The use of creatinine clearance ratios in the prevention of equine rhabdomyolysis: a report of four cases.
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Biomedical subjects
Publications and source records attributed to P Harris.
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In searching for the 'ideal' muscle relaxant for use with intravenous regional anaesthesia, muscle relaxation was assessed with and without the addition of Atracurium to Bier's Block in four volunteers. This was followed by a clinical study of 36 patients with wrist fractures to confirm the drug's safety and examine the possible clinical advantages of using a muscle relaxant. The addition of 2 mg of Atracurium to the Bier's Block improved the ease of reduction (P less than 0.025) and the quality of analgesia (P less than 0.05) (Mann-Whitney U test). The authors conclude that the addition of Atracurium to a Bier's Block is useful in selected patients with a wrist fracture.
Professional symphony musicians work in a very stressful environment which requires them to remain in asymmetric postures for long periods of time. The maladaptations (i.e., astigmatism and anisometropia) made as a result of the stress and the asymmetric postures are investigated. Forrest's astigmatism theory is restated and related to the musician with clinical data to support the theory. Stress management through imagery for the musician is discussed. A study is also discussed which shows that good sight readers in music use a fundamentally different eye scan pattern to read music from the pattern that they use to read written language.
Human carotid bodies, removed at routine necropsies, have been subjected to radioimmunoassay for various peptides. Average levels of immunoreactivity, expressed in pm/g, were: met-enkephalin 612, leu-enkephalin 162, bombesin 73, neurotensin 67, VIP 9 and substance P 16. No alpha-hANP immunoreactivity could be detected.
2-Chloroadenosine reduced the contractile tension of guinea-pig atria directly, and inhibited the increase in tension produced by beta-adrenergic stimulation of guinea-pig papillary muscle. Both effects were reduced by 8-phenyltheophylline, a competitive antagonist at extracellular P1-purinoceptors. Treatment of guinea-pigs with pertussis toxin reduced the sensitivity of both atria and ventricles to 2-chloroadenosine. Atria were significantly affected after treatment with 125 micrograms/kg toxin, but not 100 micrograms/kg. 60 micrograms/kg toxin had no effect on the sensitivity of the ventricles, but 100 and 125 micrograms/kg significantly decreased the antiadrenergic effect of 2-chloroadenosine. We conclude that both the direct and antiadrenergic effects are mediated by an inhibitory guanine nucleotide binding protein.
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The antiadrenergic effect of adenosine was investigated using isolated guinea-pig heart and guinea-pig and rabbit papillary muscle. Adenosine, 15 microM, completely abolished the increased tension stimulated by 0.1-1.0 nM isoprenaline in Langendorff-perfused guinea-pig hearts. With guinea-pig papillary muscles, adenosine decreased by 40% the increased force stimulated by 1-10 nM isoprenaline. When 5 microM 2-chloroadenosine was used in conjunction with 1 unit ml-1 adenosine deaminase, a complete inhibition of the isoprenaline-stimulated tension was seen in guinea-pig papillary muscles. The antiadrenergic effect of 2-chloroadenosine was blocked by 8-phenyltheophylline. In rabbit, there was little effect of 2-chloroadenosine (plus deaminase) on isoprenaline-stimulated tension. (-)-N6 (R-phenylisopropyl)-adenosine (PIA) had no effect on basal or isoprenaline-stimulated adenylate cyclase activity of guinea-pig or rabbit sarcolemmal membranes. We conclude that the antiadrenergic effect of adenosine is mediated by A type receptors and is seen in guinea-pig but not rabbit. Production of adenosine by superfused papillary muscle may obscure the effect of added adenosine. We find no evidence that the antiadrenergic effect is mediated by inhibition of adenylate cyclase.
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A technique is described that allows direct hybridization to the DNA of cells flow sorted onto nitrocellulose filters, which obviates an intervening DNA isolation step. The feasibility of this technique for studying small numbers of cells is demonstrated with human cord blood, which has a high proportion of nucleated cells. The cells are stained with fluorescein-conjugated anti-HLe-l, a monoclonal antibody that recognizes mature leucocytes. Anti-HLe-l-positive cells are all nucleated, and a controlled, precise number of them may be sorted directly onto a nitrocellulose membrane. In cord blood, a small percentage of anti-HLe-l-negative cells are nucleated erythrocytes, which may also serve as a source of DNA. Studies were performed on male or female newborn cells flow sorted onto nitrocellulose membranes and hybridized with either a non-specific human repeat DNA probe or a Y chromosome-specific probe. Importantly, the sex of the newborn could be determined at the DNA level from as few as 50 sorted cord blood leucocytes or 5,000 HLe-l-negative cells. Since nucleated erythrocytes are common in fetal blood but rarely found in the peripheral circulation of adults, the method has potential application for the determination of fetal sex from analysis of flow-sorted nucleated erythrocytes present in the maternal circulation during pregnancy.
A flow sorted chromosome 16-enriched recombinant library was produced to isolate DNA probes useful for constructing a linkage map of 16p, primarily for the study of adult polycystic kidney disease (APKD). The APKD locus has been mapped to chromosome 16 by linkage with the probe 3'HVR, which is located in the region 16p12----pter. Of the 48 single-copy fragments isolated from this new phage library, 39 (81%) were found to be chromosome 16 specific. Probes mapping to chromosome 16 were regionally localized by hybridizing to flow-sorted spot blots of translocation products from lymphoblastoid cell lines containing the rearrangements t(1;16) or t(11;16). Translocation breakpoints at 16p13.11 and 16p11.1 were utilized to subdivide chromosome 16 into three regions: Twenty-six probes were mapped to 16p11.1----16qter, two to 16p11.1----16p13.11, and eleven to 16p13.11----16pter. Probes from 16p were examined for their recognition of restriction fragment length polymorphisms (RFLPs). Seven polymorphic probes were found which recognized eleven RFLPs. Six of the seven probes have RFLPs which are reasonably informative (polymorphism information contents (PIC) of over 0.25). Two of these identify polymorphisms with three different alleles, one of which has a PIC value of over 0.4. These probes may aid in the diagnosis of APKD and contribute towards a linkage map of chromosome 16.
Chromosomes from the mother, father, and child of nine families were stained with ethidium bromide and analysed in flow. These flow karyotypes on average resolved separately the homologues of 4.8 of the offspring's chromosomes. A homologue's relative DNA content (calculated from the flow karyotype) was found to be an accurate marker which could be used to trace that chromosome in a family. In this way the parental origin of 74.4% of the offspring's resolved homologues was determined. In the karyotypically normal families studied no chromosome was found in a child which was clearly different from a homologue present in one of the parents. Using parental flow karyotypes to identify familial heteromorphisms, a number of dysmorphic children were studied in an attempt to detect small "de novo" abnormalities. Although no chromosome abnormality was detected in these cases, the usefulness of family studies was illustrated. In one family a large chromosome 4 homologue was found in the child and this was shown to be similar to one found in the father, suggesting an inherited heteromorphism rather than a clinically significant duplication. Flow analysis of the parents of a patient diagnosed cytogenetically as having an interstitial deletion of the X chromosome revealed the abnormality to be a "de novo" 3;X translocation. It is suggested that flow karyotype analysis in families has potential for the detection of chromosome rearrangements at the limits of resolution of conventional cytogenetics.
Subdural tension pneumocephalus in a 80-year-old man following nasal polypectomy, presenting clinically with progressive weakness of both legs, is reported and the pathogenesis is discussed. The diagnosis of tension pneumocephalus and the options of management are considered.
Arterial and coronary sinus difference for potassium, lactate, glucose, free fatty acids and creatine kinase was measured every 5 minutes in two patients undergoing successful intracoronary thrombolysis of left anterior descending occlusion. In the first patient, reperfusion, 160 minutes after the onset of pain, was followed by a transient and limited release of creatine kinase in the coronary sinus, improvement in the electrocardiogram and restitution of left ventricular contraction. In the second patient, reperfusion 365 minutes after the onset of pain, was also accompanied by a limited release of creatine kinase. Reocclusion of the left anterior descending coronary artery, however, necessitated further thrombolysis which led to a massive release of creatine kinase and permanent loss of wall-motion. It is suggested that, in this case, reperfusion damage had occurred. The arteriovenous differences showed a wash-out of potassium and lactate during reperfusion in each case. The interpretation of the entire sequence of arteriovenous changes, however, could be shown to depend critically on the state of regional perfusion.
In 1979 De Bold showed that the numbers of atrial specific granules varied with changes in water and electrolyte balance of the whole animal. Two years later, he showed that atrial extracts had a natriuretic effect. The active principle has now been identified as a polypeptide formed by cleavage of a larger precursor molecule. The rate of release of atrial natriuretic peptide-like immunoreactive material by the isolated, perfused rat heart has been shown to be increased when the right atrial pressure is raised. The mechanism of release remains, however, unknown. We describe, here, experiments which show a transient release of atrial natriuretic peptide-like immunoreactive material from isolated rat atria subjected to a constant load in an organ bath. The release appears to be specific in that it is not accompanied by a parallel release of other peptides contained in nerve fibres or of creatine kinase contained in myocytes.
Central haemodynamics and regional blood flow were studied comprehensively in conscious New Zealand White rabbits before and during the development of chronic low output cardiac failure produced by administration of the anticancer agent adriamycin. After eight weeks of adriamycin treatment, cardiac index fell from 326(40 to 225(56) ml.min-1.kg-1. This was accompanied by an increase in heart rate and total peripheral resistance but no change in mean systemic blood pressure. Myocardial function was shown to be depressed by the measurement of Frank-Starling curves, the slopes of which were appreciably flatter in adriamycin treated rabbits. Regional blood flow (measured by the radioactive microsphere technique) was redistributed. There were decreases in renal, splenic, small gut, and skeletal muscle blood flow, whereas myocardial and cerebral blood flow were unchanged. There was an increase in total body exchangeable sodium, indicating some salt and water retention. Systemic toxic effects of adriamycin could be limited by treating the animals for eight weeks with adriamycin and then allowing a two week recovery period before haemodynamic study. This would appear to be the optimal dosage schedule.
A review of the history of our knowledge and understanding of the peripheral oedema of congestive cardiac failure points to the conclusion that an inability of the heart to maintain the arterial pressure is of central importance in this condition. Although the function of the circulation is to perfuse the tissues, the body monitors the adequacy of its perfusion, not not through metabolic messengers carried from the tissues in the blood stream, but by sensing the arterial pressure; and the mechanisms evoked act to maintain the arterial pressure. In the short term this is achieved by autonomic regulation of the heart and blood vessels; in the longer term the arterial pressure is maintained through an increase in the blood volume by a retention of salt and water by the kidney. To support the latter process, intrinsic renal mechanisms are successively magnified by the renin-angiotensin-aldosterone system and by the activities of the sympathetic system and vasopressin. The natriuretic influence mediated through volume receptors and the release of atrial peptide is overruled by the arterial baroreceptors, so that the body maintains the arterial pressure at the expense of an increase in blood volume. In these ways the syndrome of congestive cardiac failure may be regarded as one which arises when the heart becomes chronically unable to maintain an appropriate arterial pressure without support.
During the course of a case of primary pulmonary hypertension occurring in a 24 year old man lung tissue became available at heart-lung transplantation in 1986 and from a lung biopsy carried out in 1981. In 1986 the sections showed classic plexogenic pulmonary arteriopathy. In 1981 they revealed migration of myofibroblasts into the intima and lumen of pulmonary arteries and arterioles, the identification of the cells being confirmed by electron microscopy. During the five years that the pulmonary vascular pathology progressed to the formation of plexiform lesions there was an increase in the number of bronchiolar endocrine cells that were immunoreactive to bombesin and calcitonin. This study demonstrates that the classic pathogenesis of primary plexogenic pulmonary arteriopathy originates years earlier as a migration of cells of muscular pedigree from the media into the intima of the pulmonary arteries and arterioles.
Highly polymorphic repeated DNA sequences were detected at the end of the long arm of human chromosome 18 by a recombinant DNA probe containing 56 bp of human DNA (pERT25). This was shown by hybridization of pERT25 to DNA from a panel of human X rodent somatic cell hybrids, by dot blot hybridization to flow-sorted human chromosomes, and by in situ hybridization to metaphase chromosomes. The high degree of polymorphism detected by this 18q DNA fragment makes it potentially useful for various applications, including investigations into the genetics of trisomy 18 (Edwards syndrome), linkage studies, and paternity testing.