Cardiovascular effects of vanadate in the dog

1980 ◽  
Vol 239 (1) ◽  
pp. H47-H56 ◽  
Author(s):  
D. J. Inciarte ◽  
R. P. Steffen ◽  
D. E. Dobbins ◽  
B. T. Swindall ◽  
J. Johnston ◽  
...  
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Brachial Artery ◽  
Cardiovascular Effects ◽  
Left Ventricular ◽  
Atpase Inhibitor ◽  
Naturally Occurring ◽  
Intracoronary Infusion ◽  
Flow Through ◽  
Artery Flow

We have investigated the cardiovascular actions of vanadate, a naturally occurring Na+-K+-ATPase inhibitor, in six series of pentobarbitalized dogs. In three of the series, isomotic sodium vanadate was infused intravenously at progressively faster rates while arterial pressure and other parameters were measured. In two other series, the solution was infused directly into the coronary artery with coronary flow held constant during measurement of perfusion pressure, left ventricular contractile force (LVCF), and dP/dt. In one series, the agent was infused into the brachial artery with brachial artery flow held constant, and small and large vessel resistances in skin and muscle were calculated. Intravenous infusion increased arterial pressure and reduced cardiac output, the latter resulting from both decreased heart rate and stroke volume. LVCF fell. Total peripheral, pulmonary, coronary, and renal resistances rose. Coronary and renal flows fell, and the latter was associated with reduced urine flow. Intracoronary infusion raised coronary resistance, but had little effect on heart rate, LVCF, and dP/dt. Intrabrachial infusion raisedthe resistance to flow through all components of the forelimb vascular bed. Thus, in the dog, vanadate activates vascular smooth muscle, but has little effect on cardiac muscle. In the latter respect, its action differs from that of ouabain.

Regional blood volume distribution during positive and negative airway pressure breathing in supine humans

1993 ◽  
Vol 75 (4) ◽  
pp. 1740-1747 ◽  
Author(s):  
J. Peters ◽  
B. Hecker ◽  
D. Neuser ◽  
W. Schaden
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Airway Pressure ◽  
Left Ventricular ◽  
Whole Body ◽  
Blood Content ◽  
Calf Blood Flow ◽  
Negative Airway Pressure

To assess the effects of continuous positive (CPAP) or negative airway pressure (CNAP) breathing (+/- 10#x2013;12 cmH2O, duration 25 min) on blood content in the body's capacitance vasculature, regional distribution of labeled red blood cells was evaluated in seven spontaneously breathing supine volunteers. Counts were acquired by whole body scans and detectors overlying the liver, intestine, left ventricle, and lower arm, and arterial pressure, heart rate, calf blood flow and vascular resistance, hematocrit, vasopressin, and atrial natriuretic peptide plasma concentrations were also obtained. With CPAP, thoracic, cardiac, and left ventricular counts diminished significantly by 7#x2013;10%, were accompanied by significant increases in counts over both the gut and liver, and remained decreased during CPAP but reversed to baseline with zero airway pressure. Calf blood flow and vascular resistance significantly decreased and increased, respectively, whereas limb counts, arterial pressure, heart rate, and hormone concentrations remained unchanged. With CNAP, in contrast, regional counts and other variables did not change. Thus, moderate levels of CPAP deplete the intrathoracic vascular bed and heart, shifting blood toward the gut and liver but not toward the limbs. No short-term compensation increasing cardiac filling during CPAP was seen. In contrast, CNAP did not alter intrathoracic or organ blood content and, therefore, does not simply mirror the effects evoked by CPAP.

Arterial pressure-flow relations in the awake standing dog

1975 ◽  
Vol 229 (5) ◽  
pp. 1261-1270 ◽  
Author(s):  
W Enrlich ◽  
FV Schrijen ◽  
TA Solomon ◽  
E Rodriguez-Lopez ◽  
RL Riley
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Rate Increase ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Heart Rate Increase ◽  
Underlying Mechanisms ◽  
The Right

The transient circulatory changes following paced heart rate increase are reported from 133 trials with 6 unanesthetized dogs with chronically implanted monitoring devices for heart rate, cardiac output, aortic blood pressure, and mean right atrial pressure. In 62 trials with 2 of the dogs, pulmonary artery, and left ventricular end-diastolic pressure, as well as left ventricular dP/dt were also studied. The sequence of changes in pressures and flows is analyzed in terms of probable underlying mechanisms, particularly with respect to the nature of vascular resistances. The rise in aortic pressure and flow during the first 3 s of paced heart rate increase, before arterial stretch receptor reflexes become active, is more consistent with an effective downstream pressure of about 49 mmHg, presumably at the arteriolar level, than with an effective downstream pressure close to 0 mmHg at the right atrial level. In the pulmonary circulation where vascular reflex effects are less prominent, the pattern of pulmonary arterial pressure and flow for the entire 30 s of observation is consistent with an effective downstream pressure of 9 mmHg, presumably at the alveolar or pulmonary arteriolar level, rather than at the level of the left ventricular end-diastolic pressure.

Prostacyclin reduces "preload" in conscious dogs via a vagal reflex mechanism

1987 ◽  
Vol 253 (6) ◽  
pp. H1477-H1483
Author(s):  
D. M. Nganele ◽  
T. H. Hintze
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Conscious Dogs ◽  
Reflex Mechanism ◽  
Capacitance Vessels ◽  
Preload Reduction ◽  
Cardiopulmonary Receptors ◽  
Electrical Pacing

The purpose of this study was to determine the effects of prostacyclin on left ventricular (LV) preload in conscious dogs. LV end-diastolic diameter (LV EDD) was used as an index of preload. Because prostacyclin reduces arterial pressure, data were sampled when mean arterial pressure, heart rate, and first derivative of LV pressure (dP/dt) had returned to control levels. There was no dose-response relationship in the preload reduction to prostacyclin, the threshold dose being 0.1 microgram/kg. Intravenous prostacyclin (2.0 micrograms/kg) reduced LV EDD 2.9 +/- 0.5% from 36 +/- 2.2 mm, (P less than 0.01). With heart rate held constant (146 +/- 2.5 beats/min) by electrical pacing, prostacyclin still reduced LV EDD by 4.0 +/- 1.0% from 32 +/- 2.5 mm (P less than 0.05). Intravenous administration of arachidonic acid (500 micrograms/kg) gave similar results. The magnitude of the preload response to prostacyclin was similar to that of nitroglycerin (25 micrograms/kg). Prazosin (1 mg/kg) or bilateral cervical vagal section completely abolished the preload response to prostacyclin but not to nitroglycerin. We, therefore, propose a mechanism where prostacyclin activates cardiopulmonary receptors with vagal afferents that results in a withdrawal of peripheral sympathetic tone to capacitance vessels to reduce preload, in contrast to nitroglycerin, whose mechanism of action is most probably a direct effect on capacitance vessels.

Roles of right versus left vagal sensory nerves in cardiopulmonary reflexes of conscious dogs

1985 ◽  
Vol 249 (3) ◽  
pp. R301-R307 ◽  
Author(s):  
K. W. Barron ◽  
V. S. Bishop
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Left Ventricular ◽  
Sensory Nerves ◽  
Inhibitory Influence ◽  
Relative Pressure ◽  
Intracoronary Administration ◽  
The Right ◽  
Vagal Sensory Nerves ◽  
Change In Mean

This study examined the relative roles of the right vs. left vagi in mediating the inhibitory influence of vagal sensory input on sympathetic outflow to the cardiovascular system. This objective was pursued through examination of responses to 1) interruption of tonic vagal input and 2) intracoronary administration of veratridine (Bezold-Jarisch effect). Bilateral vagal cold block (BVB) (n = 16) increased arterial pressure 25 +/- 3 mmHg and heart rate 66 +/- 7 beat/min, whereas right vagal cold block (RVB) and left vagal cold block (LVB) increased arterial pressure 13 +/- 2 and 4 +/- 2 mmHg, respectively. The relative differences in the change in mean arterial pressure were independent of heart rate since similar changes in arterial pressure were observed with preelevation of heart rate with atropine. Sinoaortic baroreceptor denervation augmented the pressure responses approximately fourfold, with the relative pressure changes produced by BVB, RVB, or LVB remaining proportionally the same. Intracoronary administration of veratridine (0.1 g/kg) produced a hypotension action (-44 +/- 6 mmHg), bradycardia (-48 +/- 8 beat/min), and a negative intropic effect (-482 +/- 68 mmHg/s, left ventricular (LV) (dP/dt)max. During RVB the depressor effect of veratridine was reduced to -18 +/- 5 mmHg, and changes in heart rate or LV (dP/dt)max were abolished. Veratridine administration during LVB decreased arterial pressure (-39 +/- 6 mmHg), heart rate (-22 +/- 6 beat/min), and LV (dP/dt)max (-250 +/- 60 mmHg). We conclude that in the conscious dog the tonic inhibitory influence of vagal afferent nerves on vasomotor outflow is predominantly associated with the right vagus as in Bezold-Jarisch effect.

Naturally occurring hypertension in New World nonhuman primates: potential role of the perifornical hypothalamus

2007 ◽  
Vol 292 (2) ◽  
pp. R937-R945 ◽  
Author(s):  
Orville A. Smith ◽  
Cliff A. Astley
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
New World ◽  
Critical Role ◽  
Cardiovascular Responses ◽  
Routine Laboratory ◽  
New World Primates ◽  
Naturally Occurring

Hypertension is a prominent underlying factor in the genesis of cardiovascular-related morbidity and mortality. A major impediment to the investigation into the causes of the disease is the paucity of naturally occurring animal models of the disease. There is evidence that some species of New World primates spontaneously become hypertensive. We used chronically implanted pressure transducers to assess normally occurring blood pressure and heart rate levels at rest and during routine laboratory procedures in a group of one of these New World primates ( Aotus sp.). Resting mean arterial pressure ranged from 72 to 130 mmHg. Three animals were judged to have resting mean arterial pressure levels in the hypertensive range (≥110 mmHg). In all of the animals, pressor responses to routine laboratory events were exaggerated (average highest mean pressure during 1 min from any session was 97–196 mmHg). Subsequently, the region of the perifornical/lateral hypothalamus known to produce elevated blood pressure and heart rate responses to electrical stimulation was removed, and the blood pressure responses to the laboratory routines were significantly decreased and, in some cases, eliminated. Control lesions in nearby tissue had no effect on these responses. This region may play a critical role in initiating or exacerbating cardiovascular responses that contribute to the development of essential hypertension.

Positive inotropic response to inosine in the in situ canine heart

1977 ◽  
Vol 233 (4) ◽  
pp. H438-H443 ◽  
Author(s):  
C. E. Jones ◽  
J. X. Thomas ◽  
M. D. Devous ◽  
C. P. Norris ◽  
E. E. Smith
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Substantial Effect ◽  
Contractile Force ◽  
Left Ventricular ◽  
Canine Heart ◽  
Inotropic State ◽  
Arterial Blood ◽  
The Right

Effects of inosine on left ventricular contractile force, circumflex blood flow, heart rate, and arterial pressure were investigated in mongrel dogs. Infusion of 50 ml of 10, 25, or 50 mM inosine into the right atrium over 5 min produced arterial blood inosine concentrations of 20-120 microM. Infusion of inosine concentrations of 10 mM or greater produced statistically significant increases in contractile force and circumflex blood flow (P less than 0.05). The increases in contractile force and circumflex blood flow caused by 50 inosine were approximately 40% and 110%, respectively. No statistically significant increases in heart rate or arterial pressure were observed during infusion of inosine at any concentration. Administration of propranolol (2 mg/kg) in no way altered the effects of inosine on contractile force or circumflex blood flow. Thus, the present study suggests that inosine in concentrations which may be produced in the myocardium during stressful conditions causes a substantial effect on the inotropic state of the heart and that the effects of inosine are not mediated through adrenergic mechanisms.

Baroreflex function and cardiac structure with moderate endurance training in normotensive men

1993 ◽  
Vol 74 (5) ◽  
pp. 2469-2477 ◽  
Author(s):  
M. P. McDonald ◽  
A. J. Sanfilippo ◽  
G. K. Savard
Keyword(s):  
Heart Rate ◽  
Exercise Training ◽  
Arterial Pressure ◽  
Endurance Training ◽  
Sinus Node ◽  
Left Ventricular ◽  
Control Group ◽  
Cardiac Structure ◽  
Baroreflex Function ◽  
Cardiopulmonary Baroreflex

Changes in arterial and cardiopulmonary baroreflex function and cardiac structure were followed throughout 10 wk of moderate endurance training [60 min of cycling, 3 days/wk, 60% maximal O2 uptake (VO2max)] in sedentary normotensive men (22–34 yr old). Subjects were randomly assigned to an exercise training group (ET; n = 9) or to a control group (UT; n = 4). Decreases in resting heart rate (8.9 +/- 2.6%, P < 0.01) and mean arterial pressure (7.0 +/- 2.3%, P < 0.05) and an increase in VO2max occurred after 10 wk in ET. An increase in the gain or slope of the spontaneous baroreflex response at rest was found after 10 wk in ET (50.1 +/- 6.3%, P < 0.01) but not in UT. An upward shift in the resting carotid-cardiac baroreflex response curve also occurred after 10 wk in ET, although the maximum range and gain of the response and the vagally mediated peak reflex sinus node responses were unchanged. Cardiopulmonary baroreflex function (reflex changes in forearm vascular conductance) and measured indexes of left ventricular structure were not altered in either ET or UT, although peak transmitral inflow velocity increased in ET (P < 0.05). These findings demonstrate that moderate exercise training results in an enhancement in the ability to reflexly adjust heart rate with spontaneous changes in arterial pressure within the operating range. This occurs independently of any changes in carotid-cardiac baroreflex function over the full response range in cardiopulmonary baroreflex function or in cardiac structure.

Aortic blood flow in dogs during treadmill exercise

1959 ◽  
Vol 14 (5) ◽  
pp. 809-812 ◽  
Author(s):  
Dean L. Franklin ◽  
Richard M. Ellis ◽  
R. F. Rushmer
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Treadmill Exercise ◽  
Essential Feature ◽  
Left Ventricular ◽  
Cardiac Response ◽  
Aortic Blood Flow ◽  
Direct Measurements ◽  
Flow Through ◽  
Response To Exercise

Instantaneous blood flow through the thoracic aorta was monitored continuously during spontaneous activity in intact dogs by means of a new, pulsed, ultrasonic flowmeter. Integrated flow per stroke, accumulated flow per unit time and heart rate were simultaneously derived by means of electronic computers. During treadmill exercise at 3 mph on a 5% grade, the heart rate increased by two- or threefold, but the aortic flow per stroke was only slightly increased. This observation was confirmed by direct measurements, of left ventricular diameter. An increase in stroke volume is not an essential feature of the cardiac response to exercise in these experiments. Submitted on December 15, 1958

Augmented catecholamine uptake by the heart during hemorrhage in the conscious dog

1986 ◽  
Vol 250 (1) ◽  
pp. H76-H81 ◽  
Author(s):  
O. L. Woodman ◽  
J. Amano ◽  
T. H. Hintze ◽  
S. F. Vatner
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Nerve Stimulation ◽  
Left Ventricular ◽  
Sympathetic Nerve Stimulation ◽  
Net Release

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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