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Biomedical subjects

J H Patterson

Publications and source records attributed to J H Patterson.

At least 37 records · Page 2Linked to original sources
PubMed1995

Antiarrhythmic action of pharmacological administration of magnesium in heart failure: a critical review of new data.

Congestive heart failure is characterized by contractile dysfunction and frequent complex ventricular ectopy. Despite advances in therapy, mortality from heart failure is substantial, estimated at 10-80 percent per year, and sudden death is common. Magnesium is the second most common intracellular cation, strongly influences cardiac cell membrane function, and is an important catalyst of many enzymatic reactions in the myocyte. Epidemiological studies have implicated magnesium deficit in the genesis of sudden death. Patients with congestive heart failure are predisposed to magnesium deficit for many reasons, including neurohormonal activation, poor gastrointestinal absorption, and drug therapy. Hypomagnesaemia is common in these patients and has been linked to an increased frequency of complex ventricular ectopy. Several early, uncontrolled studies have suggested a beneficial effect of magnesium administration on ventricular arrhythmias in patients with congestive heart failure. Two recent randomized, double blind, placebo-controlled trials have shown that both intravenous and oral administration of magnesium chloride results in a significant reduction in the frequency and complexity of ventricular arrhythmias in patients with congestive heart failure. Magnesium administration is well tolerated and serious adverse effects are rare. The potential mechanisms of the antiarrhythmic action of magnesium and limitations of the available data are discussed. The evidence reviewed suggests that serum magnesium concentrations should be monitored and corrected in patients with congestive heart failure. Ventricular arrhythmias may respond to acute intravenous magnesium administration, which should be considered as early therapy. Further study is needed to define magnesium dose and the effect of concomitant potassium administration. A prospective clinical trial is warranted to determine the chronic effects of magnesium administration in patients with heart failure.

Absorption↗
PubMed1994

Effect of acute magnesium administration on the frequency of ventricular arrhythmia in patients with heart failure.

BACKGROUND: There is a high incidence of ventricular arrhythmia and sudden death in patients with heart failure. Unfortunately, currently available antiarrhythmic agents have only limited efficacy and may result in proarrhythmia and hemodynamic deterioration in these patients. METHODS AND RESULTS: We studied the acute effect of intravenous magnesium chloride on the frequency and severity of ventricular arrhythmia in 30 patients with symptomatic heart failure using a double-blind, placebo-controlled crossover design. The left ventricular ejection fraction was 23.0 +/- 8.0% (mean +/- SD). No patient had a history of symptomatic ventricular arrhythmia or was receiving antiarrhythmic agents, calcium channel antagonists, or beta-blockers. Patients were randomized to receive placebo (5% dextrose [D5W] in water alone) or magnesium chloride in D5W given as a bolus of 0.3 mEq/kg over 10 minutes followed by a maintenance infusion of 0.08 mEq/kg per hour for 24 hours. The magnesium concentrations 30 minutes and 24 hours after the bolus were 3.6 +/- 0.1 and 4.2 +/- 0.1 mg/dL, respectively. There was no significant change in serum potassium concentration during magnesium administration. Blinded analysis revealed that administration of intravenous magnesium chloride, compared with placebo, significantly decreased total ventricular ectopy per hour (mean +/- SEM, 70 +/- 26 versus 149 +/- 64, P < .001), couplets per day (23 +/- 11 versus 94 +/- 59, P = .007), and episodes of ventricular tachycardia per day (0.8 +/- 0.2 versus 2.6 +/- 1.0, P = .051). CONCLUSIONS: Intravenous magnesium chloride administration reduces the frequency of ventricular arrhythmia in patients with symptomatic heart failure.

Adult↗
PubMed1993

Evaluation of 45 degrees C hyperthermia and irradiation. I. Studies in a murine rhabdomyosarcoma model.

This report describes biologic experiments using transplanted RIF-1 tumors (diameter 0.5 or 1 cm) in C3H/He inbred mice (12 to 20 per treatment group) to compare the results with heat alone (43 degrees C for 60 minutes or 45 degrees C for 15 minutes, twice weekly via radiofrequency electrodes), irradiation alone (400 cGy twice weekly for a total of 4,000 cGy with 140 kVp x-rays), or a combination of both therapies. Animals receiving combined treatment had significantly greater complete regression than those treated with either therapy alone. Tumor regrowth curves were equivalent for 43 degrees C or 45 degrees C following irradiation. In tumors 0.5 cm in diameter the overall tumor cure rates were 17% for 43 degrees C for 60 minutes and 25% for 45 degrees C for 15 minutes with heat alone and 8% with irradiation alone; the combination of irradiation and heat at both temperatures yielded comparable complete cure rates (75 and 67%). With 1-cm tumors the corresponding cure rates were 0% with heat alone (either temperature), 5% for irradiation alone, 33% for irradiation and 43 degrees C heat, and 64% for irradiation and 45 degrees C heat (p = .3). Approximately 20% of the animals in the various groups developed moist or dry desquamation in the area treated, whereas 40 to 66% exhibited moist desquamation. There was a slight increase in this sequela (73%) for mice that received irradiation and 45 degrees C compared with 50% in mice treated with 43 degrees C, but the difference was not statistically different (p = .54). Experimental studies demonstrated equivalent efficacy of 10 hyperthermia sessions at 43 degrees C or 45 degrees C combined with irradiation. Caution must be exercised in the clinical application of thermal iso-effect heat dose concepts until further clinical trials have been performed and there is a better understanding of the time-temperature relationship.

Animals↗
PubMed1991

Propranolol therapy alters estimation of potential cardiovascular risk derived from submaximal postinfarction exercise testing.

We studied the effect of propranolol administration on risk assessment based on submaximal exercise testing performed early after myocardial infarction. A total of 70 patients with recent infarction underwent modified Bruce treadmill testing with simultaneous measurement of expired gases in the absence of antianginal agents including beta-antagonists. Among these, 31 patients who had at least one of the following abnormalities--ST depression greater than or equal to 1 mm (22 patients), chest pain (four patients), or treadmill time less than 360 seconds (12 patients)--were studied in a randomized double-blind fashion and received either placebo or 240 mg of propranolol/day. A total of 28 patients completed the randomized phase and were able to undergo repeat exercise testing an average of 3.4 +/- 1.8 days later. Randomized groups were equivalent at baseline except for a higher peak oxygen consumption and carbon dioxide production (p less than 0.05) in the propranolol compared with the placebo group; these differences were taken into account in statistical analyses of the study data. Resting heart rate (59 +/- 1.2 versus 82 +/- 4.2 beats/min) and peak heart rate x systolic blood pressure (14,208 +/- 496 versus 20,075 +/- 1,062) were both significantly less (p less than 0.01) after propranolol than after placebo. Eight of nine patients treated with placebo maintained ST depression greater than or equal to 1 mm from the initial to the randomized exercise test, compared with only 4 of 13 receiving propranolol (p less than 0.01). In those with continued ST depression, time to positivity was significantly longer in those receiving propranolol compared with those taking placebo (538 +/- 73 versus 318 +/- 44 seconds, p less than 0.05). In contrast, the peak ratio between carbon dioxide production and oxygen consumption was higher in those receiving propranolol compared with those receiving placebo (0.93 +/- 0.04 versus 0.81 +/- 0.03, p less than 0.05). We conclude that propranolol therapy reduces evidence of ischemia and changes traditional estimates of potential cardiac risk derived from submaximal postinfarction exercise testing.

Cardiovascular Diseases↗
PubMed1991

Influence of calcium administration on the short-term hemodynamic and anti-ischemic effects of nifedipine.

This prospective study investigated whether pretreatment with intravenously administered calcium would influence the effect of nifedipine on rest hemodynamics and treadmill performance in patients with ischemic heart disease. Seventeen patients were studied after undergoing a qualifying treadmill exercise test that revealed ST segment depression indicative of ischemic heart disease. Study subjects performed three additional treadmill tests as part of the protocol. One treadmill test was obtained from each patient to provide baseline measurements without a preceding intravenous infusion and in the absence of all antianginal drugs including nifedipine; two additional exercise tests were preceded by an infusion and 10 mg of bite-and-swallow nifedipine. The infusions, administered in a randomized, double-blind, crossover fashion, consisted of either 10 ml of 10% calcium chloride (13.6 mEq) in 50 ml of 5% dextrose in water or 5% dextrose in water alone. Rest systolic blood pressure (134 +/- 4.6 mm Hg) was unchanged after placebo infusion (135 +/- 4.6 mm Hg) but decreased to 124 +/- 4.1 mm Hg (p less than 0.01) 25 min after nifedipine administration. Rest systolic blood pressure increased after calcium infusion (from 139 +/- 4.3 to 148 +/- 4.8 mm Hg, p less than 0.01) and then decreased significantly 25 min after nifedipine administration to 135 +/- 4.2 mm Hg (p less than 0.01). Despite a decrease at the time of peak nifedipine effect after either infusion, systolic blood pressure was significantly lower after administration of nifedipine alone than after administration of calcium and nifedipine (124 +/- 4.1 vs. 135 +/- 4.2 mm Hg, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1991

Effects of peak pressure and energy of impulses.

Peak pressure has been one of the key parameters of impulse noise used to assess the hazard to hearing. It is used in most international noise exposure limits. France uses an A-weighted energy limit. There is a rough correspondence between peak pressure and the hazard to hearing for a given type of impulse noise. However, when the effects of different types of impulses are compared, this correspondence breaks down. One of the alternate measures of impulse intensity is weighted energy. Weighted energy is appealing for a number of reasons. It does not depend on details of the pressure-time history such as the peak pressure and the more common duration measures. It should be easier to integrate with continuous or intermittent noise standards. It would make it easier to use standard hearing protector attenuation to estimate the hazard when a specific hearing protector is worn. Results of previously published articles and reports will be discussed. These reports lead to the conclusion that weighted energy is a more potent determiner of hearing hazard than peak pressure if spectral effects are controlled.

Animals↗
PubMed1990

Brain and muscle creatine kinase genes contain common TA-rich recognition protein-binding regulatory elements.

We have previously reported that the rat brain creatine kinase (ckb) gene promoter contains an AT-rich sequence that is a binding site for a protein called TARP (TA-rich recognition protein). This AT-rich segment is a positively acting regulatory element for the ckb promoter. A similar AT-rich DNA segment is found at the 3' end of the 5' muscle-specific enhancer of the rat muscle creatine kinase (ckm) gene and has been shown to be necessary for full muscle-specific enhancer activity. In this report, we show that TARP binds not only to the ckb promoter but also to the AT-rich segment at the 3' end of the muscle-specific ckm enhancer. A second, weaker TARP-binding site was identified in the ckm enhancer and lies at the 5' end of the minimal enhancer segment. TARP was found in both muscle cells (C2 and L6 myotubes) and nonmuscle (HeLa) cells and appeared to be indistinguishable from both sources, as judged by gel retardation and footprinting assays. The TARP-binding sites in the ckm enhancer and the ckb promoter were found to be functionally interchangeable. We propose that TARP is active in both muscle and nonmuscle cells and that it is one of many potential activators that may interact with muscle-specific regulators to determine the myogenic phenotype.

Animals↗
PubMed1989

The quantitative relation between sensory cell loss and hearing thresholds.

On the basis of experimental data obtained from 420 noise-exposed animals (chinchilla), the amount of sensory cell loss has been quantitatively related to the amount of permanent threshold shift at eight audiometric test frequencies between 0.125 and 16 kHz. The noise exposures, which varied extensively in spectrum, intensity and duration, produced permanent threshold shifts that ranged from 0 to 70 dB across a broad range of test frequencies. These data show: (1) consistent outer hair cell losses with less than 5 dB permanent threshold shifts (PTS) across all the test frequencies; (2) the first approximately 30 dB of PTS is established by losses of primarily outer hair cells; (3) in regions of the cochlea that transduce frequencies higher than or equal to 2 kHz, the three rows of outer hair cells show the same degree of loss for a given PTS, while in the 0.5 to 1.0 kHz region of the cochlea, the third row of outer hair cells (OHC) consistently shows less loss than do rows one and two; (4) appreciable inner hair cell (IHC) loss does not begin to appear until PTS exceeds approximately 30 dB; (5) in the virtual absence of OHC, hearing thresholds are least sensitive to IHC loss in the octave band centered at 4 kHz, i.e., the 4 kHz region can be as functional as other areas of the cochlea in spite of a greater amount of damage. The quantitative relation between cell loss and PTS varies as a function of test frequency in an orderly fashion.

Animals↗
PubMed1989

Influence of rifampin on tocainide pharmacokinetics in humans.

The effects of metabolic enzyme induction by rifampin on the pharmacokinetics of tocainide were studied in eight healthy volunteers. In an open, unrandomized fashion, volunteers received tocainide hydrochloride 600 mg orally. Blood samples were obtained immediately before and at various time intervals up to 48 hours after the dose. Urine samples were collected before and at various intervals up to 72 hours after the dose. Serum and urine samples were assayed for tocainide content by high-performance liquid chromatography. After a four-week washout period, volunteers ingested 300 mg of rifampin by mouth every 12 hours. After 10 doses, subjects received a second oral dose of tocainide hydrochloride 600 mg, and blood and urine samples were collected as before. During the sampling period, subjects continued to ingest rifampin 300 mg orally every 12 hours. Significant differences in elimination rate constant (average increase, 0.0545 to 0.0748 hr-1), elimination half-life (average reduction, 13.2 to 9.4 hours), oral clearance, and area under the concentration-time curve (average reduction, 76.8 to 55.0 mg.hr/L) between the control and rifampin treatment phases were observed. Volume of distribution and renal clearance of tocainide were not significantly different after rifampin treatment. Tocainide appears to be susceptible to significant drug-drug interactions mediated by metabolic enzyme induction.

Adult↗
PubMed1987

The effect of impulse intensity and the number of impulses on hearing and cochlear pathology in the chinchilla.

Forty-one chinchillas, divided into seven groups, were exposed to 1, 10, or 100 noise impulses (one every 3s) having peak intensities of 131, 135, 139, or 147 dB. Hearing thresholds were measured in each animal before and after exposure using an avoidance conditioning procedure; a surface preparation of the cochlear sensory epithelia was performed approximately 90 days after exposure. There was generally an orderly relation between the amount of permanent threshold shift and the severity of exposure, and a general agreement between averaged histological data and the audiometric data. For the impulses used in this study, there is a range of intensities which is bounded on the high side by the intensity which just produces injury with single impulse exposures and bounded on the low side by a critical intensity below which the injury potential drops precipitously with a reduction of impulse intensity. This region is only about 10-15 dB wide for the exposure conditions of this experiment. Within this region, the threshold of injury is a constant total energy; i.e., 10-dB change of intensity implies a tenfold change in the number of impulses for threshold injury. Detailed relations between temporary and permanent threshold shift, cochlear pathology, and exposure variables are discussed, as are the implications of these data to the development of exposure criteria.

Animals↗
PubMed1986

Effect of duration of lidocaine infusion and route of cimetidine administration on lidocaine pharmacokinetics.

The effects of the duration of lidocaine infusion and the route of cimetidine administration on lidocaine pharmacokinetics were evaluated in a randomized, three-phase crossover study of six healthy men. Lidocaine hydrochloride 100 mg was administered intravenously over two minutes, and plasma lidocaine concentrations were determined before treatment and at various intervals for three hours. Immediately after the three-hour sample was obtained, a second 100-mg dose of lidocaine hydrochloride was given, followed by a 21-hour constant infusion at a rate of 2 mg/min. Plasma lidocaine concentrations were determined at various intervals during the infusion and for eight hours afterward. Urine was collected during the last five hours of the infusion and assayed for lidocaine, monoethylglycinexylidide (MEGX), and glycinexylidide (GX). The following treatments were administered to each subject in a crossover manner: a placebo tablet every six hours, beginning two days before lidocaine administration; cimetidine 300 mg orally every six hours, beginning two days before lidocaine administration; and cimetidine hydrochloride 300 mg i.v. every six hours, beginning one hour before lidocaine administration. Each medication was given until the lidocaine infusion was discontinued. Subjects fasted and remained supine throughout each treatment period. Oral cimetidine increased the area under the concentration-time curve for lidocaine by 14.7% and increased the elimination half-life of lidocaine; i.v. cimetidine did not have a significant effect on lidocaine disposition. Lidocaine clearance was 34% lower under steady-state than single-dose conditions, but the effects of cimetidine on lidocaine disposition were similar under both conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Temporary threshold shifts produced by exposure to low-frequency noises.

Groups of human subjects were exposed for 8 or 24 h to an octave-band noise centered at 63, 125, or 250 Hz. For a 24-h exposure at 84 dBA, temporary threshold shifts (TTS) increased for 8-12 h and then either decreased or remained constant. Although TTS was less than 20 dB, complete recovery for many of the subjects required as long as 48 h. Accordingly, the higher level exposure which was planned at 94 dBA for 24 h was reduced to 90 dBA for 8 h. For this condition TTS increased throughout the 8-h exposure. TTS from the 90-dBA noise for 8 h exceeded the TTS produced by the 84 dBA; however, recovery from the 24-h exposure required as long as 48 h, whereas recovery from the 8-h exposure required only 12-24 h. Thus the time required for recovery is determined in part by the duration of exposure. TTS was not always maximal 1/2-1 oct above the band of noise, but was maximal in the frequency regions of better auditory sensitivity (350 to 750 Hz). For the 250-Hz condition, TTS increased about 1.5 dB per dB increase in noise level, whereas for the 63- and 125-Hz conditions TTS increased less than 1 dB per dB increase in noise level. More data are needed to specify the relation between TTS and the level of low-frequency noises.

Adolescent↗
PubMed1982

Congenital lacrimal sac mucoceles.

Seven infants had tense, blue-gray swellings inferior to the medial canthal tendon with otherwise normal-appearing eyelids and puncta. All lacrimal sacs transilluminated and A-scan ultrasonography performed in one case demonstrated a nonloculated cystic cavity. Four (57%) infants had uncomplicated mucoceles. One was treated with massage, and has remained asymptomatic for 14 months. The other three were cured with a single probing and irrigation of the entire lacrimal system. Three (43%) infants had developed erythema of the tissues overlying the swollen lacrimal sacs by the time of referral. Because none of the mucoceles could be decompressed by massage, prompt probing and irrigations were performed in each case. Cultures from the aspirates of all three sacs yielded Staphylococcus organisms. In contrast to the uncomplicated cases, two patients developed recurrences that necessitated additional treatment.

Erythema↗
PubMed1981

Children with normal-variant short stature: treatment with human growth hormone for six months.

Children with normal-variant short stature can be classified into four subgroups by measuring their anabolic and growth reactions to a 10-day course of human growth hormone. In Subgroup 1 there is no anabolic or growth reaction; in Subgroup 2 there is a weak anabolic reaction but no growth; Subgroups 3 and 4 have both reactions but Subgroup 4 is more responsive than Subgroup 3. We monitored growth rate and plasma immunoreactive somatomedin C concentrations in four to six children from each subgroup (age range, eight to 11 years) before, during, and after six months of injections of growth hormone (0.08 unit per kilogram of body weight per day). In children in Subgroups 3 and 4, the average somatomedin C level, which was subnormal before treatment, was restored to normal. Simultaneously, the average growth rate accelerated fivefold. In children in Subgroups 1 and 2, whose average pretreatment somatomedin C was normal, growth hormone had little effect on somatomedin level of growth rate. The somatomedin response in Subgroups 3 and 4 was apparent by the 10th day of treatment. This response provides a rapid method for identifying affected children who will benefit from longterm administration of human growth hormone.

Body Height↗