CARDIAC OUTPUT IN ACUTE EXPERIMENTAL METHEMOGLOBINEMIA

Methemoglobinemia induced in normal anesthetized dogs by intravenous infusions of aniline resulted in a decreased arterial oxygen content and a marked increase in cardiac output. Heart rate, arterial pressure, blood viscosity, and oxygen consumption increased, while total peripheral resistance and arteriovenous oxygen difference decreased. The elevation of cardiac output occurred in spite of the fact that the hematocrit level and blood viscosity increased. Ganglion-blocking doses of pentolinium bitartrate did not significantly alter the cardiovascular responses to the methemoglobinemia.

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Submaximal Cardiovascular Responses to Exercise in Children: Treadmill versus Cycle Ergometer

Pediatric Exercise Science ◽

10.1123/pes.9.4.331 ◽

1997 ◽

Vol 9 (4) ◽

pp. 331-341

Author(s):

Kenneth R. Turley ◽

Jack H. Wilmore

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Regression Analysis ◽

Oxygen Consumption ◽

Stroke Volume ◽

Peripheral Resistance ◽

Cardiovascular Responses ◽

Cycle Ergometer ◽

Individual Values ◽

Oxygen Difference

This study investigated whether cardiovascular responses at a given submaximal oxygen consumption (V̇O2, L · min-1) are different between the treadmill (TM) and cycle ergometer (CE). Submaximal cardiovascular measurements were obtained at three work rates on both the TM and CE in 7- to 9-year-old children (12 males and 12 females). Using regression analysis, it was determined that there were no differences between the TM and CE in cardiac output (L · min-1), stroke volume (SV, ml · beat-1) or heart rate (beats · min-1) at a given V̇O2 (L · min-1). There were differences in the total peripheral resistance (TPR, units) and arterial-venous oxygen difference (a-vO2 diff, ml · 100 ml-1) to V̇O2 (L · min-1) relationship. While there were statistically significant differences in TPR and a-vO2 diff between the two modalities, there was substantial overlap of individual values at any given submaximal V̇O2, thus the physiological significance is questionable. Hence, we conclude that in 7- to 9-yearold children there are no differences in submaximal cardiovascular responses between the CE and TM.

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Systemic oxygen transport in induced normovolemic anemia and polycythemia

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1962.203.4.720 ◽

1962 ◽

Vol 203 (4) ◽

pp. 720-724 ◽

Cited By ~ 44

Author(s):

John F. Murray ◽

Philip Gold ◽

B. Lamar Johnson

Keyword(s):

Cardiac Output ◽

Oxygen Transport ◽

Arterial Oxygen Saturation ◽

Peripheral Resistance ◽

Arterial Oxygen ◽

Peripheral Vascular ◽

Arterial Oxygen Content ◽

Normovolemic Anemia ◽

Systemic Oxygen ◽

Negative Linear Relationship

The hemodynamic effects of normovolemic anemia and polycythemia were studied in 14 dogs. Anemia (5 dogs) and polycythemia (5 dogs) were induced by bleeding and simultaneously infusing dextran or packed erythrocytes. Measurements included cardiac output, arterial oxygen saturation, peripheral vascular resistance, and systemic oxygen transport (cardiac output X arterial oxygen content). Cardiac output had a significant negative linear relationship to hematocrit ( r = –0.74, P < 0.01) over the range studied (13–74%). Peripheral resistance fell 46% in anemic animals and increased 152% in four of five polycythemic animals. Arterial saturation was significantly correlated to changes in hematocrit ( r = 0.62, P < 0.01) and cardiac output ( r = –0.55, P < 0.01); these values were due primarily to the linearity encountered in the anemia experiments and a reversal in these relationships tended to occur at high hematocrits. Systemic oxygen transport was maximum at normal hematocrits and decreased in anemia and polycythemia. The data indicate that hemodynamic adjustments in normovolemic anemia and polycythemia are insufficient to maintain normal oxygen delivery.

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Role of vasopressin in the cardiovascular response to hypoxia in the conscious rat

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1986.251.6.h1316 ◽

1986 ◽

Vol 251 (6) ◽

pp. H1316-H1323 ◽

Cited By ~ 4

Author(s):

B. R. Walker

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Cardiovascular Response ◽

Peripheral Resistance ◽

Cardiovascular Responses ◽

Hypoxic Exposure ◽

Conscious Rat ◽

Time Control ◽

Hemodynamic Variables

Previous experiments have demonstrated that hypoxia stimulates the release of arginine vasopressin in conscious animals including the rat. The present study was designed to test whether AVP may exert a vasoconstrictor influence during hypoxia at varying levels of CO2. Systemic hemodynamics were assessed in conscious rats for 30 min under hypocapnic hypoxic, isocapnic hypoxic, hypercapnic hypoxic, and room air conditions. Progressive effects on heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were observed with varying CO2 under hypoxic conditions. Hypocapnic hypoxia [arterial PO2 (PaO2) = 32 Torr; arterial PCO2 (PaCO2) = 22 Torr] caused HR and CO to rise and TPR to fall. Isocapnic hypoxia (PaO2 = 36 Torr; PaCO2 = 35 Torr) was associated with no significant changes in HR and CO or TPR, whereas hypercapnic hypoxia (PaO2 = 35 Torr; PaCO2 = 51 Torr) caused HR and CO to fall and TPR to rise. Room air time control experiments were associated with no change in measured hemodynamic variables. To determine the possible role of circulating AVP on these cardiovascular responses, additional experiments were performed where the specific V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP (10 micrograms/kg iv) was administered at the midpoint of hypoxic exposure. Antagonist administration had no effect on hypocapnic hypoxic animals or animals breathing room air; however, blood pressure and TPR were significantly reduced by d(CH2)5Tyr(Me)AVP in both isocapnic and hypercapnic hypoxic animals. The heart rate response to hypoxia at the various CO2 levels was unaffected; however, cardiac output and stroke volume were increased after V1-antagonism in the isocapnic and hypercapnic hypoxic animals.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension

Journal of Neurosurgery ◽

10.3171/jns.1983.59.6.0938 ◽

1983 ◽

Vol 59 (6) ◽

pp. 938-944 ◽

Cited By ~ 96

Author(s):

Quentin J. Durward ◽

A. Lorne Amacher ◽

Rolando F. Del Maestro ◽

William J. Sibbald

Keyword(s):

Cardiac Output ◽

Intracranial Hypertension ◽

Cardiovascular Responses ◽

Arterial Oxygen ◽

Optimum Level ◽

Moderate Degree ◽

Content Type ◽

Arterial Oxygen Content ◽

Head Elevation ◽

The Mean

✓ To establish if an optimum level of head elevation exists in patients with intracranial hypertension, the authors examined changes in intracranial pressure (ICP), systemic and pulmonary pressures, systemic flows, and intrapulmonary shunt fraction with the patient lying flat, and then with the head elevated at 15°, 30°, and 60°. Cerebral perfusion pressure (CPP) was calculated. The lowest mean ICP was found with elevation of the head to 15° (a fall of −4.5 ± 1.6 mm Hg, p < 0.001) and 30° (a fall of −6.1 ± 3.5 mm Hg, p < 0.001); the CPP and cardiac output were maintained. With elevation of the head to 60°, the mean ICP increased to −3.8 ± 9.3 mm Hg of baseline, while the CPP decreased −7.9 ± 9.3 mm Hg (p < 0.02), and the cardiac index also fell −0.25 ± 0.28 liters/min/sq m (p < 0.01). No significant change in filling pressures, arterial oxygen content, or heart rate was encountered at any level of head elevation. Therefore, a moderate degree (15° or 30°) of head elevation provides a consistent reduction of ICP without concomitant compromise of cardiac function. Lower (0°) or higher (60°) degrees of head elevation may be detrimental to the patient because of changes in the ICP, CPP, and cardiac output.

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Abnormal cardiovascular response to nitroglycerin in migraine

Cephalalgia ◽

10.1177/0333102419881657 ◽

2019 ◽

Vol 40 (3) ◽

pp. 266-277

Author(s):

Willebrordus PJ van Oosterhout ◽

Guus G Schoonman ◽

Dirk P Saal ◽

Roland D Thijs ◽

Michel D Ferrari ◽

...

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Stroke Volume ◽

Total Peripheral Resistance ◽

Cardiovascular Response ◽

Peripheral Resistance ◽

Cardiovascular Responses ◽

Initial Increase

Introduction Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. Methods In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg−1·min−1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. Results Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls ( p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. Discussion Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.

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Alteration of adrenergic responses by chronic cholinergic blockade

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1960.199.1.117 ◽

1960 ◽

Vol 199 (1) ◽

pp. 117-123

Author(s):

David C. Jerram

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Cardiac Output ◽

Diastolic Blood Pressure ◽

Peripheral Resistance ◽

Submaxillary Gland ◽

Chronic Administration ◽

Cardiovascular Responses ◽

Adrenergic Agents ◽

Cholinergic Blockade

The effect of the chronic administration of cholinergic blocking agents on the secretory and cardiovascular responses to epinephrine, levarterenol and isoproterenol has been determined in the dog. Chronic cholinergic blockade (CCB) produced a supersensitivity of the submaxillary gland to epinephrine and levarterenol as has been shown previously. Isoproterenol was found to have a profound secretory effect on the submaxillary gland of the dog. During CCB, the volume of secretion produced by isoproterenol was greatly increased. Changes in systolic and diastolic blood pressure, cardiac output, peripheral resistance, heart rate and duration of systole produced by graded doses of epinephrine, levarterenol and isoproterenol were not significantly or systematically altered by CCB. It was concluded that CCB does not alter the sensitivity of the vasculature to adrenergic agents. In 12 of 13 dogs, the heart rate after acute atropinization was significantly lower during CCB than in the control experiments.

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Effects of dihydroergotamine on hemodynamic molsidomine actions in anesthetized dogs

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y84-103 ◽

1984 ◽

Vol 62 (6) ◽

pp. 634-639 ◽

Cited By ~ 1

Author(s):

Volker B. Fiedler ◽

Helmut Göbel ◽

Rolf-Eberhard Nitz

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Stroke Volume ◽

Total Peripheral Resistance ◽

Peripheral Resistance ◽

Left Ventricular ◽

Venous Capacitance ◽

Heart Performance ◽

Dose Dependent Fashion ◽

Anesthetized Dogs

In pentobarbital-anesthetized mongrel dogs the intravenous actions of 0.50 mg/kg molsidomine on pulmonary artery and left ventricular (LV) end-diastolic pressures and internal heart dimensions (preload), left ventricular systolic and peripheral blood pressures, and total peripheral resistance (afterload), as well as on heart rate, dP/dt, stroke volume, and cardiac output (heart performance) were studied for 2 h. Hemodynamic molsidomine effects were influenced by increasing amounts of intravenously infused dihydroergotamine solution (DHE, 1–64 μg∙kg−1∙min−1). Molsidomine decreased preload, stroke volume, and cardiac output for over 2 h but decreased ventricular and peripheral pressures for 45 min. Systemic vascular resistance showed a tendency to decrease while heart rate and LV dP/dtmax were not altered. DHE infusion reversed molsidomine effects on the preload and afterload of the heart. The diminished stroke volume was elevated so that cardiac output also increased. Total peripheral resistance increased while heart rate fell in a dose-dependent fashion. The LV dP/dtmax remained unchanged until the highest dose of 64 μg∙kg−1∙min−1 DHE elevated the isovolumic myocardial contractility. These experiments indicate that DHE can reverse the intravenous molsidomine effects on hemodynamics. Most likely, this is mediated through peripheral vasoconstriction of venous capacitance vessels, thereby affecting moldisomine's action on postcapillary beds of the circulation.

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Effects of Bungarus candidus (Malayan krait) venom on general circulation and renal hemodynamics in experimental animals

Asian Biomedicine ◽

10.2478/abm-2010-0051 ◽

2010 ◽

Vol 4 (3) ◽

pp. 421-428 ◽

Cited By ~ 3

Author(s):

Lawan Chanhome ◽

Visith Sitprija ◽

Narongsak Chaiyabutr

Keyword(s):

Heart Rate ◽

Blood Flow ◽

Cardiac Output ◽

Renal Blood Flow ◽

General Circulation ◽

Marked Decrease ◽

Peripheral Resistance ◽

Cardiovascular Responses ◽

Renal Hemodynamics ◽

Experimental Animals

Abstract Background: Many studies have reported the occurrence of lethal acute renal failure after snakebites. Bungarus candidus (Malayan krait) is a medically important venomous snake distributed widely throughout Southeast Asia. The best known features of systemic envenoming by B. candidus are neurotoxic. Objective: Obtain more information on effects of B. candidus venom on changes in systemic and renal hemodynamics in experimental animals. Methods: Twelve adult male New Zealand white rabbits were used to study the effect of B. candidus venom on general circulation and renal hemodynamics. An anesthetized animal was intravenously injected with B. candidus venom at a dosage of 50μg/kg bodyweight. All changes of parameters were observed after initial post venom injection and recorded at 30 min intervals until 150 minutes after envenomation. Results: After envenomation, cardiovascular responses showed a marked decrease in mean arterial pressure within two minutes, afterwards gradually returning closely to baseline values. There were stepwise decreases in heart rate and cardiac output, while total peripheral resistance was slightly increased. The renal hemodynamics significantly decreased by glomerular filtration rate, effective renal plasma flow and effective renal blood flow, while the filtration fraction significantly increased. Envenomed animals showed a reduction in renal fraction, while renal vascular resistance stepwise increased. The plasma potassium level tended to increase. Animals showed stepwise decreases in urinary excretion of Na+, K+ and Cl-. A marked decrease in plasma calcium level was apparent at 120 minutes, while plasma creatine phosphokinase and lactate dehydrogenase levels increased at 30-120 minutes. Conclusion: A significant drop in blood pressure was attributed to a sustained fall in cardiac output, which would be associated with a reduction in heart rate. Sustained hypotension would contribute to reduction of renal blood flow, which results in decreased GFR.

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Cardiovascular functions during voluntary apnea in dogs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1983.245.2.r143 ◽

1983 ◽

Vol 245 (2) ◽

pp. R143-R150

Author(s):

Y. C. Lin ◽

E. L. Carlson ◽

E. P. McCutcheon ◽

H. Sandler

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Myocardial Contractility ◽

Peripheral Resistance ◽

Cardiac Pacing ◽

Cardiovascular Responses ◽

Active Role ◽

Left Ventricular ◽

Stroke Work ◽

Cardiac Power

We studied cardiovascular responses to apnea during voluntary snout immersion in conscious, chronically instrumented dogs. Voluntary snout immersion up to eye level for a duration of greater than 15 s ensured that the dog was engaged in active apnea. In a control apnea of 15-35 s, heart rate decreased by 43% from a control value of 104 beats/min. Changes in cardiac output paralleled those of heart rate. Mean aortic blood pressure did not vary during apnea, which, coupled with a reduced cardiac output, indicated a 65% increase in estimated total peripheral resistance compared with preapnea values. Treatment with atropine sulfate (0.2 mg/kg) eliminated the bradycardia response, but the peripheral vasoconstriction persisted. Treatment with propranolol (0.5 mg/kg) eliminated postapnea hypertension. Changes in myocardial contractility during apnea were observed by measuring hemodynamic parameters while maintaining a constant heart rate with cardiac pacing. Myocardial contractility was decreased during apnea as indicated by decreases in stroke volume (-13%), stroke work (-22%), cardiac output (-13%), left ventricular (dP/dt)max (-11%), and cardiac power (-24%). These changes were prevented by atropine treatment, indicating the depressed contractility was a result of vagus nerve activity. The circulatory adjustments in the dog during apnea are potential mechanisms for oxygen conservation, although the effectiveness is uncertain for the animal as a whole. It is clear that by appropriate reduction in cardiac power output, the heart itself plays an active role in conservation of limited oxygen during apnea.

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