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Biomedical subjects

E S Marks

Publications and source records attributed to E S Marks.

15 recordsLinked to original sources

Atrial natriuretic factor (ANF 103-126) enhances volume- and pressor-induced heart rate response in the conscious rat.

The reduction in blood pressure due to ANF(103-126) fails to elicit reflex cardioacceleration in the conscious rat. To examine baroreflex sensitivity, the effect of ANF(103-126) on the heart period (HP) response to rapid central volume expansion and to alterations in mean arterial pressure (MAP) induced by bolus injections of phenylephrine and sodium nitroprusside was assessed. ANF(103-126) significantly augmented the bradycardic response induced by acute volume expansion from 426 +/- 21 to 391 +/- 23 beats min-1 versus 421 +/- 23 to 405 +/- 24 without ANF(103-126). Baroreflex sensitivity was defined by the ratio of the change in heart period to the maximal change in mean arterial pressure. The dose of ANF(103-126) utilized did not affect basal heart rate or the magnitude of the mean arterial pressure response to phenylephrine but did significantly enhance the nitroprusside-induced decrease in mean arterial pressure. Baroreceptor sensitivity to phenylephrine was significantly increased by ANF(103-126): 0.997 +/- 0.07 (ms mmHg-1) during ANF(103-126) vs 0.613 +/- 0.08 during vehicle. The total duration of the heart rate response to phenylephrine was also prolonged. In contrast, ANF(103-126) did not alter the baroreceptor sensitivity (1.45 +/- 0.3 vs 1.43 +/- 0.2 ms mmHg-1) or duration of heart rate response to nitroprusside. In the conscious rat, ANF(103-126) modifies the heart rate response to changes in mean arterial pressure and acute central volume expansion. This action appears to be dependent on stimulation of cardiac vagal afferents.

Animals

Expanded eye care in the Veterans Administration hospital setting.

Over the past decade a greater number of optometrists can be found practicing in hospitals, health maintenance organizations, health clinics and other multipractitioner group settings. The impetus enabling optometry to practice in such settings is based in part on cost effectivity. Optometrists in Veterans Administration (VA) hospitals have been in the forefront in this movement to provide the full range of primary eye care services, and in becoming an integral part of the hospital/medical community.

Health Services

Neurological visual fields.

Neurological visual field defects represent lesions to the visual pathway, some of which may be life-threatening. It is, therefore, crucial that optometrists understand how to diagnose these lesions, so they may know when, and to whom to refer the patient. The following cases illustrate the management of patients with lesions to the prechiasmal, chiasmal, and postchiasmal visual pathway.

Adenoma, Chromophobe

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

Alterations in systemic haemodynamics induced by atriopeptin III.

The mechanism of the hypotensive response to the intravenous administration of atriopeptin III was investigated in rats of the Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) Okamoto strains. Cardiac performance and the systemic haemodynamic response to acute volume loading were evaluated before and during atriopeptin infusion. Cardiac output was measured by a thermo-dilution technique in conscious rats, and left ventricular pressures with differential (dP/dt) calculations were obtained in anaesthetized animals. Bolus injections followed by a 1-h continuous infusion of atriopeptin caused a progressive decrease in mean arterial pressure (MAP) and cardiac output with no significant change in heart rate. In addition there was a transient decrease, maximal at 5 min, and a subsequent increase in peripheral resistance. Atriopeptin did not alter the maximal cardiac output achieved following acute volume expansion. In the anaesthetized animals, bolus injection with a subsequent 15-min continuous infusion of atriopeptin III significantly reduced left ventricular pressures, dP/dt and mean arterial pressure. Volume expansion fully restored intraventricular pressures and dP/dt while increasing mean arterial pressure toward baseline. We conclude that the steady decrease in mean arterial pressure produced by atriopeptin III is due to a decrease in cardiac output secondary to a fall in stroke volume caused by a lowered filling pressure.

Animals

Neuropeptide Y is a potent vasoconstrictor and a cardiodepressant in rat.

Neuropeptide Y (NPY) is contained in and coreleased with norepinephrine (NE) from sympathetic nerves innervating vascular and cardiac tissues. The effects of NPY infusion on systemic hemodynamics and cardiac performance were compared with those of NE in conscious and pentobarbital sodium-anesthetized rats. A 10-min infusion of NPY (2 nmol.kg-1.min-1) decreased cardiac index (CI) 20% and stroke volume index (SVI) 9% with increases of 20% in mean arterial pressure (MAP) and 48% in total peripheral resistance (TPR). Conversely, NE (1.0 microgram.kg-1.min-1) increased SVI 14%, MAP 29%, and TRP 26%, with no change in CI. Heart rates decreased similarly (approximately 60 beats/min) but only NE-induced bradycardia was reversible by methylatropine nitrate. In anesthetized rats NPY (0.1 nmol.kg-1.min-1) increased left ventricular end-diastolic pressure (LVEDP) 20 +/- 10 mmHg (means +/- SD, n = 7) and decreased dP/dt by 8 +/- 6%. NE (0.07 microgram.kg-1.min-1) produced an equivalent pressor response, however, dP/dt rose 22 +/- 10% whereas LVEDP increased significantly less than with NPY. Thus NPY is a potent vasoconstrictor exerting similar effects to NE on MAP and TPR but, unlike NE, possesses negative inotropic and chronotropic activity.

Animals

Acute oliguric renal failure due to ibuprofen overdose.

We have described a patient who had acute oliguric renal failure after ingesting a single large overdose of ibuprofen. This patient had no predisposing underlying disease, and subsequently had complete resolution of renal failure.

Acute Kidney Injury

Pressor responsiveness to angiotensin in renovascular and steroid hypertension.

1. The pressor response to angiotensin II was reduced in rats with early (less than 6 weeks) and chronic (greater than 4 months) Goldblatt two-kidney, one-clip hypertension and enhanced in DOCA-salt hypertension. 2. Converting enzyme inhibition with captopril brought the angiotensin pressor response curves into closer proximity although the DOCA hypertensive rats were minimally hyper-responsive and rats with early and chronic renovascular hypertension showed slightly reduced responsiveness. 3. After bilateral nephrectomy the pressor responses to angiotensin were similar. 4. The pressor response to angiotensin II in these animals was inversely related to plasma renin concentration and therefore largely dependent upon receptor occupancy by endogenous angiotensin II. There is no evidence for enhanced pressor responsiveness to angiotensin in either renovascular or DOCA hypertension.

Angiotensin II

Influenza immunization in patients with chronic renal disease.

Patients receiving long-term hemodialysis (23) and patients with moderate to severe renal impairment and without hemodialysis (14) were immunized with inactivated influenza A/New Jersey/76 whole virus vaccine. Fourfold or greater increases in hemagglutinating-inhibiting antibody (HAI) titers occurred in 94% of controls, 93% of nondialyzed patients with chronic renal disease, and 87% of patients with continual hemodialysis. Postimmunization geometric mean titers in both groups of patients were equivalent to those of controls. The proportion of patients responding to vaccine was independent of levels of creatinine clearance, and the presence of preimmunization HAI titers also had no effect on frequency of seroconversion. Though some element of immunologic suppression is associated with chronic renal disease, it is not reflected in the humoral antibody response to influenza A/New Jersey/76 vaccine.

Adult