Search PubMed⌕ Search

Biomedical subjects

J N Ross

Publications and source records attributed to J N Ross.

At least 19 recordsLinked to original sources
PubMed2001

N,N'-Bis[tris(hydroxymethyl)methyl]-ethanediamide: six O-H...O hydrogen bonds generate only a two-dimensional structure.

Molecules of the title compound, C(10)H(20)N(2)O(8), adopt a conformation which is almost centrosymmetric. The molecules are disordered over two sets of sites with an occupancy ratio of 0.94:0.06. In the major form, there are two intramolecular O-H...O hydrogen bonds [O...O 2.756 (4) and 2.765 (4) A; O-H...O 144 and 146 degrees ], in which the two amidic O atoms act as acceptors. In addition, there are four intermolecular O-H...O hydrogen bonds [O...O 2.650 (3)-2.666 (3) A; O-H...O 158-171 degrees ]; these link each molecule to six others in a continuous sheet structure which contains five distinct ring motifs, two of the S(7) type, two of the R(3)(3)(10) type and one of the R(2)(2)(22) type.

Journal Article↗
PubMed1997

Acute and chronic cocaine exposure can produce myocardial ischemia and infarction in Yucatan swine.

The purpose of this study was to determine whether the acute and chronic administration of cocaine could induce myocardial infarction. Twenty-five minipigs were studied before and 4 months after balloon angioplasty of the left anterior descending artery (LAD) and balloon denudation of the left circumflex artery (LCx). Minipigs received cocaine in the initial and in the 4-month study (0.1, 0.5, and 3 mg/kg i.v.). Minipigs were randomized to group I (high-cholesterol diet + daily cocaine; 500 mg i.m.; n = 8), group II (high-cholesterol diet + no i.v. cocaine; n = 5), group III (chow diet + daily cocaine; 500 mg i.m.; n = 6), group IV (chow diet + no i.v. or i.m. cocaine; n = 6). In vivo, coronary flow significantly decreased and vascular resistance significantly increased after the administration of cocaine. Histamine significantly decreased the luminal diameters (LAD and LCx) in groups I, II and III. There were a total of five acute and 16 chronic infarctions among the three groups that received either short- or long-term cocaine; however, no infarct occurred in group IV. The combination of daily cocaine abuse with a cholesterol-rich diet enhanced coronary vasoreactivity in vivo and in vitro. We conclude that long-term or sporadic cocaine abuse can induce myocardial infarction.

Animals↗
PubMed1996

Cocaine-induced microvascular vasoconstriction but differential systemic haemodynamic responses in Yucatan versus Yorkshire varieties of swine.

1. Systemic and coronary haemodynamics were measured in 6 Yorkshire swine and 6 Yucatan miniature swine under isoflurane anaesthesia to investigate the influence of cocaine following its intravenous administration at 1, 3 and 7 mg kg-1. 2. Cocaine in Yorkshire swine decreased mean arterial pressure and rate pressure product (systolic pressure x heart rate), suggesting a cardiac depressant effect, whereas cocaine in Yucatan miniature swine increased these parameters, consistent with a hyperadrenergic state. 3. Cocaine in both Yorkshire swine and Yucatan miniature swine decreased coronary blood flow and coronary flow reserve, and increased coronary vascular resistance. 4. A modest generalized epicardial coronary artery constriction was observed by angiography, without evidence of focal spasm. 5. Our results confirm a marked vasoconstrictor effect of cocaine on the coronary arterial circulation, predominantly distal to the epicardial coronary arteries, but also indicate important differences in the systemic cardiovascular responses to the drug between two closely related strains of animals within the same species. Due to the similarities between the swine and human coronary arterial vasculature, we suggest that vasoconstriction in the coronary microcirculation may produce cardiac toxicity in man.

Angiocardiography↗
PubMed1995

Cocaine and the porcine coronary microcirculation: effects of chronic cocaine exposure and hypercholesterolemia.

OBJECTIVE: To examine the acute effect of cocaine on the coronary microcirculation and whether chronic cocaine administration with or without a concomitant high-cholesterol diet affects beta-adrenoceptor and endothelial functions in the coronary microcirculation. DESIGN: Prospective experimental study. SETTING: Laboratory and animal research facility. PARTICIPANTS: Yorkshire pigs. INTERVENTIONS: Pigs were fed a high (2%)-cholesterol diet or a regular diet for 3 months. Animals in both groups received cocaine chronically (7 mg/kg/day, IM). Control animals were fed a regular diet. MEASUREMENTS AND MAIN RESULTS: Responses of the porcine coronary arterioles (90 to 190 microns in diameter) were examined in vitro in a pressurized (40 mmHg) no-flow state using a video-imaging apparatus. Acute application of cocaine caused a significant contraction with a mean maximal diameter decrease of 14% +/- 5%, which was markedly reduced by muscarinic blockade but not significantly affected by alpha 1-adrenergic blockade. Lidocaine or procainamide had no vasoconstrictor effect. Chronic exposure of animals to cocaine diminished contractile responses to cocaine and reduced relaxation responses to the nonselective beta-adrenergic receptor agonist isoproterenol. Phenylephrine caused a minimal (< 4%) contraction of vessels in all groups. Chronic cocaine administration with concomitant high-cholesterol feeding attenuated endothelium-dependent relaxations to serotonin, whereas endothelium-dependent relaxations to bradykinin were unaffected. Endothelium-independent relaxations to sodium nitroprusside were similar in all groups. CONCLUSIONS: These results suggest that cocaine can exert a direct vasoconstrictor effect on the porcine coronary microcirculation via a muscarinic mechanism. Chronic exposure to cocaine significantly decreases beta-adrenoceptor-mediated relaxation and blunts endothelium-dependent relaxation to a small degree.

Adrenergic alpha-Antagonists↗
PubMed1994

Cardiogenic shock induced by cocaine in swine with normal coronary arteries.

OBJECTIVE: The aim was to test the hypothesis that acute intravenous cocaine administration can cause coronary microvascular constriction culminating in myocardial ischaemia and cardiogenic shock. METHODS: Systemic haemodynamic variables and coronary blood flow were measured in 14 Yorkshire swine at baseline and following intravenous administration of 1, 3, and 10 mg.kg-1 of cocaine. Epicardial coronary artery diameter was measured from coronary arteriograms and coronary flow velocity was recorded with a Doppler flow wire. RESULTS: Cocaine produced a decrease in mean arterial pressure (65%), cardiac output (80%), and stroke volume (80%), and an increase in pulmonary artery diastolic pressure (60%). Although coronary blood flow decreased by 70%, epicardial coronary cross sectional area decreased by only 37-45%. Pretreatment with prazosin did not abolish the decrease in coronary blood flow. After administration of 10 mg.kg-1 of cocaine, five of 14 animals developed myocardial ischaemia and cardiogenic shock, culminating in ventricular fibrillation and death. CONCLUSIONS: In anaesthetised Yorkshire swine, cumulative intravenous doses of cocaine caused a significant reduction in coronary blood flow resulting in myocardial ischaemia, which cannot be attributed to epicardial vasoconstriction alone. This suggest that cocaine-induced coronary ischaemia may result from microvascular constriction, which is only partially prevented by alpha 1 blockade. In addition, direct toxic effects of cocaine on the myocardium may also contribute to the development of cardiogenic shock.

Animals↗
PubMed1994

Cocaine-induced microvascular spasm in Yucatan miniature swine. In vivo and in vitro evidence of spasm.

The purpose of the present study was to determine the maximal coronary flow reserve (CFR) before and after the administration of successive cocaine doses (0.1, 0.5, 3, and 7 mg/kg IV) for 2 minutes at 10-minute intervals in eight miniature swine. CFR was assessed by the administration of adenosine (0.03, 0.3, and 3 mg IC). Hemodynamic and flow measurements were performed 3 minutes after each dose. Coronary flow (CF) was measured with a Doppler-tipped wire in the proximal left anterior descending coronary artery (LAD). Also, microvessels were dissected, and vessel diameters were measured by a videoelectronic dimension analyzer. In vivo, LAD CF increased fourfold, CFR increased twofold, and coronary vascular resistance (CVR) decreased fourfold after the administration of adenosine. In contrast, LAD CF decreased threefold, CFR decreased onefold, and CVR increased sixfold 3 minutes after the administration of cocaine. Adenosine (3 mg) was repeated 4 minutes after the administration of cocaine, and LAD CF increased 1.4-fold, CVR increased 2.5-fold, and CFR decreased onefold. Thus, adenosine partially reversed the potent cocaine constrictor effect. In vitro, 10(-9) mol/L cocaine decreased the diameter of the coronary microvessels from 129 +/- 12 to 127 +/- 12 microns, and 10(-4) mol/L cocaine decreased coronary microvessel diameter to 114 +/- 15 microns (P < .05). In conclusion, cocaine in vivo decreases CFR, and consistent with the in vivo effect, cocaine in vitro produced constriction of vessels < 200 microns. These results indicate that cocaine can produce profound microvascular spasm. This may contribute to the ischemia/infarction reported in patients who abuse cocaine and who are subsequently found to have normal epicardial coronary arteries.

Adenosine↗
PubMed1994

Effects of cocaine on carotid vascular reactivity in swine after balloon vascular injury.

BACKGROUND AND PURPOSE: The use of cocaine has been associated with stroke. To evaluate carotid vasospasm as a potential mechanism of cocaine-induced stroke, we studied 12 swine immediately and 10 weeks after angioplasty. METHODS: We compared the short- and long-term vasoconstrictor responses of normal and injured arterial segments to nitroglycerin, histamine, and cocaine in vivo by carotid angiography. We also compared the isometric contractile force responses to different vasoactive substances in normal and injured vascular rings in vivo, and we tested the direct action of cocaine on both arterial segments. RESULTS: In in vivo studies, immediately after angioplasty, luminal diameter in the control segment decreased by 30% with histamine 30 micrograms/kg and by 23% with cocaine 10 mg/kg (P < .001). In contrast, neither histamine nor cocaine produced vasoconstriction in the angioplasty segment. Thus, a transient loss of vasoconstriction occurred at the angioplasty site. Ten weeks later, histamine 30 micrograms/kg significantly (P < .001) decreased luminal diameter by 34% in the control and by 33% in the angioplasty segment; similarly, cocaine 10 mg/kg significantly (P < .001) decreased luminal diameter by 26% in the control and by 34% in the angioplasty segment. Thus, 10 weeks after angioplasty, the transitory loss of carotid vasoconstriction in response to histamine and cocaine reverted, and a moderate generalized vasoconstriction occurred in both segments without localized vasospasm. In vitro, the maximal isometric tension responses to KCl, acetylcholine, histamine, and phenylephrine were similar in vascular rings from normal and angioplasty segments. The median effective doses to histamine and phenylephrine were similar. In contrast, cocaine in concentrations from 10(-7) to 10(-3) mol/L failed to produce any isometric contraction in vitro. CONCLUSIONS: Cocaine in vivo produced a generalized carotid vasoconstriction without evidence of localized vasospasm; since there was no response to cocaine in vitro, the in vivo effect was most likely mediated by neurohumoral factors rather than by a direct action of cocaine on vascular smooth muscle.

Angioplasty, Balloon↗
PubMed1992

Alternative treatment of heartworm disease.

Conventional adulticidal therapy may cause acute death due to embolism in major pulmonary arteries resulting in severe infarction of the lung. To avoid this problem removing a significant number of worms with flexible alligator forceps prior to adulticidal therapy is recommended. Before surgery, an accurate diagnosis and critical evaluation of the patient is mandated for proper choice and sequence of treatment.

Animals↗
PubMed1991

Variance of indirect blood pressure measurements and prevalence of hypertension in clinically normal dogs.

In a series of 3 studies, indirect blood pressure measurements were obtained to define normal variance, identify hypertension, and estimate the prevalence of hypertension in apparently healthy dogs. In part 1, we measured values in 5 clinically normal dogs twice weekly for 5 weeks in a home setting. Mean +/- SD systolic arterial pressure (SAP) and diastolic arterial pressure (DAP) was 150 +/- 16 and 86 +/- 13 mm of Hg, respectively. The DAP significantly (P less than 0.01) decreased with repeated measurements over the 5-week period. In part 2, we assessed the variation between blood pressures measured in a clinic vs those measured in the home. Within a 2-week period, measurements were obtained from 10 clinically normal dogs in a private veterinary clinic and again in their home. Significant differences were not observed between clinic and home measurements of SAP and DAP; however, heart rate was significantly (P less than 0.05) higher in the clinic. In part 3, SD about the SAP and DAP mean values were determined in 102 clinically normal dogs. Canine hypertensive status was determined, using statistical methods and data from 102 clinically normal dogs. Values of SAP greater than 202 mm of Hg and DAP greater than 116 mm of Hg were determined to be 2 SD beyond the mean and, therefore, were interpreted to be hypertensive. Approximately 10% of the 102 apparently healthy dogs measured in this study were considered hypertensive on the basis of these criteria. In addition, a border zone of suspected hypertension was estimated, using the mean + 1.282 SD. The SAP border zone was between 183 and 202 mm of Hg, whereas the DAP border zone was between 102 and 113 mm of Hg. Of the 102 dogs, 12 had values within these zones of suspected hypertension.

Animals↗
PubMed1987

M-mode echocardiographic values in sheep.

M-mode echocardiograms were recorded from 21 adult sheep (20 ewes, 1 whether). Fifteen echocardiographic measurements were taken and compared with body weights or heart rates, using linear regression equations. Significant correlations (P less than 0.05) were found when body weight was compared with left ventricular internal dimensions in systole (Yo = 0.187 Xo + 18.60, P less than 0.05) and diastole (Yo = 0.346 Xo + 26.69, P less than 0.02), septal thickness in systole (Yo = 0.0876 Xo + 7.64, P less than 0.05) and diastole (Yo = 0.0673 Xo + 4.45, P less than 0.05), aortic root dimension (Yo = 0.129 Xo + 23.40, P less than 0.05), and left atrial dimension (Yo = 0.194 Xo + 15.95, P less than 0.005). Heart rate was significantly correlated (P less than 0.05) with body weight (Yo = -0.245 X 96.71, P less than 0.05), ejection time (Yo = -0.0013 Xo + 0.376, P less than 0.001), velocity of circumferential fiber shortening (Yo = 0.0061 Xo + 0.928, P less than 0.05), mean velocity of mitral valve middiastolic closure (Yo = -0.184 Xo + 1.65, P less than 0.02), and left atrial dimension (Yo = -0.109 + 40.55, P less than 0.005). Fractional shortening of the left ventricle was (mean) 37.2 +/- 5.7% and the left atrial to aortic root ratio was (mean) 0.92 +/- 0.10.

Animals↗
PubMed1984

TMJ + MPD?

Explore the source record for details and available documents.

Humans↗
PubMed1983

Electron microscopy of intimal lesions in the pulmonary trunk of a dog with Dirofilaria immitis.

Protruding intimal lesions in canine pulmonary trunk induced by naturally occurring heartworm disease were further characterized at light and electron microscopic levels. The pulmonary trunk was dissected free, fixed and subdivided into many specimens which were routinely prepared for scanning electron microscopy (SEM). After SEM observation, selected samples were embedded in Epon-Araldite and sectioned for correlated light (LM) and transmission electron microscopic (TEM) observation. SEM observation revealed protruding lesions of various sizes and shapes on the luminal surface. These ranged from papillae to complex lamellar projections extending far into the lumen. This suggests a progressive growth pattern. A layer of cells covered most of the lesion surface and between the lesions. These cells had a rounded conformation and no uniform orientation on the luminal surface. Other areas of the lesion surface appeared fibrous and devoid of cells. LM and TEM sections of the SEM specimens revealed three types of surfaces on the protruding fibro-muscular lesion. The lesion was primarily covered by cells which were (1) endothelial or (2) non-endothelial in nature. The non-endothelial surface cells were separated from each other and did not have the typical characteristics of endothelial cells. The third region was acellular and had the fibrous appearance of extracellular matrix. The acellular and non-endothelial portions formed a significant amount of the lesion surface. Previous reports have indicated these lesions were covered by typical endothelium. This report indicates that further characterization and quantitation of the cells covering the lesion surfaces is necessary.

Animals↗
PubMed1980

Scanning electron microscopy of an elastic fiber network which forms the internal elastic lamina in canine saphenous vein.

Scanning electron microscopy (SEM) was used to study the arrangement of elastic fibers in the canine saphenous vein as the basis for further studies of veins used in by-pass grafting operations. The elastic fiber arrangement in distended and non-distended veins was examined in both immersion-fixed and perfusion-fixed vessels. Transmission electron microscope (TEM) observation of the SEM samples confirmed the identity of these fibrillar structures as elastic fibers. In addition, specific stains for elastic fibers (Verhoeff's iron hematoxylin and orcein) were used. The elastic fibers forming the internal elastic lamina were arranged in a fishnet-like pattern. Large-diameter fibers, running longitudinally along the vascular wall, were interconnected by smaller oblique fibers. Together the fibers formed an elastic cylindrical network between the endothelium and the smooth muscle cells. The thicker longitudinal fibers were the same diameter in distended and non-distended veins. By contrast, the oblique fibers were thinner and more complexly branched in distended veins. The architecture of the elastic fiber network contributes to vascular flexibility and allows circumferential distension. The interconnecting oblique fibers presumably serve to distribute internal pressure equally around the venous wall.

Animals↗
PubMed1979

Quantification of myocardial ischemia and infarction with 201thallium scintigraphy.

A quantitative method for the analysis of 201thallium myocardial scintigrams, developed in an experimental infarcted dog heart model, has been compared with two nonquantitative methods for interpretation of stress myocardial scintigrams in two groups of patients studied with coronary angiography: 11 with normal coronary arteries and 14 with coronary artery disease. Three independent observers interpreted scintigrams which were 1) not computer processed; 2) corrected for background activity in lungs and chest wall; and 3) processed by a computer method which uses a uniform threshold of counts determined from the dog model to define perfusion defects. Interobserver variability as well as sensitivity and specificity of detecting coronary disease were examined. In patients with coronary artery disease interobserver variability was improved by using the computer technique: observers agreed as to the existence of a perfusion defect in 93% of the scintigrams as compared to 55% and 81% for the unprocessed and background-subtracted images respectively. No false positive indications of coronary disease were obtained by any of the three techniques. Use of the computer method did not improve the sensitivity of detecting coronary disease, however--71% compared to 64% for unprocessed images and 79% for background-substracted images. The advantages of this quantitative computer method are increased consistency of interpretation and lack of false positive diagnoses of coronary disease. An improved sensitivity of detection may be gained by varying thallium count thresholds according to anatomic location in the heart.

Animals↗