Effects of inotropic agents on arterial resistance and venous compliance in anesthetized dogs

1982 ◽  
Vol 60 (7) ◽  
pp. 968-976 ◽  
Author(s):  
R. I. Ogilvie
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Time Constant ◽  
Right Atrial ◽  
Fast Time ◽  
Vascular Effects ◽  
Venous Compliance ◽  
Peripheral Vasculature ◽  
Arterial Resistance ◽  
Flat Dose

Systemic vascular effects of dopamine, dobutamine, and prenalterol were studied in 45 anesthetized open-chest dogs. Blood flow [Formula: see text] and right atrial pressure (Pra) were independently controlled by a right heart bypass. Transient changes in central blood volume after an acute reduction in Pra at a constant [Formula: see text] showed that blood was draining from two vascular compartments with different time constants, one fast and the other slow. Dopamine (2.5–10 μg∙kg−1∙min−1) was the most active drug with dose-related increases in heart rate 6–19%, arterial pressure (Pa) 3–36%, and venous compliance 2–25%. Small doses of dopamine (2.5 and 5 μg∙kg−1∙min−1) reduced arterial resistance of the slow time-constant compartment increasing [Formula: see text] distribution to that compartment 21–42%, whereas larger doses increased both arterial resistance and venous compliance in that compartment. Arterial resistance in the fast time-constant compartment increased with all doses of dopamine. Dobutamine (2.5–10 μg∙kg−1∙min−1) modestly increased heart rate 2–11% and Pa 9–12%) without altering [Formula: see text] distribution demonstrating a relatively flat dose response. Dobutamine 2.5–5 μg∙kg−1∙min−1 increased venous compliance 5–10% while 10 μg∙kg−1∙min−1 had no effect or decreased compliance of both compartments. Prenalterol 3 μg∙kg−1∙min−1 increased Pa 9% primarily by increasing arterial resistance in the fast time-constant compartment without altering heart rate or blood flow distribution. Doses of prenalterol 10–100 times greater caused dose-dependent reductions in Pa and vascular compliance. In this animal model of the circulation with a fixed cardiac output, dopamine had the greatest effect on the peripheral vasculature and chronotropy.

Comparative effects of vasodilator drugs on flow distribution and venous return

1985 ◽  
Vol 63 (11) ◽  
pp. 1345-1355 ◽  
Author(s):  
R. I. Ogilvie
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Time Constant ◽  
Venous Return ◽  
Flow Distribution ◽  
Fast Time ◽  
Central Blood Volume ◽  
Slow Time ◽  
Arterial Resistance ◽  
Slow Time Constant

Systemic vascular effects of hydralazine, prazosin, captopril, and nifedipine were studied in 115 anesthetized dogs. Blood flow [Formula: see text] and right atrial pressure (Pra) were independently controlled by a right heart bypass. Transient changes in central blood volume after an acute reduction in Pra at a constant [Formula: see text] showed that blood was draining from two vascular compartments with different time constants, one fast and the other slow. At three dose levels producing comparable reductions in systemic arterial pressure (30–40% at the highest dose), these drugs had different effects on flow distribution and venous return. Hydralazine and prazosin had parallel and balanced effects on arterial resistance of the two vascular compartments, and flow distribution was unaltered. Captopril preferentially reduced arterial resistance of the compartment with a slow time constant for venous return (−26 ± 6%, −30 ± 6%, −50 ± 5% at 0.02, 0.10, and 0.50 mg∙kg−1∙h−1, respectively; [Formula: see text]) without altering arterial resistance of the fast time-constant compartment. Blood flow to the slow time-constant compartment was increased 43 ± 14% at the highest dose, and central blood volume was reduced 108 ± 15 mL. In contrast, nifedipine had a balanced effect on arterial resistance with the lowest dose (0.025 mg/kg) but caused a preferential reduction in arterial resistance of the fast time-constant compartment at higher doses (−38 ± 4% and −55 ± 2% at 0.05 and 0.10 mg/kg, respectively). Blood flow to the slow time-constant compartment was reduced 36 ± 5% at the highest dose of nifedipine, and central blood volume was increased 66 ± 12 mL. Total systemic venous compliance was unaltered or slightly reduced by each of the four drugs. These results add further evidence to the hypothesis that peripheral blood flow distribution is a major determinant of venous return to the heart.

Cardiovascular Effects of Marihuana in Man

1974 ◽  
Vol 52 (3) ◽  
pp. 706-719 ◽  
Author(s):  
S. C. Clark ◽  
C. Greene ◽  
G. W. Karr ◽  
K. L. MacCannell ◽  
S. L. Milstein
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Physiological Responses ◽  
Vagal Tone ◽  
Cardiovascular Effects ◽  
Cardiovascular Responses ◽  
Venous Compliance ◽  
Double Blind ◽  
Arterial Resistance

Twenty-eight subjects, matched by sex and Cannabis experience, received by controlled inhalation under single- and double-blind conditions 600 mg marihuana placebo and marihuana. Forearm, venous and arterial pressures, forearm blood flow, and heart rate were recorded while supine. Derived functions such as "dp/dt", regional arterial resistance, and venous compliance were calculated from these variables. (1) Placebo produced no intoxication or consistent physiological responses. (2) Marihuana produced intoxication in all Cannabis-experienced and half the non-experienced subjects. (3) Cardiovascular responses occurred in response to marihuana in the absence of intoxication, indicating that they were not psychogenically mediated. (4) Inhibition of vagal tone may contribute to the tachycardia seen with marihuana. (5) Reflexly mediated sympathetic responses may be muted in the presence of marihuana.

Contrasting neurovascular findings in chronic orthostatic intolerance and neurocardiogenic syncope

2003 ◽  
Vol 104 (4) ◽  
pp. 329-340 ◽  
Author(s):  
Julian M. STEWART ◽  
Amy WELDON
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Orthostatic Intolerance ◽  
Peripheral Vascular ◽  
Neurocardiogenic Syncope ◽  
Control Subjects ◽  
Arterial Resistance ◽  
Vascular Physiology ◽  
Venous Resistance

Simple faint (neurocardiogenic syncope) and postural tachycardia syndrome (POTS) characterize acute and chronic orthostatic intolerance respectively. We explored the hypothesis that vascular function is similar in the two conditions. We studied 29 patients with POTS and compared them with 20 patients with neurocardiogenic syncope who were otherwise well, and with 15 healthy control subjects. We measured continuous heart rate, respiration and blood pressure, and used venous occlusion strain gauge plethysmography to measure calf and forearm blood flow, peripheral arterial resistance, peripheral venous resistance and venous pressure (Pv). Upright tilt was performed to 70° for 10min, during which calf blood flow and volume were measured. Calf Pv was increased (to 27.2±2.0mmHg) in a subgroup of POTS patients, who also had increased arterial resistance (57±6mmHg·ml-1·min-1·100ml-1 tissue), increased venous resistance (2.4±0.3mmHg·ml-1·min-1·100ml-1 tissue), and decreased peripheral flow (1.0±0.2ml·min-1·100ml-1 tissue) in the calf; other POTS patients with a normal Pv had decreased arterial resistance (18±2mmHg·ml-1·min-1·100ml-1 tissue) and increased blood flow (3.8±0.3ml·min-1·100ml-1 tissue). Syncope patients were not different from controls (Pv = 11.4±0.5mmHg; calf flow = 3.1±0.2ml·min-1·100ml-1 tissue; arterial resistance = 27±2mmHg·ml-1·min-1·100ml-1 tissue; venous resistance = 1.2±0.3mmHg·ml-1·min-1·100ml-1 tissue). When upright, syncope patients and control subjects had similar increases in heart rate and calf volume, stable blood pressure, and decreases in blood flow. POTS patients had markedly increased heart rate and calf blood flow, unstable blood pressure, and pooling in the lower extremities, regardless of subgroup. We conclude that peripheral vascular physiology in patients with POTS is abnormal, in contrast with normal peripheral vascular physiology in neurocardiogenic syncope.

Abstract 240: Comparison of Hemodynamics Generated by Synchronized and Interposed Compressions During Treatment of Pseudo Electro-mechanical Dissociation

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Joshua W Lampe ◽  
Jill K Badin ◽  
Lyra Clark ◽  
Jeff R Gould ◽  
Karen L Moodie ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Chest Compression ◽  
Right Atrial ◽  
Compression Rate ◽  
Chest Compressions ◽  
Blood Flows ◽  
Mechanical Dissociation ◽  
Life Threatening ◽  
Integrated Or

Introduction: Pseudo electro-mechanical dissociation (P-EMD) is a cardiac arrest variant characterized by a life-threatening reduction in cardiac output in the presence of organized electrical activity. Synchronization of chest compressions to the R-wave in the ECG may be preferable to the delivery of standard CPR. However, in the bradycardic P-EMD state, synchronization may result in inadequate blood flow due to the low compression/heart rate. This pilot study examined the hemodynamic effect of interposing additional chest compressions between synchronized chest compressions during bradycardic P-EMD to increase the compression rate. Methods: P-EMD was induced via hypoxia in three female swine (~30 kg) and treated with synchronized compressions until the onset of asystole (HR<12 BPM). Interposed compressions were added when the heart rate fell below 60 BPM. A chest compression was classified as synchronized or interposed depending on the presence or absence of a co-incident R-wave. Hemodynamic parameters were integrated or averaged over each compression interval. Results: Synchronized compressions tended to produce larger aortic pressures, larger carotid blood flows, and lower right atrial pressures than interposed compressions. Data from one experiment are shown in Figure 1. The relative hemodynamic benefit of a synchronized chest compression appears to depend on the effectiveness of the underlying heart contraction. The interposed chest compressions generated forward carotid blood flow and increased the compression rate during bradycardia. Discussion: During bradycardic P-EMD, synchronized compressions may generate better hemodynamics than interposed compressions, and the combination of synchronized and interposed compressions may result in more blood flow than the delivery of synchronized compressions alone. Figure 1. Comparison of hemodynamics generated by synchronized compressions (blue) and interposed compressions (red).

Capsaicin-induced bronchial vasodilation in dogs: central and peripheral neural mechanisms

1993 ◽  
Vol 74 (1) ◽  
pp. 259-266 ◽  
Author(s):  
T. E. Pisarri ◽  
J. C. Coleridge ◽  
H. M. Coleridge
Keyword(s):  
Blood Flow ◽  
Bronchial Artery ◽  
Neutral Endopeptidase ◽  
Right Atrial ◽  
Vagus Nerves ◽  
Vascular Effects ◽  
Vascular Conductance ◽  
Axon Reflex ◽  
C Fibers ◽  
The Right

In 21 anesthetized dogs, we placed a flow probe around the right bronchial artery and examined changes in bronchial blood flow and bronchial vascular conductance when pulmonary C-fibers were stimulated by right atrial injection of capsaicin. When vagus nerves were intact, capsaicin evoked a pulmonary depressor chemoreflex and increased bronchial blood flow by 125% and bronchial vascular conductance by 175%; flow in an adjacent intercostal artery did not increase. Injection of color-coded microspheres revealed that blood flow to mucosa of lower trachea and to a peripheral bronchus doubled, whereas flow to posterior tracheal wall increased little. Cooling (to -1 degree C) or cutting cervical vagi (in 17 dogs) abolished the pulmonary chemoreflex and abolished all bronchial vascular effects in nine dogs but 33% of the vasodilation persisted in eight. In five of six dogs, this persisting vasodilation was potentiated by phosphoramidon (a neutral endopeptidase inhibitor that retards breakdown of neuropeptides released by C-fibers). Atropine reduced the capsaicin-induced bronchial vasodilation by approximately 30%. We conclude that the bronchial vasodilation was largely due to a centrally mediated vagal reflex and that a neuropeptide-dependent axon-reflex component was also present in about one-half the dogs.

Cardiopulmonary effects of unilateral airway pressure changes in intact infant lambs

1984 ◽  
Vol 56 (5) ◽  
pp. 1439-1448 ◽  
Author(s):  
B. P. Fuhrman ◽  
J. Everitt ◽  
J. E. Lock
Keyword(s):  
Blood Flow ◽  
Airway Pressure ◽  
Left Lung ◽  
Right Atrial ◽  
Pulmonary Vasculature ◽  
Direct Effects ◽  
Vascular Effects ◽  
Lung Blood Flow ◽  
End Tidal ◽  
Pressure Changes

Direct effects of airway pressure changes on the pulmonary vascular bed of the intact infant lamb were studied under chloralose anesthesia using a preparation developed to permit independent ventilation of right and left lungs and independent measurement of right and left lung blood flow. A specially designed endobronchial tube eliminated the need for thoracotomy the day of study. Unilateral changes in positive end-expiratory pressure (PEEP) during volume-regulated ventilation increased ipsilateral but not contralateral airway pressure, confirming adequate separation of right and left lungs and suggesting rigidity of the mediastinum. Such interventions ( UPEEP ) at levels of 5, 10, and 15 cmH2O reduced ipsilateral but not contralateral pulmonary blood flow (by 10, 25, and 46%, respectively) but did not alter end-tidal PCO2 of either lung. UPEEP had less effect on cardiac output, stroke volume, right atrial, left atrial, esophageal, and pulmonary arterial pressures than did PEEP applied to both lungs. Because this preparation separates the predominantly direct effects of UPEEP on the ipsilateral lung from its indirect effects on the contralateral lung, it is well suited to studies of direct pulmonary vascular effects of airway pressure changes in an intact closed-chest preparation with reactive pulmonary vasculature.

Altered control of skin blood flow at high skin and core temperatures

1975 ◽  
Vol 38 (5) ◽  
pp. 839-845 ◽  
Author(s):  
C. R. Wyss ◽  
G. L. Brengelmann ◽  
J. M. Johnson ◽  
L. B. Rowell ◽  
D. Silverstein
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Skin Temperature ◽  
Linear Model ◽  
Skin Blood Flow ◽  
Forearm Blood Flow ◽  
Right Atrial ◽  
Esophageal Temperature ◽  
Cooling Period ◽  
Blood Temperature

Five subjects were studied during periods of controlled increases and decreases in skin temperature (Ts) over the Ts range of 34–40 degrees C. One protocol was designed to observe changes in forearm blood flow (FBF) and heart rate (HR) with changes in core temperature (Tc; right atrial blood temperature and esophageal temperature were measured) with Ts held constant at two levels. FBF and HR changed linearly with Tc in the Tc range of 37–38 degrees C with Ts constant at 38 degrees C. A second protocol imposed Ts changes at two levels of Ts and Tc; this protocol also included a prolonged cooling period. The influence of Ts on FBF and HR was reduced when Ts changes occurred at an elevated Ts and Tc, and FBF showed considerable hysteresis during cooling. We conclude that a linear model for the control of FBF or HR is inadequate as a tool for predicting the control of these variables.

scholarly journals Orthostasis fails to produce active limb venoconstriction in adolescents

2001 ◽  
Vol 91 (4) ◽  
pp. 1723-1729 ◽  
Author(s):  
Julian M. Stewart ◽  
Jean Lavin ◽  
Amy Weldon
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Venous Occlusion ◽  
Upper Body ◽  
Sympathetic Activation ◽  
Prior Work ◽  
Blood Flows ◽  
Arterial Resistance ◽  
Capacitance Vessel ◽  
Vessel Volume

Orthostasis is characterized by translocation of blood from the upper body and thorax into dependent venous structures. Although active splanchnic venoconstriction is known to occur, active limb venoconstriction remains controversial. Based on prior work, we initially hypothesized that active venoconstriction does occur in the extremities during orthostasis in response to baroreflex activation. We investigated this hypothesis in the arms and legs of 11 healthy volunteers, aged 13–19 yr, using venous occlusion strain gauge plethysmography to obtain the forearm and calf blood flows and to compute the capacitance vessel volume-pressure compliance relation. Subjects were studied supine and at −10, +20, and +35° to load the baroreflexes. With +20° of tilt, blood flow decreased and limb arterial resistance increased significantly ( P < 0.05) compared with supine. With +35° of tilt, blood flow decreased, limb arterial resistance increased, and heart rate increased, indicating parasympathetic withdrawal and sympathetic activation with arterial vasoconstriction. The volume-pressure relation was unchanged by orthostatic maneuvers. The results suggest that active venoconstriction in the limbs is not important to mild orthostatic response.

Effects of angiotensin on pulmonary and systemic hemodynamics

1962 ◽  
Vol 202 (4) ◽  
pp. 690-694 ◽  
Author(s):  
John E. Chimoskey ◽  
Pedro C. Blaquier ◽  
A. C. Taquini ◽  
David F. Bohr
Keyword(s):  
Heart Rate ◽  
Renin Angiotensin System ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Pulmonary Resistance ◽  
Angiotensin System ◽  
Arterial Resistance ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial

In ten morphine-urethan anesthetized dogs single injections of 2.0 µg/kg of synthetic valine 5 angiotensin II amide elevated systemic and pulmonary arterial pressures and depressed heart rate. Thirty-minute intravenous infusions of angiotensin (0.4 and 1.0 µg/kg/min) in eight dogs elevated systemic arterial pressure and diminished heart rate. Pulmonary arterial, pulmonary wedge, left ventricular end-diastolic, and right atrial pressures were all slightly elevated; mean cardiac output did not change. Calculated total pulmonary resistance and pulmonary arterial resistance were diminished; central blood volume was elevated. These findings suggest that elevated systemic pressure and resistance increase myocardial work and induce reflex bradycardia, thereby elevating left ventricular end-diastolic, pulmonary wedge, and pulmonary arterial pressures. Systemic vasoconstriction also contributes to the elevated right atrial pressure and distention of the pulmonary vascular bed, which diminishes total pulmonary and pulmonary arterial resistance. These findings are not incompatible with the theory that the renin-angiotensin system is active in essential hypertension.

Local endogenous opiate activity in dog myocardium: receptor blockade with naloxone

1985 ◽  
Vol 248 (3) ◽  
pp. H382-H388 ◽  
Author(s):  
J. L. Caffrey ◽  
J. F. Gaugl ◽  
C. E. Jones
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Coronary Blood Flow ◽  
Opiate Receptor ◽  
Rapid Onset ◽  
Contractile Force ◽  
Left Ventricular ◽  
Right Atrial ◽  
Receptor Blockade ◽  
Endogenous Opiates

The participation of endogenous opiates in myocardial performance and coronary blood flow was investigated. Heart rate, left ventricular contractile force (LVCF), left coronary blood flow (LCBF), and left ventricular oxygen extraction were monitored in anesthetized dogs before and after intracoronary opiate receptor blockade with naloxone. LVCF consistently increased in a dose-dependent fashion following intracoronary naloxone. The increasing LVCF was accompanied by significant increases in LCBF and myocardial oxygen consumption, without changes in heart rate. Rapid onset of responses suggested the presence of endogenous opiates operating locally within the myocardium. Similar effects did not follow right atrial injection of naloxone, ruling out a systemic mechanism. Furthermore, naloxone injected into the isolated left anterior descending artery selectively increased contractile force in that perfusion territory while the adjacent untreated circumflex territory showed no change. The administration of dynorphin into the coronaries produced a depression of LVCF qualitatively consistent with these effects. The effect of dynorphin was subsequently reversed with naloxone. These results support the concept that endogenous opiates participate in the regulation of myocardial function through local mechanisms at the myocardial level.

Sign in / Sign up

Export Citation Format

Share Document