and Lycopersicon esculentum lectin bound primarily to the luminal plasmalemma in the microvascular beds of the myocardium and diaphragm. In the cerebral cortex, labeling of the microvasculature was clearly different: Griffonia simplicifolia I bound primarily to pericytes and vascular smooth muscle cells whereas Lycopersicon esculentum labeled only the microvascular endothelium. Lysates prepared from the myocardium, diaphragm and cerebral cortex were processed through Griffonia simplicifolia I lectin affinity separation followed by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) analysis of the fraction obtained. A number of putative endothelium-specific glycoproteins was detected and found to differ qualitatively and quantitatively from organ to organ. The most prominent polypeptide, approximately 97 kDa, was present in substantial amounts in the myocardium and diaphragm, but in considerably lower concentration in the cerebral cortex. The reverse applied for a approximately 55 kDa protein. The preferential distribution of the approximately 97 kDa protein parallels differences in Griffonia simplicifolia I lectin binding by fluorescence and electron microscopy on sections of the corresponding organs. The results provide further evidence for the existence of endothelial glycoproteins specific for different microvascular beds and possibly connected with local functional differentiations.

Animals↗
PubMed1990

Nephrotoxicity of common drugs used by urologists.

Many clinically popular drugs, such as aminoglycoside antibiotics, amphotericin B, radiographic contrast media, analgesics, platinum-based cancer chemotherapy, and cyclosporine, can cause deterioration of kidney function even when the dose has been adjusted properly for renal insufficiency. The authors review the pathophysiologic mechanisms of nephrotoxicity of these drugs and prevention and treatment strategies.

Aminoglycosides↗
PubMed1989

Contrast-associated nephropathy.

Contrast nephropathy can be defined as an acute impairment of renal function that follows exposure to radiocontrast materials and for which alternative explanations for renal impairment have been eliminated. Based on reported studies, the incidence of contrast associated nephropathy (CAN) varies from 0 to 22%. This wide variation can be traced to differences in study design and the criteria used to designate significant renal impairment. Irrespective of the exact incidence, 2 defined risk factors have been identified: preexisting renal disease and diabetes mellitus. Whereas preexisting renal insufficiency is the single most influential risk factor for CAN, when diabetes coexists the incidence approaches 100%. The clinical presentation of CAN is distinct, having a temporal relation between the performance of the contrast study in the high-risk patient and the onset of an increase in serum creatinine levels within the next 24 hours. Serum creatinine values greater than 50% of baseline or rising 1 mg/dl or more is diagnostic. The peak serum creatinine level occurs within 3 to 5 days of the contrast study and oliguria is associated in approximately 30% of the cases. Monitoring serum creatinine is the most useful clinical procedure in high-risk patients after angiography. At least 5 potential pathophysiologic mechanisms of CAN have been proposed: interference with renal perfusion, altered glomerular perm-selectivity, direct tubular injury, intraluminal obstruction, and immunologic mechanisms. Support for each mechanism, either singularly or in combination, can be found in published reports; however, none has achieved universal acceptance. The single most important clinical axiom regarding the prevention and management of CAN is, "Always use the least invasive diagnostic procedure available."(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1989

Risk factors for toxic nephropathies.

The best definition of risk factors for renal injury, irrespective of the aetiological agent, comes from observations in patients with acute renal failure. From such observations, two subdivisions have evolved, i.e., acute insults and host risk factors. Acute renal insults include: hypertension, sepsis, use of nephrotoxic drugs (e.g., aminoglycoside antibiotics and contrast media), haemoglobinuria or myoglobinuria, liver disease and extracellular volume depletion. Host risk factors include: advanced age, hypertension, gout and hyperuricaemia, diabetes mellitus, chronic renal failure and use of diuretics. Furthermore, the mechanism of acute renal injury can be correlated with different risk factors: for a tubular toxic agent, acting either directly on the cells or haemodynamically, a dose-dependency is characteristic; while for immunologically mediated injury, genetic predisposition is more important. The identification of risk factors for chronic toxic injury is confounded by the possibilities of multiple episodes of subclinical renal injury, the distinct possibility that a major component of the ageing process may be a loss of renal reserve, and a progressive body burden, of, e.g., cadmium, which may deplete intrinsic protective mechanisms. However, clinically relevant risk factors can alert the clinician to exercise additional caution when prescribing medications that are potentially nephrotoxic. Such factors include dehydration, pre-existing renal disease, age, co-existing diseases that cause renal ischaemia, gender, concomitantly administered drugs, and electrolyte abnormalities.

Age Factors↗
PubMed1988

The influence of tobramycin dosage regimens on nephrotoxicity, ototoxicity, and antibacterial efficacy in a rat model of subcutaneous abscess.

The influence of dosage regimen on the nephrotoxicity, ototoxicity, and antibacterial efficacy of tobramycin was assessed in Fisher rats with Pseudomonas aeruginosa subcutaneous abscesses. A subcutaneous tobramycin dose of 10 mg/kg every 4 h resulted in peak and trough serum concentrations that approximated those currently recommended for patients. Subsequently, the influence of this subcutaneous dosage regimen was compared with three other regimens that administered the same total daily dose: 20 mg every 8 h, 30 mg every 12 h, and 60 mg every 24 h. Renal injury was assessed by measuring inulin clearance and in vivo synthesis of renal DNA and by histopathology. Cochlear histology was also assessed. The number of P. aeruginosa per abscess was quantitated. In animals with infected abscesses, there was a consistent trend of greater kidney injury with the more-frequent dosage regimens. There was no evidence of cochlear toxicity in any group. All regimens were equally effective in reducing the number of P. aeruginosa in subcutaneous abscesses.

Abscess↗
PubMed1987

Maturation of myocardial capillaries in the fetal and neonatal rat: an ultrastructural study with a morphometric analysis of the vesicle populations.

The ultrastructural morphology of the cellular and extracellular components of the developing myocardial capillary wall--from the 16-day-gestation fetus of the rat to the 21-day neonate--was examined. A morphometric analysis of plasmalemmal vesicles and of coated vesicles and pits of capillary endothelial cells was performed during the same developmental period. As the lateral extensions of the capillary endothelial cells change from irregular to regular in their thickness during development, there is an increase in the number of plasmalemmal vesicles and a progression from clusters of plasmalemmal vesicles to a uniform distribution in the endothelial cell. The ratio of vesicles which are open to the luminal front, which are "free" in the cytoplasm, or which are open to the abluminal front of the endothelial cell was consistent throughout development. The numerical density of plasmalemmal vesicles demonstrates a gradual and significant increase. In contrast, the numbers of coated vesicles and pits are variable within a very narrow range, and no pattern of increase or decrease is discernible during development. Similarly, there is no change in interendothelial cell junctions, which consist of occluding and primitive adhesive junctional types, during development. The lamina densa of the basal lamina gradually develops from discontinuous, patchy densities along the abluminal surface of the endothelial cells to a continuous and distinct layer by 21 days gestation. The presence of the proteoglycan species in the developing basal lamina was assessed with the cationic dye ruthenium red (RR), and the appearance of RR-marked proteoglycans was found to parallel the appearance of lamina densa material. found to parallel the appearance of lamina densa material. The RR sites appear discontinuously in patches; and later, the RR sites appear in a continuous and regular planar lattice in the lamina rara interna and externa at 21 days gestation. A complete array of RR-stainable anionic sites outside a continuous lamina densa near birth indicates that the basal laminae of developing capillaries in the heart are morphologically, and in part biochemically, mature by the end of the first neonatal week. Our results show that the endothelial cells and the subtending basal lamina of myocardial capillaries gradually mature morphologically during the final days of gestation and the first neonatal week.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1987

Myocardial capillaries in the fetal and the neonatal rat: a morphometric analysis of the maturing myocardial capillary bed.

Developing myocardial capillaries from 16-day-gestation fetus to adult undergo several morphological changes including a thinning of the lateral extensions of the capillary endothelial cells, the formation of a basal lamina, and an increase in the number of plasmalemmal vesicles. A decrease in the extracellular space, an increase in the number of capillaries, and a decrease in the capillary diameter were also observed during the developmental period. In view of these ultrastructural changes, a morphometric analysis was made on the developing myocardial wall to demonstrate specific quantitative changes. The volumes which were occupied by capillary endothelial cells, capillary lumina, extracellular space, and myocardial myocytes within a reference volume of myocardium were measured; and we found that 8% of the reference myocardial volume was occupied by capillary endothelial cells, 85% was occupied by myocardial myocytes, 4% was occupied by capillary lumina, and, except for a significant change in extracellular space at 16 days gestation, 3% was occupied by extracellular space. Each volume ratio was found to be nearly constant throughout the studied period. In contrast to this constancy in the volume ratios, other parameters which were measured demonstrated significant changes during the developmental period studied. These overall changes include a 135% increase in capillary density, a 63% increase in luminal surface area of capillary endothelial cells, a 24% decrease in capillary diameter, a 12% decrease in diffusion distance, and a 35% decrease in the diameter of the erythrocyte population.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Functional maturation of the capillary wall in the fetal and neonatal rat heart: permeability characteristics of developing myocardial capillaries.

The development of the functional components of the myocardial capillary wall was characterized by time-course studies of transendothelial transport of intravascularly injected probes of graded size from 16 days of gestation in the fetal rat to seven days postpartum. Despite the morphological changes occurring in the developing endothelial cells, the interaction of the probes was similar throughout the developmental period studied. The carbon particles were retained within the capillary lumina without any association with interendothelial junctions or with plasmalemmal vesicles. Carbon also was associated with coated vesicles. In contrast to carbon, ferritin was localized sequentially, over 60 sec of circulation, in plasmalemmal vesicles on the lumenal surface, in the cytoplasm, and on the ablumenal surface of the endothelial cells as well as in the interstitial space. Ferritin was located also in coated pits and vesicles and, after 90 sec of circulation, in multivesicular bodies. Within 30 sec of circulation, reaction product of myoglobin was located in plasmalemmal vesicles, coated vesicles, and transendothelial cell channels. Also within 30 sec, myoglobin partially filled the interendothelial space from the capillary lumina to the level of the tight junction. At all developmental ages studied, the interendothelial cell junctions appeared structurally tight and were impermeable to all of the probes. Once ferritin or myoglobin had reached the ablumenal space, the basal lamina did not appear to restrain the passage of the probes. Plasmalemmal vesicles are the capillary structures which transendothelially transport ferritin and myoglobin in developing myocardial capillaries.

Animals↗
PubMed1987

Assimilate Unloading from Maize (Zea mays L.) Pedicel Tissues : I. Evidence for Regulation of Unloading by Cell Turgor.

Sugar and (14)C-assimilate release from the pedicel tissue of attached maize (Zea mays L.) kernels was studied following treatment with solute concentrations of up to 800 millimolal. Exposure and collection times ranged from 3 to 6 hours. Sugar and (14)C-assimilate unloading and collection in agar traps was reduced by 25 and 43%, respectively, following exposure to 800 millimolal mannitol. Inhibition of unloading was not specific to mannitol, since similar concentrations of glucose, fructose, or equimolar glucose plus fructose resulted in comparable inhibition. Ethylene glycol, a rapidly permeating solute which should not greatly influence cell turgor, did not inhibit (14)C-assimilate unloading. Based on these results, we suggest that inhibition of unloading by high concentrations of sugar or mannitol was due to reduced pedicel cell turgor. Changes in pedicel cell turgor may play a role in the regulation of assimilate transfer within the maize kernel.

Journal Article↗
PubMed1987

Assimilate Unloading from Maize (Zea mays L.) Pedicel Tissues : II. Effects of Chemical Agents on Sugar, Amino Acid, and C-Assimilate Unloading.

Sugar, amino acid, and (14)C-assimilate release from attached maize (Zea mays L.) pedicels was studied following treatment with several chemical inhibitors. In the absence of these agents, sugar release was nearly linear over a 7-hour period. At least 13 amino acids were released with glutamine comprising over 30% of the total. Release was not affected by potassium concentration, 10-minute pretreatments with p-chloromercuribenzene sulfonic acid (PCMBS) or dithiothreitol, and low concentrations of CaCl(2). Three hours or more exposure to PCMBS, dinitrophenol, N-ethylmaleimide, or 2,4,6-trinitrobenzene sulfonic acid strongly inhibited (14)C-assimilate, sugar, and amino acid release from the pedicel. These treatments also reduced (14)C-assimilate movement into the kernel bases. It is, therefore, likely that reduced unloading, caused by these relatively long-term exposures to chemical inhibitors, was related to reduced translocation of assimilates into treated kernels. Whether this effect is due to disruption of kernel metabolism and sieve element function or reduced assimilate unloading and subsequent accumulation of unlabeled assimilates within the pedicel tissues cannot be determined at this time.

Journal Article↗
PubMed1985

Sugar Efflux from Maize (Zea mays L.) Pedicel Tissue.

Sugar release from the pedicel tissue of maize (Zea mays L.) kernels was studied by removing the distal portion of the kernel and the lower endosperm, followed by replacement of the endosperm with an agar solute trap. Sugars were unloaded into the apoplast of the pedicel and accumulated in the agar trap while the ear remained attached to the maize plant. The kinetics of (14)C-assimilate movement into treated versus intact kernels were comparable. The rate of unloading declined with time, but sugar efflux from the pedicel continued for at least 6 hours and in most experiments the unloading rates approximated those necessary to support normal kernel growth rates. The unloading process was challenged with a variety of buffers, inhibitors, and solutes in order to characterize sugar unloading from this tissue.Unloading was not affected by apoplastic pH or a variety of metabolic inhibitors. Although p-chloromercuribenzene sulfonic acid (PCMBS), a nonpenetrating sulfhydryl group reagent, did not affect sugar unloading, it effectively inhibited extracellular acid invertase. When the pedicel cups were pretreated with PCMBS, at least 60% of sugars unloaded from the pedicel could be identified as sucrose. Unloading was inhibited up to 70% by 10 millimolar CaCl(2). Unloading was stimulated by 15 millimolar ethyleneglycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid which partially reversed the inhibitory effects of Ca(2+). Based on these results, we suggest that passive efflux of sucrose occurs from the maize pedicel symplast followed by extracellular hydrolysis to hexoses.

Journal Article↗