ISSN:0009-7330    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

We have found that myocardial oxygen consumption is linearly correlated with the systolic pressure-volume area in the canine left ventricle. This pressure-volume area is a specific area in the pressure-volume diagram that is circumscribed by the end-systolic pressure-volume relation line, the end-diastolic pressure-volume relation curve, and the systolic segment of the pressure-volume trajectory. This area is equivalent to the total mechanical energy generated by ventricular contraction, consisting of the external mechanical work and the mechanical potential energy. In the present study, we specifically changed the course of the diastolic segment of the pressure-volume trajectory without changing the systolic segment of the pressure-volume trajectory and the systolic pressure-volume area. Although the fractions of external mechanical work and mechanical potential energy in the pressure-volume area were markedly changed, the simultaneously measured left ventricular oxygen consumption remained unchanged. This result indicates that the myocardial oxygen consumption is predominantly determined by the total mechanical energy generated during systole, or the systolic pressure-volume area, independent of how the total mechanical energy is converted effectively to external mechanical work during the cardiac cycle.

ISSN:0009-7330    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Interaction of carotid sinus and aortic arch reflex control of total peripheral resistance was studied in eight dogs anesthetized with sodium pentobarbital and placed on constant flow cardiac bypass. Carotid sinus and aortic arch baroreceptor areas were isolated and separately perfused at controlled pressures. Combinations of carotid sinus and aortic arch pressures were delivered at random in steps of 25 mm Hg over the 50–225 mm Hg pressure range, and systemic arterial pressure was measured. Changes in arterial pressure reflected changes in total peripheral resistance. A multiple linear regression showed that both carotid sinus and aortic arch pressures exhibited a sigmoidal relationship with arterial pressure. Independent of carotid and aortic baroreceptor pressures, arterial pressure was found to be a periodic function of time (period = 2 hours) in all dogs. The average carotid sinus reflex open loop gain was found to be 0.231 ± 0.092, while average aortic arch open loop gain was 0.141 ± 0.088. The gain of either the carotid sinus or aortic arch reflex was not influenced by the absolute pressure level of the other receptor area. In a separate series of experiments performed in the same dogs, we tested the hypothesis that a nonlinear temporal summation of the reflex control of total peripheral resistance might exist when the inputs to carotid and aortic baroreceptors are changed simultaneously. With both inputs held at the region of maximum gain, 25 mm Hg step changes were imposed first on carotid sinus pressure, then on aortic arch pressure, and then on both simultaneously. A temporal inhibition of the two reflexes showed that simultaneous excitation of both receptors resulted in a smaller reflex response than the sum of individual responses.

ISSN:0009-7330    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

When the left coronary artery was perfused with nonpulsatile pressure, the onset of diastole was accompanied by a capacitance overshoot in flow with an exponential decay back to a steady state. Time constant for that decay ranged from 55 msec when tone was present to 105 msec with maximal dilation. Since the transient resulted from a fall in tissue pressure, this represents an estimation of intramural arterial capacitance only. Transients in perfusion pressure, which would also affect epicardial arteries, yielded similar time constants. We concluded that most of the coronary capacitance resides in the small intramural vessels. Analysis of transients yielded a value for capacitance of between 0.01 and 0.05 ml/mm Hg per 100 g. We then used the data from the transients to construct coronary pressure flow curves which were free of any back flow from capacitance. When coronary tone was present, the curves indicated that flow ceased at 30 mm Hg. With maximal dilation, flow ceased at only 18 mm Hg. Long diastoles in those same hearts indicated that flow ceased at about' 10 mm Hg higher pressure. Although capacitance causes critical closing pressure as determined by a long diastole to be artifacrually high, critical closing pressure is still appreciable in the heart, and tone dependent. Finally, three computer models were built, one of which included only small vessel capacitances, the second, only vascular waterfalls, and the third, both of the above. Only model 3 was capable of reproducing the flow patterns which were actually seen.

ISSN:0009-7330    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The aim of this study was to examine whether control of vascular resistance by vagal afferents is altered in the early as well as late stage of hypertension. We examined the effects of vagotomy on hindlimb vascular resistance as well as on arterial baroreflex control of hindlimb vascular resistance in spontaneously hypertensive rats and Wistar-Kyoto rats, 12 and 35 weeks old. Vagotomy in rats with the intact baroreceptors increased hindlimb vascular resistance in all four groups. Hindlimb vascular responses to graded sympathetic nerve stimulation were closely linear up to 6 Hz in all groups, and the slope of the response was approximately 1.4 times steeper in spontaneously hypertensive than in Wistar-Kyoto rats, in both the young and old groups. The increase in hindlimb vascular resistance after vagotomy normalized by the slope of the response to sympathetic nerve stimulation was greater in young spontaneously hypertensive rats than in young Wistar-Kyoto rats, but was less in old spontaneously hypertensive rats than in old Wistar-Kyoto rats. Vagotomy increased the gain of arterial baroreflex control of hindlimb vascular resistance in young spontaneously hypertensive rats, and in two groups of Wistar-Kyoto rats, but not in old spontaneously hypertensive rats. The percent increase in the gain of arterial baroreflex control of hindlimb vascular resistance after vagotomy tended to be greater in young spontaneously hypertensive than in young Wistar-Kyoto rats, but was less in old spontaneously hypertensive than in old Wistar-Kyoto rats. Central venous pressure and left ventricular enddiastolic pressure were higher in spontaneously hypertensive than in Wistar-Kyoto rats in both young and old groups. Left atrial distensibility assessed by obtaining the atrial pressure-volume relationship was comparable between young spontaneously hypertensive and young Wistar-Kyoto rats, but was less in old spontaneously hypertensive than in old Wistar-Kyoto rats. These results indicate that vagal afferents exert tonic inhibition on control of hindlimb vascular resistance in spontaneously hypertensive as well as in Wistar-Kyoto rats, and that tonic inhibitory influence of afferents on control of hindlimb vascular resistance is altered in spontaneously hypertensive rats, augmented in young, but attenuated in old, spontaneously hypertensive rats, compared with that in age-matched Wistar-Kyoto rats. It is considered that altered control of vascular resistance by vagal afferents in spontaneously hypertensive rats may result from changes in vagal afferent activity.

ISSN:0009-7330    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Ouabain (80 γgAg) injected into the lateral cerebroventricles (ICV) of rats produced a prompt and sustained increase in arterial blood pressure. A diastolic blood pressure increase of about 40 mm Hg began within 10 minutes of injection and lasted at least 1 hour. This dose of ouabain had no effect on arterial pressure when given intravenously. The vasopressor response to intracerebroventricularly administered ouabain was not blocked by prior intravenous administration of phentolamine (1 γg/kg) or hexamethonium (3 mg/kg). However, continuous intravenous infusion of saralasin (2 mg/kg per min) prevented the pressor response to intracerebroventricularly administered ouabain. In addition, bilateral nephrectomy, adrenalectomy, pretreatment with intravenously administered propranolol (2 mg/kg) or captopril (10 mg/kg) abolished the increase in blood pressure evoked by intracerebroventricularly administered ouabain. Plasma renin and epinephrine levels at the peak of the pressor response to intracerebroventricularly administered ouabain were respectively, about 2.5- and 2-fold higher than in control rats. Our data indicate that ouabain administered into the central nervous system produces a hypertensive effect which does not primarily involve peripheral α-adrenergic receptors, but appears to be due to angiotensin II produced by renin of renal origin. These data suggest that digitalis agents can interact with sites in the central nervous system to induce a release of renin from the kidney; this release appears to involve activation of β-adrenergic receptors by catecholamines from the adrenal medulla, perhaps through a direct adrenal-kidney vascular network.

ISSN:0009-7330    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

We investigated the effects of exogenous leukotriene D4, synthesis inhibitors, and a leukotriene receptor antagonist upon chloralose anesthetized, mechanically ventilated, neonatal piglets with constant left pulmonary blood flow and upon piglets with uncontrolled pulmonary blood flow. Leukotriene D4(100–10,000 mg, intravenously) caused dose-dependent increases in peak tracheal pressure, pulmonary vascular resistance, and systemic vascular resistance coupled with dose-dependent decreases in cardiac output and systemic arterial pressure. In a limited number of experiments, cardiovascular responses to exogenous leukotriene C4were qualitatively similar but quantitatively less than those to leukotriene D4. Neither treatment with diethylcarbamazine or the lipoxygenase inhibitor nordihydroguaiaretic acid, nor with the leukotriene receptor antagonist, FPL55712, altered any baseline cardiovascular parameter measured, suggesting the absence of any influence of leukotrienes on resting hemodynamics. Hypoxia or hypoxia combined with mild hypercapnia caused pulmonary vasoconstriction. Neither treatment with diethylcarbamazine or the lipoxygenase inhibitor nordihydroguaiaretic acid, nor with the leukotriene receptor antagonist FPL55712, altered the pulmonary vasoconstrictor response to hypoxia or combined hypoxia/hypercapnia. We conclude that endogenous leukotrienes do not appear to have an influence on resting cardiovascular function, neither do they appear to be necessary for hypoxic pulmonary vasoconstriction in the neonatal piglet, although exogenous leukotrienes are capable of producing cardiovascular effects.

ISSN:0009-7330    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

The purpose of this study was to discover the cause and magnitude of changes in the body-surface potentials occurring when: (1) fluids of various conductivity were added to the pericardial sac, or (2) the volume of the blood within chambers of the heart was either increased or decreased. Fluids added to the pericardium were physiological saline, whole-blood, and mineral oil. Magnitudes of body-surface potentials were compared to the predictions based on a mathematical eccentric spheres model of the heart and torso developed previously by Rudy and Plonsey. Data demonstrated conclusively that there is a nonlinear relationship between the body-surface potentials and the conductivity of the pericardial layer. This relationship is one in which the body-surface potentials of the anterior chest were found to decrease when conductivity of the pericardial layer was either increased or decreased. These changes in body-surface potentials were caused solely by alterations in the conductivity and volume of the fluid effusate. It was demonstrated that these changes were not caused by any “stretching” or “compression” of the cardiac tissue caused by the altered fluid volumes in and around the heart. Findings were accurately predicted by the eccentric spheres model, thereby confirming the model's usefulness as a predictive instrument. The model provides an explanation for the nonlinear relationship that was exhibited by the data.

ISSN:0009-7330    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

Hybridomas were prepared from mice immunized with myosin from the enlarged left ventricle of a 53-year-old female with an obstructive cardiomyopathy. The specificity of 15 monoclonal antibodies to myosin heavy chains was assessed by the reactivity of muscle extracts and of chymotryptic myosin fragments of different sizes with these antibodies, as determined by the immune replicate technique; some of the monoclonal antibodies cross-reacted only with the ventricular V3-type myosin from hypothyroid rats, whereas the other antibodies cross-reacted both with the latter and with the ventricular VI-type myosins from normal young rats. Immunological heterogeneity of the fibers from human atrial muscles and from human ventricular muscles was detected by some of the antimyosin antibodies by means of indirect immunofluorescence. Histochemical fiber heterogeneity was also detected by adenosine triphosphatase staining of the same tissues. Because of the close correspondence observed between the immunological and histochemical responses of atrial fibers, it has been postulated that at least two distinct types of myosin exist in the human atrium, each myosin form being histochemically related to either α-or β-like ventricular myosin heavy chains. In contrast, there was no direct correspondence between the two experimental approaches in human ventricles, and it is postulated that at least three distinct types of myosin exist within the human ventricles, one VI-type myosin, presumably corresponding to the very rare fibers with an alkaline-stable adenosine triphosphatase activity, and two other V3-type myosins corresponding to immunologically different fibers, each having an alkaline-labile adenosine triphosphatase activity. Monoclonal antibodies that can distinguish among the different myosin variants were further used to provide the basis for an anatomical description of fiber types and myosin types within the human atrial and ventricular myocardium in the whole hearts of two young boys who died sudden violent deaths. Small zones of myosin variation were seen to be scattered, but probably not randomly distributed, within large areas of myocardium in which the cellular distribution of myosin was constant; the large areas had one myosin distribution specific for each cardiac cavity. No clear-cut conclusions can yet be made concerning the physiological role of the regional variations observed in the distribution of the different molecular forms of myosin.

ISSN:0009-7330    

出版商:OVID    

年代:1984

数据来源: OVID

摘要:

In a preceding paper, we employed an initially spherical, modified membrane model of the infarcted ventricle to investigate the relation between ventricular function and both infarct size and infarct stiffness. In the present paper, we have applied the same model to a set of different questions, namely, the consequences of enhanced or depressed inotropic state within the noninfarcted myocardium. When infarcted ventricles containing up to 41percent; infarction are examined, stroke volume appears to be relatively insensitive to increases in inotropic state. However, stroke volume falls rapidly when inotropic state is depressed below 80percent; of normal. For the case of a ventricle with a large, weakly contracting segment which is not totally infarcted, stroke volume is impaired only when the contractility of the weak region is diminished below 50percent; of normal. Finally, the stress concentration around a region of infarction appears to be dependent more strongly on the inotropic state of the noninfarcted tissue than on the infarct size

ISSN:0009-7330    

出版商:OVID    

年代:1984

数据来源: OVID