Aortocaval fistula delays gastric emptying of liquid test meal in awake rats

2013 ◽  
Vol 304 (10) ◽  
pp. H1397-H1405 ◽  
Author(s):  
Moisés T. B. Silva ◽  
Raimundo C. Palheta ◽  
Francisca G. V. Oliveira ◽  
Juliana B. M. de Lima ◽  
José Antunes-Rodrigues ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Gastric Emptying ◽  
Central Venous Pressure ◽  
Test Meal ◽  
Venous Pressure ◽  
Aortocaval Fistula ◽  
Central Venous ◽  
Dye Retention ◽  
Awake Rats

Arteriovenous anastomoses disrupt cardiovascular and renal homeostasis, eliciting hemodynamic adjustments, resetting the humoral pattern, and inducing cardiac hypertrophy. Because acute circulatory imbalance alters gut motor behavior, we studied the effects of arteriovenous fistula placement on the gastric emptying (GE) of a liquid meal in awake rats. After laparotomy, we created an aortocaval fistula (ACF) by aorta and cava wall puncture with a 21-, 23-, or 26-gauge needle. The ACF was not created in the control group, which underwent sham operation. After 12, 24, or 48 h, mean arterial pressure, heart rate, and central venous pressure were continuously recorded, and cardiac output was estimated by thermal dilution. The rats were then gavage fed a test meal (i.e., phenol red in glucose solution), and fractional dye retention was determined 10, 20, or 30 min later. The effect of prior bleeding on ACF-induced GE delay, the role of neuroautonomic pathways, and changes in plasma hormone levels (i.e., angiotensin II, arginine vasopressin, atrial natriuretic peptide, corticosterone, and oxytocin) were evaluated. When compared with the sham-operated group, ACF rats exhibited arterial hypotension, higher ( P < 0.05) heart rate, central venous pressure, and cardiac output values and increased ( P < 0.05) gastric dye retention, a phenomenon prevented by bilateral subdiaphragmatic vagotomy and hexamethonium treatment. Pirenzepine also impaired the occurrence of gastric delay in subjects with ACF. In addition to causing hyperkinetic circulation, ACF placement delayed the GE of liquid in awake rats, an effect that likely involves a parasympathetic pathway.

Endurance training in dogs increases vascular responsiveness to an alpha 1-agonist

1988 ◽  
Vol 65 (2) ◽  
pp. 625-632 ◽  
Author(s):  
Y. M. Evans ◽  
J. N. Funk ◽  
J. B. Charles ◽  
D. C. Randall ◽  
C. F. Knapp
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Central Venous Pressure ◽  
Endurance Training ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Central Venous ◽  
Vascular Responsiveness

The effects of endurance training on vascular responsiveness to an alpha 1-agonist and the associated changes in baroreflex modulation of heart rate and vascular resistance were studied. Graded dosages of phenylephrine were given to eight treadmill-trained dogs and to eight untrained dogs; both groups were chronically instrumented and were sedated and resting when tested. These dosages were repeated after ganglionic blockade. Aortic pressure, cardiac output, central venous pressure, peripheral resistance, and heart rate were each averaged over 30 s before injection and 90 s after injection. The slope of the peripheral resistance-dose relationship was significantly increased in trained compared with untrained dogs in both the unblocked and blocked cases [unblocked: trained 0.89, untrained 0.47; blocked: trained 4.30, untrained 2.05 (mmHg.l-1.min)/(microgram.kg-1)]. The unblocked resistance slopes were reduced with respect to the blocked slopes by 77 (untrained) and 79% (trained). The slope of the heart rate-aortic pressure response was reduced, but not significantly, by endurance training. We conclude that 6 wk of endurance training in dogs resulted in a doubling of the vascular responsiveness to an alpha 1-agonist, with no significant change in the baroreflex regulation of resistance or heart rate.

Active recovery attenuates the fall in sweat rate but not cutaneous vascular conductance after supine exercise

2004 ◽  
Vol 96 (2) ◽  
pp. 668-673 ◽  
Author(s):  
Thad E. Wilson ◽  
Robert Carter ◽  
Michael J. Cutler ◽  
Jian Cui ◽  
Michael L. Smith ◽  
...  
Keyword(s):  
Heart Rate ◽  
Central Venous Pressure ◽  
Sweat Rate ◽  
Venous Pressure ◽  
Thoracic Impedance ◽  
Active Recovery ◽  
Central Venous ◽  
Cycle Exercise ◽  
Vascular Conductance ◽  
Cutaneous Vascular Conductance

The purpose of this study was to identify whether baroreceptor unloading was responsible for less efficient heat loss responses (i.e., skin blood flow and sweat rate) previously reported during inactive compared with active recovery after upright cycle exercise (Carter R III, Wilson TE, Watenpaugh DE, Smith ML, and Crandall CG. J Appl Physiol 93: 1918-1929, 2002). Eight healthy adults performed two 15-min bouts of supine cycle exercise followed by inactive or active (no-load pedaling) supine recovery. Core temperature (Tcore), mean skin temperature (Tsk), heart rate, mean arterial blood pressure (MAP), thoracic impedance, central venous pressure ( n = 4), cutaneous vascular conductance (CVC; laser-Doppler flux/MAP expressed as percentage of maximal vasodilation), and sweat rate were measured throughout exercise and during 5 min of recovery. Exercise bouts were similar in power output, heart rate, Tcore, and Tsk. Baroreceptor loading and thermal status were similar during trials because MAP (90 ± 4, 88 ± 4 mmHg), thoracic impedance (29 ± 1, 28 ± 2 Ω), central venous pressure (5 ± 1, 4 ± 1 mmHg), Tcore (37.5 ± 0.1, 37.5 ± 0.1°C), and Tsk (34.1 ± 0.3, 34.2 ± 0.2°C) were not significantly different at 3 min of recovery between active and inactive recoveries, respectively; all P > 0.05. At 3 min of recovery, chest CVC was not significantly different between active (25 ± 6% of maximum) and inactive (28 ± 6% of maximum; P > 0.05) recovery. In contrast, at this time point, chest sweat rate was higher during active (0.45 ± 0.16 mg·cm-2·min-1) compared with inactive (0.34 ± 0.19 mg·cm-2·min-1; P < 0.05) recovery. After exercise CVC and sweat rate are differentially controlled, with CVC being primarily influenced by baroreceptor loading status while sweat rate is influenced by other factors.

Alteration in heart rate response to hemorrhage in conscious dogs with volume overload

1978 ◽  
Vol 235 (4) ◽  
pp. H422-H428
Author(s):  
M. M. LeWinter ◽  
J. S. Karliner ◽  
J. W. Covell
Keyword(s):  
Heart Rate ◽  
Central Venous Pressure ◽  
Pulse Pressure ◽  
Pressure Pulse ◽  
Heart Rate Response ◽  
Parasympathetic Nervous System ◽  
Venous Pressure ◽  
Volume Overload ◽  
Conscious Dogs ◽  
Central Venous

The heart rate response to hemorrhage was studied in conscious dogs before and up to 2 mo after the establishment of volume overload due to systemic arteriovenous (a-v) fistulas. Before a-v fistula, heart rate increased markedly during hemorrhage. When hemorrhage was preceded by dextran infusion, bleeding resulted in a gradual reduction in heart rate. The a-v fistula caused marked increases in resting heart rate, central venous pressure, pulse pressure, and blood volume. During hemorrhage, heart rate initially remained constant, but then declined abruptly from the resting value of 121 +/- 3.7 beats/min to a nadir of 89 +/- 6.5 beats/min (P less than 0.01). Although mean arterial pressure decreased markedly, there was no significant change in pulse pressure, and central venous pressure tended to stabilize with the heart rate decline. The abrupt heart rate decline was prevented by atropine but unaltered by propranolol. The response was observed as early as 5 days after a-v fistula. We conclude that an alteration in the heart rate response to hemorrhage appears early during volume overload. This alteration appears to be reflex in nature and to be mediated by the parasympathetic nervous system.

Cardiovascular actions of histamine and potassium

1959 ◽  
Vol 197 (5) ◽  
pp. 1005-1007 ◽  
Author(s):  
Calvin Hanna ◽  
Patricia B. McHugo ◽  
William H. MacMillan
Keyword(s):  
Cardiac Output ◽  
Central Venous Pressure ◽  
Potassium Chloride ◽  
Venous Pressure ◽  
Plasma Potassium ◽  
Dilution Method ◽  
Cardiac Rate ◽  
Central Venous ◽  
Arterial Blood ◽  
Cardiovascular Actions

The cardiovascular actions of intravenous histamine, in doses from 2.5 to 20 µg/kg of the free base, were studied in the pentobarbitalized dog using the dye dilution method. With the small dose there was a consistent but small initial increase in cardiac output and with the larger doses there was a biphasic change in output. Cardiac rate, central venous pressure, central blood volume, hematocrit and the mean circulation time were essentially unchanged. Infusions of histamine and of potassium chloride at the rate of 1 µg and 1 mg/kg/min., respectively, moderately increased the cardiac output. Potassium chloride had no effect on the arterial blood pressure, cardiac rate and central venous pressure. Both the infusion of potassium chloride and injection of histamine produced a comparable elevation of the plasma potassium. It is possible that the actions of histamine to increase the plasma potassium contribute to the cardiovascular actions of this amine, especially on the cardiac output.

ANP-mediated volume depletion attenuates renal responses in humans

1992 ◽  
Vol 263 (6) ◽  
pp. R1303-R1308 ◽  
Author(s):  
T. J. Ebert ◽  
L. Groban ◽  
M. Muzi ◽  
M. Hanson ◽  
A. W. Cowley
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Central Venous Pressure ◽  
Sodium Excretion ◽  
Healthy Subjects ◽  
Venous Pressure ◽  
Urine Volume ◽  
Positive Pressure ◽  
Plasma Norepinephrine ◽  
Central Venous

Brief low-dose infusions of atrial natriuretic peptide (ANP) that emulate physiological plasma concentrations in humans have little if any effect on renal excretory function. This study explored the possibility that ANP-mediated reductions in cardiac filling pressures (through ANP's rapid effect on capillary dynamics) could attenuate its purported renal effects. Protocol A consisted of 16 healthy subjects (ages 19-27 yr old) who underwent three consecutive 45-min experimental sequences: 1) placebo, 2) ANP (10 ng.kg-1 x min-1), and 3) ANP alone (n = 8) or ANP with simultaneous lower body positive pressure (LBPP, n = 8). Electrocardiogram and direct measures of arterial and central venous pressures were continuously monitored. Blood was sampled at the end of each 45-min sequence before subjects stood to void. Compared with control (placebo), ANP produced a hemoconcentration and increased plasma norepinephrine, but did not change heart rate, blood pressure, plasma levels of renin, aldosterone, or vasopressin, or renal excretion of volume or sodium. In subjects receiving LBPP to maintain central venous pressure during the last 45 min of ANP infusion, norepinephrine did not increase and urine volume and sodium excretion increased (P < 0.05). In a second study (protocol B), five healthy subjects received a placebo infusion for 45 min followed by two consecutive 45-min infusions of ANP (10 ng.kg-1 x min-1). Central venous pressure was maintained (LBPP) at placebo baseline throughout the two ANP infusion periods. Urine volume and sodium excretion rates increased progressively and significantly during both ANP infusion periods (P < 0.05) without significant changes in creatinine clearance, blood pressure, or heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiopulmonary Effects of Intrathoracic Insufflation in Dogs

2002 ◽  
Vol 38 (6) ◽  
pp. 515-520 ◽  
Author(s):  
Curt M. Daly ◽  
Karen Swalec-Tobias ◽  
Anthony H. Tobias ◽  
Nicole Ehrhart
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Healthy Adult ◽  
Venous Pressure ◽  
Minute Volume ◽  
Mechanical Ventilator ◽  
Central Venous ◽  
Anesthetized Dogs ◽  
Pressure Standard

This study was designed to quantify the effects of incremental positive insufflation of the intrathoracic space on cardiac output (CO), heart rate (HR), arterial pressure (AP), central venous pressure (CVP), and percent saturation of hemoglobin with oxygen (SPO2) in anesthetized dogs. Seven healthy, adult dogs from terminal teaching laboratories were maintained under anesthesia with isoflurane delivered with a mechanical ventilator. The experimental variables were recorded before introduction of an intrathoracic catheter, at intrathoracic pressures (IP) of 0 mm Hg, 3 mm Hg insufflation, and additional increments of 1 mm Hg insufflation thereafter until the SPO2 remained &lt;85% despite increases in minute volume. Finally the variables were measured again at 0 mm Hg IP. The cardiac output and systolic and diastolic AP significantly (P&lt;0.05) decreased at 3 mm Hg IP. Significant decreases in SPO2 were seen at 10 mm Hg IP. Significant increase in CVP was noted at 6 mm Hg IP. Heart rate decreased significantly at 5 to 6 mm Hg IP but was not decreased above 6 mm Hg IP. Given the degree of CO decrease at low intrathoracic pressures, insufflation-aided thoracoscopy should be used with caution and at the lowest possible insufflation pressure. Standard anesthetic monitoring variables such as HR and AP measurements may not accurately reflect the animal’s cardiovascular status.

Microcirculatory Perfusion during Volume Therapy

1995 ◽  
Vol 82 (4) ◽  
pp. 975-982. ◽  
Author(s):  
Wolfgang Funk ◽  
Verena Baldinger
Keyword(s):  
Heart Rate ◽  
Oxygen Partial Pressure ◽  
Partial Pressure ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Tissue Perfusion ◽  
Volume Replacement ◽  
Surface Oxygen ◽  
Tissue Oxygen ◽  
Central Venous

Background Because of the passage of water and salt molecules into the interstitial space, volume replacement with crystalloid solutions requires an amount at least four times that of lost blood. The resulting tissue edema may interfere with nutritive capillary perfusion and oxygen delivery. To prove this hypothesis, the effects of isovolemic hemodilution (hematocrit 30%) with Ringer's lactate solution or dextran 60 on tissue perfusion and oxygenation were investigated in awake Syrian golden hamsters. Methods Experiments were performed by using a chronic dorsal skinfold window giving access to skeletal muscle tissue (musculus cutaneus) with in vivo microscopy, quantitative video image analysis, and surface oxygen partial pressure electrodes. Central venous and arterial pressures were measured by means of chronically implanted jugular venous and carotid catheters. Results Isovolemic exchange of blood with dextran caused no significant changes in arterial or central venous pressure, heart rate, capillary flow velocity, functional capillary density, or surface oxygen partial pressure during the 1-h observation period. A volume of Ringer's solution equal to four times of the amount of blood lost maintained arterial pressure and heart rate when central venous pressure was kept at predilution control values. However, tissue perfusion determined by counting perfused capillaries per terminal arteriole was reduced by 62%, and mean tissue oxygen partial pressure decreased from 19 to 8 mmHg. Conclusions In this model, volume replacement with artificial colloids yielded hemodynamic stability and adequate tissue oxygen supply, whereas administration of crystalloids alone jeopardized tissue perfusion and oxygenation.

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