Biomedical subjects

T P Stopps

Publications and source records attributed to T P Stopps.

8 recordsLinked to original sources

PubMed1990

Rapid ventricular pacing of dogs to heart failure: biochemical and physiological studies.

Chronic, rapid ventricular pacing produces congestive heart failure in dogs. The objectives of this study were to determine whether or not (i) in vitro myocardial biochemical alterations reported for heart failure by volume or pressure overload also occurred with heart failure due to rate overload, and (ii) these biochemical alterations were related to relevant in vivo cardiac physiologic alterations. We compared 27 dogs that were paced to advanced heart failure with 21 sham-operated dogs. Dogs with heart failure had 55% lower left ventricular ejection fraction (22.5 +/- 7.6 vs. 50.5 +/- 5.1%) and cardiac index (81 +/- 22 vs. 178 +/- 48 mL.min-1.kg-1), 287% higher pulmonary capillary wedge pressure (27.5 +/- 6.8 vs. 7.1 +/- 3.4 mmHg; 1 mmHg = 133.3 Pa), and 64% greater left ventricular diastolic area (18.4 +/- 3.7 vs. 11.2 +/- 1.3 cm2) (all p less than 0.05). Dogs with heart failure also had (i) 69% lower norepinephrine (232 +/- 139 vs. 747 +/- 220 ng/g protein), (ii) 25-50% lower activities of myofibrillar Ca ATPase (0.188 +/- 0.026 vs. 0.253 +/- 0.051 U/mg myofibrils), sarcoplasmic reticulum Ca-transport ATPase (0.155 +/- 0.074 vs. 0.288 +/- 0.043 U/mg membrane), and the glycolytic enzyme phosphofructokinase (33.4 +/- 10.0 and 47.7 +/- 15.8 U/g), (iii) 32% higher activity of the beta-oxidation enzyme hydroxyacyl-CoA dehydrogenase (11.43 +/- 1.48 vs. 8.67 +/- 1.70 U/g), and (iv) 60% higher activity of Krebs cycle oxoglutarate dehydrogenase (2.89 +/- 0.77 vs. 1.81 +/- 0.95 U/g) (all p less than 0.05). No differences between groups were observed for isozyme patterns and ATPase activity of myosin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

A new method for hemodynamic and echocardiographic assessment of conscious dogs: comparison with thiopental-morphine anaesthesia.

A method allowing assessment of cardiac structure and function in the conscious dog using readily available instrumentation is desirable and should provide physiologic advantages when compared to anaesthesia. Accordingly, we studied 19 dogs (22 +/- 2.5 kg), using two-dimensional echocardiographic and Swan-Ganz and femoral artery catheterization; ten were conditioned to permit conscious studies and nine received anaesthesia. Dogs receiving anaesthesia were induced with intravenous thiopental (16 +/- 4 mg/kg), followed by a maintenance dose (7 +/- 1 mg/kg/h) plus morphine sulphate (213 +/- 5 micrograms/kg/h). Cardiac index, mean blood pressure, and systemic vascular resistance were similar between groups. However, anaesthesia as compared to conscious studies resulted in a marked tachycardia (147 +/- 30 bpm, vs 98 +/- 19 bpm, p less than 0.0005), significantly lower right atrial pressure (5 +/- 2 mmHg vs 8 +/- 2 mmHg, p less than 0.05), and a trend towards a lower pulmonary capillary wedge pressure (6 +/- 5 mmHg vs 9 +/- 3 mmHg). Simultaneous echocardiography showed left ventricular diastolic cross sectional area to be smaller in the anaesthesia group (8.5 +/- 1.7 cm2 vs 10.4 +/- 1.5 cm2, p less than 0.05); however, ejection fraction in the two groups was similar. Velocity of circumferential fiber shortening (Vcf), normalized for heart rate and preload, was significantly lower in the anaesthetised dogs (0.63 +/- 0.22 circ/sec vs 0.89 +/- 0.26 circ/sec, p less than 0.05); this decline in Vcf, in association with a lower systolic wall stress (85 +/- 29 10(3) dynes/cm2 vs 119 +/- 23 10(3) dynes/cm2, p less than 0.05) indicates that thiopental-morphine anaesthesia depresses contractility.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗

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

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

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↗

PubMed1986

Rapid ventricular pacing in the dog: pathophysiologic studies of heart failure.

We examined rapid ventricular cardiac pacing as a means of inducing heart failure in the dog to establish the sequence and nature of physiologic compensation in this preparation. Seven animals paced at 250 beats/min for 3 weeks (VP1 group) showed an increase in cardiac size from 78.5 +/- 9.5(SD) to 105.8 +/- 13.0 cm2, a reduction in mean arterial pressure from 149 +/- 7 to 130 +/- 21 mm Hg, a fall in cardiac index from 196 +/- 57 to 125 +/- 37 ml/kg/min, and an increase in left ventricular filling pressure from 6 +/- 5 to 22 +/- 9 mm Hg and in right atrial pressure from 2 +/- 2 to 5 +/- 3 mm Hg. An additional series of six animals (VP2 group) was paced until a clear biologic end point for heart failure was reached (average 5.3 +/- 1.9 weeks) and they showed similar but more advanced changes compared with the VP1 group. The changes in cardiac size and hemodynamics in the VP1 and VP2 groups were significantly different from those in parallel studies of 10 sham-operated animals. Plasma norepinephrine and renin activity were unchanged in sham-operated animals, whereas in the VP1 group, plasma norepinephrine rose from 338 +/- 118 to 764 +/- 567 pg/ml (p less than .05), but plasma renin activity did not change. In the VP2 group norepinephrine rose from 471 +/- 285 to 999 +/- 425 pg/ml (p less than .025) and plasma renin rose from 2.1 +/- 1.5 to 8.0 +/- 7.1 ng/ml/hr (p less than .05). There was an excellent correlation between plasma norepinephrine and renin activity before the animals were killed in both the VP1 and VP2 groups (r = .88, p less than .001). No change was evident in atrial natriuretic factor content, as determined by bioassay, in sham-operated or VP1 group animals. However, there was a significant reduction in atrial natriuretic activity from the right atrium that was inversely correlated with the level of right atrial pressure in the VP2 group.

Animals↗

PubMed1984

Ultrastructural study of developing rabbit diaphragm.

Diaphragms obtained from forty rabbit fetuses during the last third of gestation and from five rabbits one week old were studied ultrastructurally. Four gestational ages were chosen for the investigation. The diaphragm at 20 days gestation revealed early myogenesis which was characterised by many myogenic cells in the process of mitosis and by fusion of myoblasts to form myotubes. A large number of lipid droplets and a moderate quantity of glycogen were observed in the myotubes. These myotubes contained a few myofibrils peripherally. At 22 days of gestation, the myotubes exhibited a relatively large number of myofibrils and large amounts of glycogen. They also showed sarcolemmal modifications which appeared to be developing motor end plates. Mitosis of the myogenic cells persisted even after fusion. At 25 days of gestation, connective tissue sheaths appeared around the muscle fibres as well as further differentiation of the muscle fibres. At 30 days of gestation, the muscle fibres exhibited nearly complete differentiation, with the formation of myotendinous junctions. At one week post partum, the diaphragm showed full development of its muscle fibres. These morphological observations suggest a very rapid functional differentiation of the rabbit diaphragm during the last third of gestation.

Animals↗

PubMed1983

The effects of cesarean section anesthesia on heat loss and heat production in the newborn rabbit.

The newborn of some smaller animals rely upon heat produced by nonshivering thermogenesis in the brown fat to prevent a fall in body temperature after birth. Because of their pharmacological properties, some drugs may affect nonshivering thermogenesis. Therefore, in this study, the ability of newborn rabbits delivered under Innovar-Vet, ketamine hydrochloride, methoxyflurane and epidural anesthesia to maintain the rectal, subcutaneous interscapular and lumbar temperature was investigated at an ambient temperature of 35 degrees C or 22 degrees C and the results compared with control newborns delivered without anesthesia. When the newborns were exposed to 35 degrees C, the anesthetics studied had no effect on the ability of the newborn to maintain the rectal temperature and the subcutaneous temperature over the interscapular fat pad was similar to the lumbar subcutaneous temperature thereby indicating that nonshivering thermogenesis was not activated. However, at an ambient temperature of 22 degrees C Innovar-Vet or methoxyflurane reduced the temperature difference between interscapular and lumbar temperatures to 1.6 degrees C compared to 2.5 degrees C in controls and the difference between core temperature and ambient temperature to 3.5 degrees C greater compared to 7.5 degrees C in controls. Ketamine hydrochloride or lidocaine hydrochloride plus meperidine has less effect because these compounds lack adrenergic blocking properties. These data suggest that newborns delivered under anesthetics or tranquillizers that have adrenergic blocking properties require a warm (35 degrees C) environment to prevent a fall in core temperature.

Anesthesia, Obstetrical↗