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Biomedical subjects

G W Moe

Publications and source records attributed to G W Moe.

44 records · Page 3Linked to original sources
PubMed1989

Alterations in serum sodium in relation to atrial natriuretic factor and other neuroendocrine variables in experimental pacing-induced heart failure.

The pathophysiologic role of atrial natriuretic factor and other neuroendocrine variables in relation to serum sodium and renal function was evaluated in 15 conscious dogs with severe chronic ventricular pacing-induced heart failure (250 beats/min for 5.1 +/- 0.4 weeks). Six sham-operated dogs observed over an 8 week period served as controls. Development of heart failure was characterized by a progressive increase in plasma norepinephrine, renin activity and aldosterone from control values of 293 +/- 15 pg/ml, 1.4 +/- 0.4 ng/ml per h and 124 +/- 42 pg/ml, respectively, to 1,066 +/- 96 pg/ml, 10.2 +/- 2.4 ng/ml per h and 577 +/- 151 pg/ml (all p less than 0.01), respectively, at severe heart failure. In contrast to other neuroendocrine variables, plasma atrial natriuretic factor increased from a control level of 243 +/- 74 pg/ml to a peak concentration of 724 +/- 149 pg/ml (p less than 0.01) at 2 weeks, then declined and plateaued at twice the level of the control value as severe heart failure developed. At severe heart failure, serum sodium decreased from 147 +/- 0.6 to 141.8 +/- 2.1 mmol/liter (p less than 0.05), whereas urea increased from 6.0 +/- 0.5 to 7.8 +/- 0.6 mmol/liter (p less than 0.05). The change in serum sodium concentration correlated with plasma renin activity and aldosterone (r = -0.77, -0.88, respectively, both p less than 0.01), but not with norepinephrine or atrial natriuretic factor. When sinus rhythm was restored, 14 dogs were observed for 48 to 72 h and 8 dogs were followed up for another 4 weeks after cessation of pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Congestive heart failure.

Congestive heart failure (CHF) is a condition that is increasing in incidence and is associated with significant morbidity and mortality rates. The main abnormality that underlies CHF is depressed myocardial function. The resulting decrease in cardiac output activates several peripheral compensatory mechanisms, which may further impair ventricular function and worsen the prognosis. Although systolic dysfunction is the traditional descriptor of CHF, diastolic dysfunction is increasingly recognized as a distinct entity. In prescribing therapy the predominant type of ventricular dysfunction and the peripheral components of the heart failure should be identified. The ultimate aim is to alleviate symptoms, minimize complications and prolong survival. Recent data from two multicentre trials have suggested that vasodilators can achieve these goals. Trials are under way to assess the impact of early vasodilator therapy on CHF.

Calcium Channel Blockers↗
PubMed1988

Intravenous nisoldipine in severe congestive heart failure.

The acute hemodynamic effects of intravenous nisoldipine were studied in 10 patients with severe congestive heart failure. Nisoldipine was administered in three consecutive doses (1.5, 3.0, and 6.0 micrograms/kg) at least 150 min apart. Following the first dose, mean arterial pressure declined from 96 +/- 17 to 87 +/- 16 mm Hg (p less than 0.01), cardiac index increased from 2.1 +/- 0.7 to 2.4 +/- 0.7 L/min/m2 (p less than 0.025), and systemic vascular resistance fell from 27 +/- 10 to 19 +/- 6 units (p less than 0.01). Maximal hemodynamic effects occurred by 2 to 5 min and gradually waned over the next 120 min. There were no significant changes in heart rate or filling pressures. The time course for the hemodynamic effects were similar with subsequent doses but the magnitude of change was significantly greater. There was a dose-dependent increase in peak arterial nisoldipine concentration. Baseline plasma norepinephrine and renin were high but did not change with nisoldipine administration. No significant changes were seen after nisoldipine administration. No major side effects were observed. These data suggest that nisoldipine is a potent arterial vasodilator that can be of benefit in patients with low output cardiac failure.

Adult↗
PubMed1988

Recovery from heart failure: structural and functional analysis in a canine model.

Chronic, rapid ventricular pacing produces congestive heart failure in the dog. Using echocardiography, the features of developing heart failure were analysed and the capacity of this model for recovery was assessed once pacing had been discontinued. Fifteen dogs were studied; nine were paced at 250 beats/min (bpm) to severe heart failure (5.0 +/- 1.8 weeks) and six served as sham controls. In the paced animals at severe heart failure, two-dimensional echocardiography demonstrated a significant increase in diastolic cross-sectional cardiac area (from 11 +/- 3 to 16 +/- 2 cm2, p less than 0.05), associated with a marked fall n area ejection fraction (54 +/- 8 to 21 +/- 8%, p less than 0.05), and significant left ventricular wall thinning (from 6.0 +/- 0.7 to 4.7 +/- 0.9 mm, p less than 0.05). In addition, significant increases in heart rate (77 +/- 7 to 126 +/- 13 bpm, sinus rhythm; p less than 0.05), respiratory rate (41 +/- 13 to 80 +/- 20 cycles/min, p less than 0.05), and body weight (21 +/- 1 to 24 +/- 3 kg, p less than 0.05) were noted. Serum sodium fell (146 +/- 3 to 140 +/- 8 mmol/L, p less than 0.05), while blood urea nitrogen (6 +/- 2 to 10 +/- 2 mmol/L, p less than 0.05) and creatinine (86 +/- 12 to 101 +/- 15 mmol/d, p less than 0.05) increased. Recovery was characterized by rapid improvement such that all measured parameters normalized by 1 week, except for cross-sectional cardiac area which remained dilated up to 4 weeks (14 +/- 3 cm2, p less than 0.05 versus control).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Physiological effects of synthetic atrial natriuretic factor in normal conscious dogs.

The objective of this study was to examine the integrative physiologic effects of atrial natriuretic factor (ANF). Synthetic 99-126 ANF was administered to 6 normal conscious dogs as two consecutive infusions (0.02 and 0.1 microgram/kg/min respectively) each over 30 min: each infusion was preceded by a priming dose of 1 microgram/kg. With the first infusion, mean arterial pressure declined from 113 +/- 2 to 103 +/- 4 mmHg, pulmonary capillary wedge pressure declined from 9.6 +/- 0.5 to 7.2 +/- 0.7 mmHg and right atrial pressure declined from 9.8 +/- 0.4 to 8.0 +/- 0.7 mmHg (all p less than 0.05). No change in heart rate was seen. Despite very high plasma ANF concentrations, no further decline in arterial or central filling pressures were seen in the second infusion. In contrast, cardiac output declined progressively from 3.8 +/- 0.2 to 2.8 +/- 0.21/min (p less than 0.01) by the end of second infusion. Plasma renin activity declined from 2.2 +/- 0.7 to 0.9 +/- 0.3 ng/ml/hr (p less than 0.05) while plasma norepinephrine remained unchanged. Urine output and sodium excretion increased in a dose dependent manner. The diverse time course of the hemodynamic, renal and neuroendocrine effects suggests these effects of ANF are mediated by different mechanisms. Furthermore, the failure of heart rate and plasma norepinephrine to increase despite a significant decline in blood pressure and cardiac output suggests ANF may have a depressant effect on the sympathetic nervous system.

Animals↗
PubMed1988

Early recovery from heart failure: insights into the pathogenesis of experimental chronic pacing-induced heart failure.

Chronic rapid ventricular pacing (250 beats/min) induces severe heart failure in a canine model. To assess the potential for recovery after cessation of pacing, simultaneous hemodynamic and two-dimensional echocardiographic studies were conducted in nine conscious dogs paced to severe heart failure (4.3 +/- 1.7 weeks). Heart failure was characterized by elevated left and right ventricular filling pressures from 9 +/- 3 and 7 +/- 2 mm Hg to 25 +/- 6 and 15 +/- 3 mm Hg (both p less than 0.01), respectively. Left ventricular cross-sectional area (an estimate of preload) and systolic wall stress (an estimate of afterload) increased from 12 +/- 2 cm2 and 119 +/- 23 10(3) dynes/cm2 to 17 +/- 3 cm2 and 210 +/- 46 10(3) dynes/cm2 (both p less than 0.01), respectively. Left ventricular ejection fraction decreased from 54% +/- 7% to 13% +/- 5% (p less than 0.01). When pacing was discontinued to allow resumption of sinus rhythm, left and right ventricular filling pressures declined rapidly at 48 hours after resumption of sinus rhythm, by 36% and 53%, respectively. Ejection fraction doubled, although left ventricular cross-sectional area and wall stress remained elevated at 48 hours. The recovery of systolic function in the absence of major changes in loading conditions suggests that pacing-induced heart failure is mediated by a decrease in left ventricular contractility. Moreover, the persistent dilation of the left ventricle after cessation of pacing suggests that structural remodeling of the left ventricle occurs during the development of pacing-induced heart failure.

Animals↗
PubMed1987

A comparative evaluation of hemodynamic and neurohumoral effects of nitroglycerin and nifedipine in congestive heart failure.

Nitroglycerin and nifedipine have been suggested as useful agents in the therapy of congestive heart failure. Because of the rapid action and feasability for sublingual administration of both drugs, their comparative hemodynamic and neurohumoral effects were studied in 12 patients with congestive heart failure. After sublingual nitroglycerin, there was a significant decrease in mean arterial pressure (96 +/- 17 to 90 +/- 15 mm Hg, p less than 0.01), left ventricular (LV) filling pressure (30 +/- 12 to 22 +/- 10 mm Hg, p less than 0.01), right atrial pressure (15 +/- 6 to 10 +/- 5 mm Hg, p less than 0.01) and systemic vascular resistance (21.5 +/- 7.7 to 19.3 +/- 6.2 units, p less than 0.05) and an increase in cardiac index (2.2 +/- 0.6 to 2.4 +/- 0.7 liters/min/m2, p less than 0.05) and LV stroke work index (20.4 +/- 7.0 to 24.5 +/- 8.6 gm-m/m2, p less than 0.01). After sublingual nifedipine, there was also a significant decrease in mean arterial pressure (96 +/- 16 to 89 +/- 14 mm Hg, p less than 0.01) and systemic vascular resistance (22.1 +/- 7.1 to 18.0 +/- 6.1 units, p less than 0.01) and an increase in cardiac index (2.1 +/- 0.6 to 2.4 +/- 0.6 liters/min/m2, p less than 0.01); in contrast to nitroglycerin, this was unaccompanied by significant changes in right- or left-sided filling pressures or LV stroke work index.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗