Comparison of the response of muskrat, rabbit, and guinea pig heart muscle to hypoxia

1982 ◽  
Vol 243 (3) ◽  
pp. R245-R250
Author(s):  
T. McKean ◽  
R. Landon

Papillary muscles were removed from anesthetized muskrats and rabbits and mounted in a muscle chamber maintained at 29 degrees C. Muscles were stimulated at a rate of 12/min and subjected to 30 min of hypoxia followed by 30 min of reoxygenation. Peak tension in muskrats declined less than peak tension in rabbits during oxygen deprivation. During reoxygenation, peak tension in muskrats rapidly returned to control levels and then exceeded control, whereas peak tension in rabbits never recovered. Time to peak tension was largely unaffected in muskrats during hypoxia and decreased in rabbits. During reoxygenation, time to peak tension increased in muskrats and returned to control in rabbits. Hearts from muskrats and guinea pigs were removed under ether anesthesia and perfused retrograde with a physiological saline solution. Developed tension, heart rate, coronary blood flow, and lactate dehydrogenase (LDH) output were monitored. During 30 min of hypoxia, muskrat hearts developed a profound bradycardia compared to guinea pigs. Coronary flow increased in both species but less so in muskrats. Guinea pig hearts developed contracture whereas muskrat hearts relaxed. During reoxygenation heart rate and coronary blood flow returned toward normal but cells released large amounts of LDH, indicating cell damage. It is concluded that the isolated heart of the muskrat, a diving mammal, is better able to deal with hypoxia than the heart of the nondividing guinea pig and rabbit.

1982 ◽  
Vol 242 (5) ◽  
pp. H805-H809 ◽  
Author(s):  
G. R. Heyndrickx ◽  
P. Muylaert ◽  
J. L. Pannier

alpha-Adrenergic control of the oxygen delivery to the myocardium during exercise was investigated in eight conscious dogs instrumented for chronic measurements of coronary blood flow, left ventricular (LV) pressure, aortic blood pressure, and heart rate and sampling of arterial and coronary sinus blood. After alpha-adrenergic receptor blockade a standard exercise load elicited a significantly greater increase in heart rate, rate of change of LV pressure (LV dP/dt), LV dP/dt/P, and coronary blood flow than was elicited in the unblocked state. In contrast to the response pattern during control exercise, there was no significant change in coronary sinus oxygen tension (PO2), myocardial arteriovenous oxygen difference, and myocardial oxygen delivery-to-oxygen consumption ratio. It is concluded that the normal relationship between myocardial oxygen supply and oxygen demand is modified during exercise after alpha-adrenergic blockade, whereby oxygen delivery is better matched to oxygen consumption. These results indicate that the increase in coronary blood flow and oxygen delivery to the myocardium during normal exercise is limited by alpha-adrenergic vasoconstriction.


1957 ◽  
Vol 190 (3) ◽  
pp. 425-428 ◽  
Author(s):  
Richard M. Hoar ◽  
William C. Young

Oxygen consumption and heart rate during pregnancy were measured in untreated, thyroxin-injected and thyroidectomized guinea pigs given I131. From impregnation until parturition, oxygen consumption increased 7.9% in untreated females. The increase continued until 5 days postpartum when a sharp decrease occurred. The increase is not accounted for by growth of the fetal mass. Comparable increases occurred in thyroxin-injected (16.2%) and thyroidectomized (11.9%) females, although the levels throughout were higher and lower, respectively, than in intact females. Heart rate did not increase. On the contrary, statistically significant decreases occurred in the untreated and thyroxin-injected females. Although the mechanism associated with the increased metabolic rate is not known, the possibility of thyroid participation would seem to be excluded. Involvement of the adrenal cortex is suggested by morphological differences in the cells of the zona fasciculata in pregnant and nonpregnant females and by evidence cited from other studies.


Mathematics ◽  
2020 ◽  
Vol 8 (8) ◽  
pp. 1205
Author(s):  
Timur Gamilov ◽  
Philipp Kopylov ◽  
Maria Serova ◽  
Roman Syunyaev ◽  
Andrey Pikunov ◽  
...  

In this work we present a one-dimensional (1D) mathematical model of the coronary circulation and use it to study the effects of arrhythmias on coronary blood flow (CBF). Hydrodynamical models are rarely used to study arrhythmias’ effects on CBF. Our model accounts for action potential duration, which updates the length of systole depending on the heart rate. It also includes dependency of stroke volume on heart rate, which is based on clinical data. We apply the new methodology to the computational evaluation of CBF during interventricular asynchrony due to cardiac pacing and some types of arrhythmias including tachycardia, bradycardia, long QT syndrome and premature ventricular contraction (bigeminy, trigeminy, quadrigeminy). We find that CBF can be significantly affected by arrhythmias. CBF at rest (60 bpm) is 26% lower in LCA and 22% lower in RCA for long QT syndrome. During bigeminy, trigeminy and quadrigeminy, respectively, CBF decreases by 28%, 19% and 14% with respect to a healthy case.


1971 ◽  
Vol 50 (6) ◽  
pp. 1635-1641 ◽  
Author(s):  
William K. Elwood

β-Streptococcal infection and its sequelae did not play a significant role in the development of hypoplastic enamel defects. Hypoplastic enamel faults occurred that could not be related to any of the experimental procedures. A genetic or other component may influence the susceptibility of guinea pigs to hypoplastic enamel lesions.


1980 ◽  
Vol 49 (1) ◽  
pp. 28-33 ◽  
Author(s):  
G. R. Heyndrickx ◽  
J. L. Pannier ◽  
P. Muylaert ◽  
C. Mabilde ◽  
I. Leusen

The effects of beta-adrenergic blockade upon myocardial blood flow and oxygen balance during exercise were evaluated in eight conscious dogs, instrumented for chronic measurements of coronary blood flow, left ventricular pressure, aortic blood pressure, heart rate, and sampling of arterial and coronary sinus venous blood. The administration of propranolol (1.5 mg/kg iv) produced a decrease in heart rate, peak left ventricular (LV) dP/dt, LV (dP/dt/P, and an increase in LV end-diastolic pressure during exercise. Mean coronary blood flow and myocardial oxygen consumption were lower after propranolol than at the same exercise intensity in control conditions. The oxygen delivery-to-oxygen consumption ratio and the coronary sinus oxygen content were also significantly lower. It is concluded that the relationship between myocardial oxygen supply and demand is modified during exercise after propranolol, so that a given level of myocardial oxygen consumption is achieved with a proportionally lower myocardial blood flow and a higher oxygen extraction.


1989 ◽  
Vol 257 (6) ◽  
pp. H1983-H1993 ◽  
Author(s):  
J. M. Capasso ◽  
M. W. Jeanty ◽  
T. Palackal ◽  
G. Olivetti ◽  
P. Anversa

To determine the consequence of acute nonocclusive constriction of the epicardial coronary artery on the adaptation of the left ventricle and its impact as a function of age, the left main coronary artery was narrowed in rats 4 and 12 mo of age, and the animals were killed 45 min later. Similar reductions in the luminal diameter, averaging 4%, were obtained in both groups of animals, and this change resulted in an increase in left ventricular end-diastolic pressure and a decrease in positive and negative change in pressure overtime (dP/dt) and in peak-developed ventricular pressure. Left ventricular volume increased by 66% and 56% at 4 and 12 mo because of increases in both the longitudinal and transverse chamber diameters. In contrast, wall thickness decreased by 27% and 35%, whereas sarcomere length increased only by 8.0% and 6.0%, respectively. These changes implied the occurrence of side-to-side slippage of myocytes within the wall to accommodate the larger chamber volume. The alterations in myocardial performance combined with the variations in ventricular size and wall thickness produced a marked elevation in diastolic and systolic wall stress. Moreover, myocyte cell damage in the form of contraction bands and disorganization of the intercalated disc region was seen. No consistent difference was found in any of the parameters measured as a function of age. Measurements of resting coronary blood flow across the left ventricular wall before coronary artery narrowing were comparable with those obtained 45 min after constriction. In conclusion, acute nonocclusive coronary artery stenosis has profound detrimental effects on the function and structure of the myocardium in the absence of an impairment of resting coronary blood flow.


2002 ◽  
Vol 282 (6) ◽  
pp. H2031-H2038 ◽  
Author(s):  
Christine Barbé ◽  
Eric Dubuis ◽  
Annie Rochetaing ◽  
Paul Kreher ◽  
Pierre Bonnet ◽  
...  

A physiological role of carbon monoxide has been suggested for coronary myocytes; however, direct evidence is lacking. The objective of this study was to test the effect of chronic carbon monoxide exposure on the K+ currents of the coronary myocytes. The effect of 3-wk chronic exposure to carbon monoxide was assessed on K+ currents in isolated rat left coronary myocytes by the use of the patch-clamp technique in the whole cell configuration. Moreover, membrane potential studies were performed on coronary artery rings using intracellular microelectrodes, and coronary blood flow in isolated heart preparation was recorded. Carbon monoxide did not change the amplitude of global whole cell K+ current, but it did increase the component sensitive to 1 mM 4-aminopyridine. Carbon monoxide exposure hyperpolarized coronary artery segments by ∼10 mV and, therefore, increased their sensitivity to 4-aminopyridine. This effect was associated with an enhancement of coronary blood flow. We conclude that chronic carbon monoxide increases a 4-aminopyridine-sensitive current in isolated coronary myocytes. This mechanism could, in part, contribute to hyperpolarization and to increased coronary blood flow observed with carbon monoxide.


1986 ◽  
Vol 250 (1) ◽  
pp. H76-H81 ◽  
Author(s):  
O. L. Woodman ◽  
J. Amano ◽  
T. H. Hintze ◽  
S. F. Vatner

Changes in arterial and coronary sinus concentrations of norepinephrine (NE) and epinephrine (E) in response to hemorrhage were examined in conscious dogs. Hemorrhage (45 +/- 3.2 ml/kg) decreased mean arterial pressure by 47 +/- 6%, left ventricular (LV) dP/dt by 38 +/- 6%, and mean left circumflex coronary blood flow by 47 +/- 6%, while heart rate increased by 44 +/- 13%. Increases in concentrations of arterial NE (5,050 +/- 1,080 from 190 +/- 20 pg/ml) and E (12,700 +/- 3,280 from 110 +/- 20 pg/ml) were far greater than increases in coronary sinus NE (1,700 +/- 780 from 270 +/- 50 pg/ml) and E (4,300 +/- 2,590 from 90 +/- 10 pg/ml). Net release of NE from the heart at rest was converted to a fractional extraction of 66 +/- 9% after hemorrhage. Fractional extraction of E increased from 16 +/- 6% at rest to 73 +/- 8% after hemorrhage. In cardiac-denervated dogs, hemorrhage (46 +/- 2.8 ml/kg) decreased mean arterial pressure by 39 +/- 15%, LV dP/dt by 36 +/- 10%, and mean left circumflex coronary blood flow by 36 +/- 13%, while heart rate increased by 24 +/- 10%. Hemorrhage increased arterial NE (1,740 +/- 150 from 210 +/- 30 pg/ml) and E (3,050 +/- 880 from 140 +/- 20 pg/ml) more than it increased coronary sinus NE (460 +/- 50 from 150 +/- 30 pg/ml) and E (660 +/- 160 from 90 +/- 20 pg/ml) but significantly less (P less than 0.05) than observed in intact dogs. These experiments indicate that hemorrhage, unlike exercise and sympathetic nerve stimulation, does not induce net overflow of NE from the heart.(ABSTRACT TRUNCATED AT 250 WORDS)


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