Limitation of a pulsed Doppler velocimeter for blood flow measurement in small vessels

The performance of a new and simplified flow probe construction and the Iowa 545C-4 pulsed Doppler velocimeter was evaluated for measurement of blood flow over several months in small arteries of awake animals. Calibrations were performed over a wide range of intraluminal pressures and physiological flow velocities. Pressure-dependent differences in slope of the Doppler shift-volume flow relationship were detected in some probes. Signal strength was maintained at hematocrits > 10%. Distortion of pulsed Doppler signal peaks occurred in the conscious rabbit at peak aortic velocities, at which Reynold's number for turbulence was exceeded and the Doppler shift surpassed the Nyquist limit of 31.25 kHz for the velocimeter. Although the Doppler shift-volume flow relationship is linear at < 5 kHz, in some cases at higher Doppler shifts and blood flow velocities the relationship may become nonlinear, thus causing the volume flow rate to be underestimated by up to 38%. The cause of this phenomenon may be "aliasing" and/or the consequence of the range control capability of the velocimeter selectively sampling changing velocity profiles and flow disturbances in the central stream at higher velocities

Recent views on integrated coronary control: significance of non-uniform regional control of coronary flow conductance

Previous work from this laboratory and others has shown that powerful autonomic influences modulate coronary flow. In particular, the parasympathetic nervous system produces vasodilatation when activated by baroreceptors via the vagus nerve. Differences exist in baroreflex coronary vasodilator mechanisms among the right, circumflex and anterior descending coronary vascular beds in the awake chronically instrumented dog. Our hypothesis is that neurogenic acetylcholine acting from the adventitial side and endothelial nitric oxide from the luminal aspect of coronary smooth muscle compete with powerful intrinsic myogenic constrictor mechanisms to regulate regional flow conductance. There is also increasing evidence that heterogeneity of control systems exists in different-sized coronary vessels within an individual coronary vascular bed. It is concluded that coronary vessels in vascular beds can no longer be assumed to respond in a uniform manner to neural, myogenic, metabolic or humoral factors. These new perspectives of regional control mechanisms have important implications for understanding pathophysiological mechanisms inducing and sustaining tachyarrhythmias involved in ischaemic heart disease

Venous hydrostatic indifference point as a marker of postnatal adaptation to orthostasis in swine

The postulate that venous adaptation assists postural baroreflex regulation by shifting the hydrostatic indifference point (HIP) toward the heart was investigated in eight midazolam-sedated newborn piglets. Whole body head-up (+15, +30, and +45°) and head-down (-15 and -30°) tilt provided a physiological range of orthostatic strain. HIP for all positive tilts shifted toward the heart (P < 0.05), +45° HIP shifted most [6.7 ± 0.3, 5.9 ± 0.5, and 3.6 ± 0.3 (SE) cm caudal to right atrium on days 1, 3, and 6, respectively]. HIP for negative tilts (3.0 ± 0.2 cm caudal to right atrium) did not shift with postnatal age. Euthanasia on day 6 caused 2.1 ± 0.3-cm caudal displacement of HIP for positive and negative tilts (P < 0.05). HIP proximity to right atrium was not altered by α-, β-adrenoceptor and cholinoceptor blockade on day 5. It is concluded that early HIP migration reflects enhancement of venous pressure control to head-up orthostatic strain. The effect is independent of baroreflex-mediated adrenoceptor and cholinoceptor mechanisms

Effect of fentanyl on baroreflex control of circumflex coronary conductance

Summary: 1. Fentanyl, a synthetic μ-opioid receptor agonist, is the preferred induction and maintenance anaesthetic agent in cardiac surgery. 2. Its actions on myocardial blood flow are poorly understood. There are reports of intra-operative myocardial ischaemia. Its reported actions on cardiorespiratory control vary widely, but do involve hypertension, bradycardia and peripheral vasoconstriction. 3. Accordingly, the postulate that fentanyl would cause coronary vasoconstriction and myocardial disadvantage was examined in awake dogs with a continuous wave Doppler flow probe mounted on the circumflex coronary artery. 4. Continuous intravenous infusion of fentanyl citrate (550 ng/kg per min) raised plasma concentrations of fentanyl to 3.37 ng/mL in a linear fashion at 20 min. There was a fall in core temperature of 0.7°C and, although no apparent depression of ventilation or fall in arterial or coronary sinus PO₂, there was a rise in PCO₂ and H⁺ concentration. Some dogs salivated and panted transiently. Thus, fentanyl may reset temperature regulation in low doses but, at higher doses, is associated with metabolic acidosis. 5. In sinus rhythm, the arterial pressure of the dogs fell slightly, then rose to 115% of resting control. Circumflex flow and conductance rose early, then conductance steadily declined to 83%. Heart rate fell, then rose before returning to pre-infusion levels. The early circumflex coronary vasodilator effects, but not the later vasoconstrictor effects, were reduced in dogs with paced hearts. 6. In dogs with paced hearts, a dose–effect study using 138, 275, 550 and 1100 ng/kg per min fentanyl suggested that, at low plasma concentrations of 1–2 ng/mL, vasodilatation does occur in both coronary and systemic circulations; however, at higher doses, intense coronary and systemic vasoconstriction supervenes. 7. The dose–response effect of fentanyl on arterial baroreflex control of circumflex conductance was examined during the immediate 8 s circumflex vasodilator response to a step rise in aortic pressure caused by inflation of an intra-aortic balloon. At low plasma concentrations of fentanyl, baroreflex control of circumflex conductance appears to be enhanced but, with increasing plasma concentrations of fentanyl, appears to be depressed. 8. Therefore, the effects of fentanyl are dose dependent. At low plasma concentrations, left ventricular blood flow and its baroreflex control is enhanced but, at higher concentrations, it is depressed

Heart-lung interactions: the sigh and autonomic control in the bronchial and coronary circulations

1. The Darwin hypothesis that human and animal expressions of emotion are the product of evolution and are tied to patterns of autonomic activity specified to progress the emotion remains under challenge. 2. The sigh is a respiratory behaviour linked with emotional expression in animals and humans from birth to death. The aim of the present study was to explore Darwin’s hypothesis with respect to tied autonomic activity underlying sigh-induced changes in the bronchial and coronary circulations. 3. Awake dogs were prepared using pulsed ultrasonic flow probes on the right bronchial artery, parent intercostal artery and brachial artery, or on the right, circumflex and anterior descending coronary arteries. Central venous (CVP) and arterial pressures (AP) were measured; heart rate and flow conductances were derived. Three spontaneous sighs were monitored before and during random blockade of individual and combinations of cholinoceptors, -adrenoceptors and β-adrenoceptors using methscopolamine, phentolamine and propranolol infusions. The data were subject to a 2 3 factorial analysis. 4. A spontaneous sigh is marked by a transient fall and return (< 3 s) in CVP of 18 mmHg (from 4±1 to –14±2 mmHg), usually followed by apnoea lasting 23±2 s. There is an immediate tachycardia and small rise in AP (phase 1) then, during apnoea, bradycardia and a fall in AP (phase 2). During phase 2, bronchial and coronary blood flow and conductance rise two- to three-fold over 30 s (peak at 8 s). The vascular changes are absent in parent intercostal and brachial beds. 5. The phase 1 tachycardia is entirely cholino/adrenoceptor in origin and is due to cholinoceptor withdrawal and positive β-adrenoceptor plus β-adrenoceptor/cholinoceptor interaction activity, in the ratio 1.75 : 1. The phase 2 bradycardia is entirely cholinoceptor. However, only 17% of the peak rise in bronchial conductance is due to -/β-adrenoceptor interactions (sympathetic withdrawal); 83% is due to non-cholino/adrenoceptor mechanisms. In a separate four animals, the total sigh-induced conductance rise is virtually abolished by prior infusion of NG-nitro- L-arginine methyl ester. 6. Therefore, the mechanism of the sigh-induced bronchial and conductance effects may be an efferent nitrergic component of an arterial chemoreceptor reflex induction of sighing. An alternative hypothesis invokes local stretch-sensitive C-fibre sensory nerve endings releasing substance P–calcitonin gene-related peptide–neurokinin A in response to cardiovascular distortion secondary to the sudden transmural pressure rise when intrapleural pressure falls. Whatever the case, these effects and the cholino/adrenoceptor base for the heart rate and broncho/coronary changes support the Darwin hypothesis