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Biomedical subjects

R E Patterson

Publications and source records attributed to R E Patterson.

At least 91 records · Page 5Linked to original sources
PubMed1991

Adenosine receptor blockade with 8-p-sulfophenyltheophylline aggravates coronary constriction.

We examined the role of adenosine in modulating the coronary constrictor effect of neuropeptide Y (NPY). Anesthetized dogs (n = 22) were instrumented to record hemodynamics and to collect arterial and coronary venous blood. In control dogs (n = 7), during the first 30 min before NPY, baseline coronary resistance fell slightly. By 10 min after NPY (42 nmol over 4 min), coronary resistance was increased by 30% and fell slowly to pre-NPY levels over the ensuing hour. Intravenous (7.5 mg/kg, n = 3) or intracoronary (to 100 microM arterial concentration, n = 12) infusion of 8-p-sulfophenyltheophylline (8-THEO) blocked the vasodilator effects of adenosine but did not alter the peak dilation seen with papaverine or reactive hyperemia. Over 30 min before NPY, infusion of 8-THEO increased baseline resistance by 31% as it reduced coronary blood flow, despite no change in other hemodynamic parameters or myocardial oxygen consumption. The coronary constrictor effect of NPY was magnified in the presence of adenosine receptor blockade. At 3 min, coronary resistance was increased by 34%, at 5 min by 52%, and at 10 min by 59%. The effect of adenosine receptor blockade on constriction due to NPY could not be attributed to a nonspecific alteration in cardiac function or oxygen consumption. In addition, the increase in baseline coronary resistance following receptor blockade correlated with the worsening of the coronary constriction following NPY (r = 0.48, P less than 0.05). Thus it appears that adenosine modulates an imposed constriction of coronary vessels and acts as a "host defense" to restore coronary tone toward normal.

Adenosine↗
PubMed1989

Importance of epidemiology and biostatistics in deciding clinical strategies for using diagnostic tests: a simplified approach using examples from coronary artery disease.

The explosion of costly new medical diagnostic technologies demands a common sense approach to help physicians decide appropriate indications and strategies for use of these tests. This simple, nonmathematical review focuses on the assessment of coronary artery disease, but the approach can be generalized to other medical problems. This clinical approach to diagnostic testing strategies is based on seven sequential questions: 1. What is the clinical probability that this patient has a specific disease characteristic based on clinical data? 2. What is the overall objective for management of this patient based on the overall status of the patient? 3. Most importantly, what specific questions need to be answered about the patient's condition before the physician can recommend the most appropriate management (e.g., whether the patient has coronary disease, whether an anatomic lesion is functionally significant, whether a myocardial region is reversibly ischemic or irreversibly infarcted, whether a particular therapy has had good or bad effects or what is the patient's prognosis)? The key point is for the physician to formulate a specific clinical question about the patient before the test. 4. The physician must then ask how well does the test answer the particular clinical question about the patient. Here the physician needs to understand the sensitivity and specificity of the test, especially because they are influenced by various clinical biases. 5. Next, the physician must ask how to interpret the reliability of a positive or negative test result in the individual patient. This requires understanding predictive value and predictive error of a given result and how they are influenced by the clinical data as described by Bayes' theorem. 6. Next, the physician must ask what further tests or therapies will be recommended for the patient. The physician can estimate in advance how different test results would alter management plans and he can then allow this estimate to help determine indications for the test. There is some controversy concerning whether to use Bayes' theorem or multivariate analysis to estimate the final probability of a disease characteristic. 7. Finally, in this era of quality assurance, professional review and cost containment, it behooves each physician to ask whether the data provided by the particular tests were worth the cost, inconvenience and risk for that particular patient.

Bayes Theorem↗
PubMed1989

Coronary constriction due to neuropeptide Y: alleviation with cyclooxygenase blockers.

Intra-arterial administration of neuropeptide Y (NPY), a peptide endogenous to sympathetic nerves, increases coronary vascular resistance by 30-40%. To test whether blockade of prostaglandin synthesis altered the severity of the NPY-induced coronary vasoconstriction, dogs (n = 25) were anesthetized and instrumented to record hemodynamic parameters. In control animals (n = 11) paired infusions of NPY (42 nmol/3 min) were given at 0 and 120 min. NPY produced similar increases in coronary resistance by 10 min, 31 +/- 7% (mean +/- SD) with the first dose vs. 32 +/- 12% with the second dose. The increases in resistance were due to an initial decrease in coronary flow (10 +/- 6%) followed by a prolonged increase in aortic pressure (15-20% over 20 min). Each infusion of NPY decreased heart rate (-10 +/- 7%) but did not alter left ventricular dP/dt. The effects of NPY lasted 40-60 min. In a separate group, a cyclooxygenase inhibitor (COI), indomethacin (n = 6) or ibuprofen (n = 8), was given 1 h before the second dose of NPY. The increases in coronary resistance were blunted significantly after cyclooxygenase blockade from a predrug value of 36 +/- 13 to 19 +/- 12%. In these treated animals, the decrease (-12 +/- 6%) in coronary blood flow seen with the first dose of NPY was prevented (4 +/- 14%) during the second dose (P less than 0.05). Of the two drugs, ibuprofen appeared to restore coronary flow more than did indomethacin. Neither drug affected the base line or the NPY-elicited changes in aortic pressure, heart rate, dP/dt, or myocardial oxygen demands.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Neuropeptide-Y. A peptide found in human coronary arteries constricts primarily small coronary arteries to produce myocardial ischemia in dogs.

Neuropeptide-Y (NPY), a brain peptide, is located in the walls of human coronary arteries. This study assessed the effects of NPY on the coronary circulation in 40 chloralose-anesthetized, open-chest dogs. Intracoronary NPY (42 nmol over 5.2 min) caused a 39% reduction in coronary blood flow without changing heart rate or aortic pressure. To determine whether this vasoconstriction could produce ischemia, intramyocardial pH was measured in seven dogs (group I) and decreased from 7.45 +/- 0.06 to 7.37 +/- 0.06 pH units after NPY in the subendocardium (P less than 0.0002), and from 7.45 +/- 0.06 to 7.40 +/- 0.05 pH units (P less than 0.04) in the subepicardium of the infused zone. Left ventricular ejection fraction (LVEF), measured by radionuclide angiography, decreased from 0.52 +/- 0.08 to 0.42 +/- 0.12 U (n = 5, P less than 0.01) during NPY. NPY-induced vasoconstriction was also associated with ST-T wave changes on the electrocardiogram (ECG) in eight of nine other animals (group V). In another group of six dogs (group IV), the change in small vessel resistance accounted for 94% of the increase in total resistance, so that the primary vasoconstrictor effect of NPY was exerted on small coronary arteries. Thus, NPY, a peptide found in human coronary arteries, caused constriction of primarily small coronary arteries that was severe enough to produce myocardial ischemia as determined by ECG ST-T wave changes, and decreases in intramyocardial pH and LVEF in dogs.

Animals↗
PubMed1989

Contrasting effects of verapamil and nifedipine on pH of ischemic myocardium in the dog.

It remains unknown whether the actions of verapamil to depress and nifedipine to enhance contractile function of ischemic myocardium influence the degree of myocardial ischemic injury. Thus, we measured intramyocardial pH using fiberoptic pH probes in 43 anesthetized open-chest dogs pretreated for 30 min with verapamil, or nifedipine in doses that decreased aortic pressure 10 to 15 mm Hg before ligation of the left anterior descending coronary artery for 15 min. Drugs were continued during the 15-min ischemic period until the animals were euthanized without reperfusion: verapamil, 10-20 micrograms/kg/min and nifedipine, 2 to 4 micrograms/kg/min i.v. Verapamil-treated dogs showed higher pH of ischemic subendocardium after 15 min ischemia (6.75 +/- 0.07) than did the nifedipine (6.48 +/- 0.04) or placebo (6.43 +/- 0.05) groups, even if the animals were paced (6.71 +/- 0.11) to prevent the negative chronotropic effect of verapamil (P less than 0.01). Neither verapamil nor nifedipine changed collateral myocardial blood flow from 0.10 +/- 0.02 in the subendocardium and 0.17 +/- 0.03 ml/min/g in the subepicardium. Left ventricular function estimated by left ventricular dp/dt was depressed 15% by verapamil and enhanced 26% by nifedipine. Thus, verapamil, but not nifedipine, relieves acidosis of ischemic myocardium after acute coronary occlusion in doses that sustain a 10 to 15 mm Hg decrease in aortic pressure. Nifedipine, in doses that produced the same 10 to 15 mm Hg decrease in mean aortic pressure, did not increase intramyocardial pH, as it enhanced contractile function, estimated by left ventricular dp/dt.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Calcium channel binding characteristics in the human heart.

The number, affinity, pharmacologic specificity and regional distribution of calcium channel binding sites in human hearts obtained at autopsy and open heart surgery were characterized using the radioligand [3H]nitrendipine. Scatchard analyses of saturation data from 6 autopsy hearts revealed a homogeneous distribution of high affinity binding sites (affinity-1 [KD] = 0.44 +/- 0.06, 0.52 +/- 0.07, 0.32 +/- 0.02, 0.30 +/- 0.03, and 0.45 +/- 0.01 nM; binding capacity [Bmax] = 30 +/- 4, 27 +/- 6, 25 +/- 7, 33 +/- 3, and 28 +/- 4 fmol/mg protein in right atrium, right ventricle, left atrium, left ventricle and ventricular septum, respectively). In ligand competition experiments, nifedipine and nitrendipine completely displaced binding with partial displacement by verapamil and 35% enhancement of binding by 10(-5) M diltiazem at 37 degrees. Analyses of right atrial appendages obtained at open heart surgery from 5 coronary artery bypass patients provided similar results (KD = 0.2 +/- 0.03 nM, Bmax = 42 +/- 2 fmol/mg protein). In addition, no significant differences in KD or Bmax were found in 3 hamster hearts assayed at the time of death or up to 18 hours postmortem at either 4 or 25 degrees. In contrast, there was a significant increase in Bmax (110 fmol/mg protein) with no change in KD (0.3 nM) in a myomectomy specimen from a patient with obstructive hypertrophic cardiomyopathy compared with either autopsy or surgical specimens. These studies illustrate the feasibility and potential advantages of studying calcium channels directly in human hearts.

Adult↗
PubMed1988

Normal SPECT thallium-201 bull's-eye display: gender differences.

The bull's-eye technique synthesizes three-dimensional information from single photon emission computed tomographic 201TI images into two dimensions so that a patient's data can be compared quantitatively against a normal file. To characterize the normal database and to clarify differences between males and females, clinical data and exercise electrocardiography were used to identify 50 males and 50 females with less than 5% probability of coronary artery disease. Results show inhomogeneity of the 201TI distributions at stress and delay: septal to lateral wall count ratios are less than 1.0 in both females and males; anterior to inferior wall count ratios are greater than 1.0 in males but are approximately equal to 1.0 in females. Washout rate is faster in females than males at the same peak exercise heart rate and systolic blood pressure, despite lower exercise time. These important differences suggest that quantitative analysis of single photon emission computed tomographic 201TI images requires gender-matched normal files.

Adult↗
PubMed1987

Correlation of changes in cardiac calcium channels with hemodynamics in Syrian hamster cardiomyopathy and heart failure.

We compared hemodynamics with [3H]nitrendipine (calcium channel) binding to cardiac membranes from Bio 14.6 cardiomyopathic Syrian hamsters at 4 and 10 months with their F1B controls. A 50% increase in the number (Bmax) of nitrendipine binding sites (calcium channels) was seen only in the 4 month old myopathic vs controls (Bmax = 468 +/- 11 vs 309 +/- 10 fmol/mg prot with no change in affinity (KD) (KD = .65 +/- .12 vs .75 +/- .14 nM), while no differences in Bmax or KD were seen at 10 months (Bmax = 375 +/- 9 vs 362 +/- 7 fmol/mg prot/KD = .82 +/- .18 vs .89 +/- .17 nM) myopathic vs control respectively. Hemodynamic studies revealed no significant differences in cardiac output, cardiac index, stroke volume, heart rate, mean arterial pressure, peripheral resistance, body weight, heart weight at 4 months, but a significant decrease in peripheral resistance (1120 +/- 360 vs 2080 +/- 240) increase in body weight (118 +/- 2 vs 94 +/- 2 grams) and heart weight (97 +/- 5 vs 78 +/- 2 gms/100 gms body weight) in 10 month myopathic vs control animals. We conclude that the onset of cardiomyopathy at 4 months is associated with a selective increase in calcium channel binding sites and heart failure at 10 months is associated with a relative decrease in these sites.

Animals↗
PubMed1987

Use of cross-correlation function to detect patient motion during SPECT imaging.

We have developed a procedure to detect patient motion during a tomographic acquisition. The method uses frame-to-frame cross-correlation functions of the summed profiles in the vertical and horizontal directions of the planar images. The quantitative output derived from examination of the variation of the change in the pixel value, corresponding to the maximum of the cross-correlation function at each view, provides an effective and nonsubjective means of performing quality control on the presence and amount of movement during a single photon emission computed tomographic scan. In contrast to cine mode and sinogram display, easy to interpret hard copy can be generated through this procedure.

Algorithms↗
PubMed1986

Functional consequences and intracoronary localization of alpha-adrenergic stimulation of the canine coronary circulation.

Although alpha-adrenergic stimulation can increase coronary vascular resistance, it remains unknown whether the vasoconstriction can override intrinsic coronary regulatory influences to produce ischemia. Methoxamine, 2 to 4 mg, was infused into the circumflex coronary artery of 23 chloralose-anesthetized open chest dogs, and resulted in a 68% increase in coronary vascular resistance. The functional consequence of this increased coronary vascular resistance was assessed by gated radionuclide ventriculography and ST-T wave changes on the electrocardiogram. In six dogs (Group I), aortic pressure changed trivially (less than 5 mm Hg) to allow distinction between direct effects of the flow reduction and indirect effects of increased aortic pressure. In this group, coronary blood flow decreased 33% from a control value of 44 +/- 10 ml/min (p less than 0.001) and left ventricular ejection fraction decreased from 0.54 +/- 0.12 to 0.46 +/- 0.10 (p less than 0.025). In eight dogs (Group II) in which aortic pressure increased by more than 5 mm Hg, left ventricular ejection fraction decreased from 0.46 +/- 0.07 to 0.39 +/- 0.09 (p less than 0.002). Pressure gradients were measured between the aorta and a distal coronary artery branch to calculate small and large vessel resistances separately in four other dogs (Group III). The resistance of small coronary arteries accounted for 92% of the total increase in coronary vascular resistance produced by methoxamine. In five other dogs (Group IV), intracoronary methoxamine, 2 mg, produced ST-T wave changes suggestive of ischemia as it increased coronary vascular resistance by 33%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Agonists↗
PubMed1986

Factors related to obesity in preschool children.

The purpose of this research was to examine the following variables for their relationship to the prevalence of preschool obesity: familial aggregation of obesity, infant feeding practices, socioeconomic status, and parents' attitudes toward the use of food for non-nutritive purposes. Parents completed a biographical data form. Height, weight, and skinfold measurements were obtained from 94 preschool children and their biological parents. Both parents answered a Child Feeding Opinion Questionnaire. Anthropometric measurements were evaluated using percentile rankings from NHANES. On the assumption that subjects over the 75th percentile for triceps skinfold were overweight and those above the 90th percentile were obese, 23.4% and 7.5% of the children, 9.6% and 5.3% of the mothers, and 29.8% and 10.6% of the fathers were overweight or obese, respectively. Most parent-child anthropometric correlations were statistically significant. No statistically significant relationships were found between infant feeding practices and childhood obesity. Mothers' educational level varied inversely with the children's weight for height. Mothers and fathers opposed the use of food for reward, punishment, soothing, or affection. The parents' child feeding attitudes had no obvious relationship with the children's anthropometric measurements.

Attitude↗
PubMed1985

Comparative effects of calcium-channel blocking agents on left ventricular function during acute ischemia in dogs with and without congestive heart failure.

To examine the relative potencies of verapamil, nifedipine and diltiazem on left ventricular (LV) function under ischemic conditions, 20 conscious closed-chest dogs that had partial occlusion of their circumflex coronary arteries were studied. Myocardial blood flow was measured by microspheres, LV function by radionuclide angiography. Drug effects were compared at doses causing equal decreases in mean arterial pressure (MAP) and in coronary vascular resistance of the nonischemic zone. Global ejection fraction (EF) and EF of the ischemic region were significantly decreased by verapamil (p less than 0.002) and increased by nifedipine (p less than 0.001); diltiazem caused no significant changes. Verapamil significantly increased peak diastolic filling rate (p less than 0.001); nifedipine also increased diastolic filling rate but only at doses that markedly decreased MAP and coronary vascular resistance. Diltiazem was not significantly different from placebo. For doses causing an equal decrease in MAP, verapamil decreased heart rate (p less than 0.001), and diltiazem and nifedipine increased heart rate (p less than 0.05). Myocardial ischemic zone flow remained unchanged during placebo, verapamil, diltiazem or nifedipine infusion. To study the influence of heart failure on the hemodynamic effects of the calcium-channel blocking agents, 6 foxhounds underwent total occlusions of the left anterior descending coronary artery, resulting in myocardial infarction, volume loading to increase left atrial pressure and partial occlusion of the circumflex coronary artery. Verapamil depressed global left ventricular ejection fraction and increased left atrial pressure to as high as 40 to 45 mm Hg. In contrast, nifedipine decreased left atrial pressure and increased global EF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Effect of verapamil on pH of ischemic canine myocardium.

Verapamil has been shown to depress the contractility of ischemic myocardium. The present study was designed to determine whether that effect is due to an increase in ischemic injury caused by the drug or whether it might reflect a protective effect. A critical partial occlusion was effected on the left anterior descending coronary artery of 16 open chest foxhounds. A fiberoptic pH probe was implanted in the subendocardium of the ischemic zone, and coronary blood flow was reduced by 79% from a control value of 38 +/- 4 ml/min and held constant. Mean coronary perfusion pressure was decreased 48% from its control value of 90 +/- 6 mm Hg and remained constant. Eight animals were treated with intravenous verapamil, beginning 20 to 30 minutes after the onset of ischemia, in incremental doses (5, 10 and 20 micrograms/kg per min) and eight were treated with placebo. The pH of the ischemic zone increased after institution of treatment in the verapamil group (+ 0.04 +/- 0.05 pH unit) whereas it decreased in the placebo group (- 0.06 +/- 0.4 pH unit) during the first dose (p less than 0.05). Although the difference in pH between the two groups was marked at all doses (p less than 0.03) compared with control partial occlusion, verapamil caused no significant change in heart rate (+ 0.1 +/- 1 beat/min in the verapamil group versus + 0.6 +/- 4.5 beats/min in the placebo group), mean arterial pressure (- 7.5 +/- 4 versus - 4.3 +/- 3 mm Hg, respectively) or cardiac output (- 0.2 +/- 0.07 versus - 0.02 +/- 0.04 liters/min, respectively) comparing control with the first or the second dose of verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

A new device for the efficient pulverisation and extraction of myocardial biopsies for high energy phosphate analysis.

We developed a new device for processing frozen myocardial biopsies. Frozen samples of 20 to 50 mg were dropped into a 25 ml stainless steel centrifuge tube held in a custom-made aluminium container precooled in liquid nitrogen. A stainless steel pestle attached to a stainless steel disk was driven by a modified heavy-duty staple gun to pulverise the tissue rapidly at low temperatures. The tissue powder was extracted with 0.3N PCA at 0 degree C in the centrifuge tube which was then transferred to a Sorvall super-speed centrifuge. Values for adenosine triphosphate (ATP) were 5.6 +/- 0.7 mumol . g-1 wet weight (mean +/- SD). Creatine phosphate (CP) yield was 12.2 +/- 3 mumol . g-1 wet weight. The % recovery of an added internal standard for ATP was 86 +/- 18% and for CP 90 +/- 16% with the new method.

Adenosine Triphosphate↗
PubMed1984

Adenosine uptake sites in dog heart and brain; interaction with calcium antagonists.

[3H] Nitrobenzylthioinosine (NBI) binding is characterized in dog heart and brain. Evidence is presented suggesting that [3H]NBI is binding to the adenosine uptake site in both tissues. Physiologic studies in open-chested dogs clearly demonstrate that NBI acts as a coronary vasodilator, consistent with an action at the adenosine uptake site. The binding is reversible, saturable and of high affinity (KD = 0.78 +/- .06 nM for heart and 0.52 +/- .05 nM for brain). Both dipyridamole and hexobendine are high potency inhibitors of [3H]NBI binding in heart and brain while other antihypertensives and vasodilators such as propranolol and nitroglycerin have no effect. The inhibition of [3H]NBI binding observed with dipyridamole was competitive indicating that both agents are acting at the same site. The dihydropyridine calcium antagonists also inhibited binding with a lower potency than the adenosine uptake blockers. Non-dihydropyridine calcium antagonists were much less potent in this regard. The inhibition of [3H]NBI binding observed with the dihydropyridine calcium antagonists was non-competitive suggesting that the calcium channel and adenosine uptake site may be coupled to each other.

Adenosine↗