Effect of Acetaldehyde on the Isolated, Non-working Guinea-Pig Heart: Independence of the Coronary Flow Increase from Changes in Heart Rate and Oxygen Consumption

1974 ◽  
Vol 52 (3) ◽  
pp. 602-612 ◽  
Author(s):  
Minh-Hau Nguyen ◽  
L. Gailis

Guinea-pig hearts were perfused at constant pressure with Krehs–Henseleit bicarbonate buffer equilibrated with 95% O2 – 5% CO2. Acetaldehyde at 1 and 5 mM increased coronary flow, oxygen consumption, and heart rate. At 0.2 mM, it increased coronary flow and oxygen consumption only. In the rapidly paced heart, 1 mM acetaldehyde increased coronary flow, but not heart rate or oxygen consumption. Acetaldehyde increased coronary flow and oxygen consumption of the potassium-arrested heart. Acetaldehyde increased all parameters of the hypoxic heart (25% O2 gas phase), but the anoxic heart was not affected (coronary flow was already maximal).Reserpine (in vivo) and catecholamine β blockers (dichloroisoproterenol and propranolol) (in vitro) blocked the heart rate increases and moderated the rise in oxygen consumption. Dichloroisoproterenol plus phentolamine blocked the increases of both heart rate and oxygen consumption. None of the compounds affected the increase of coronary flow produced by acetaldehyde. Epinephrine, norepinephrine, and tyramine increased the heart rate and oxygen consumption, but not the coronary flow. Theophylline increased all three parameters. Neither tranylcypromine nor atropine modified the acetaldehyde effect. We conclude that the increase in heart rate is mediated by catecholamine β receptors. The increase in coronary flow is independent of the increase in heart rate or oxygen consumption and is not mediated by catecholamines.

1996 ◽  
Vol 11 (6) ◽  
pp. 289-302 ◽  
Author(s):  
Jiang Xu ◽  
Sina Zaim ◽  
Amir Pelleg

1960 ◽  
Vol 199 (1) ◽  
pp. 179-182 ◽  
Author(s):  
Abraham Guz ◽  
George S. Kurland ◽  
A. Stone Freedberg

Coronary flow, heart rate, myocardial oxygen consumption and Walton strain gauge tension were determined in the isolated rabbit heart perfused with hemoglobin solutions of varying oxygen content. Perfusion was carried out under constant pressure and with the hemoglobin solution in equilibrium with 3% CO2 and 97% air under atmospheric tension. Oxygen content was varied from 2 to 18 vol. % by diluting hemoglobin with Ringer-Locke solution. Change from a higher to lower oxyhemoglobin concentration resulted in increased coronary flow; the reserve led to decreased flow. Heart rate, myocardial tension and oxygen consumption were constant at oxygen capacity above 2 vol. %.


2010 ◽  
Vol 20 (2) ◽  
pp. 150-158 ◽  
Author(s):  
Cecilia Falkenberg ◽  
Stefan Hallhagen ◽  
Krister Nilsson ◽  
Boris Nilsson ◽  
Ingegerd Östman-Smith

AbstractBackgroundThe arterial switch operation is the corrective operation for transposition of the great arteries, defined as the combination of concordant atrioventricular and discordant ventriculo–arterial connections, but there have been concerns about silent subendocardial ischaemia on exercise and coronary artery growth. The arterial switch divides the majority of the sympathetic nerves entering the heart; we have studied the effects of coronary flow and sensitivity to catecholamine stimulation in an animal model.MethodsA total of 10 piglets were operated on cardiopulmonary bypass with section and resuturing of aortic trunk, pulmonary artery and both coronary arteries, with 13 sham-operated controls. After 5–7 weeks of recovery, seven simulated switch survivors and 13 controls were studied.ResultsBasal heart rate was significantly higher in switch piglets: in vivo mean (standard deviation) 112 (12) versus sham 100 (10) beats per minute, (p = 0.042); in vitro (Langendorff preparation): 89 (9) versus sham 73 (8) beats per minute (p = 0.0056). In vivo maximal heart rate in response to epinephrine was increased in switch piglets, 209 (13) versus 190 (17) beats per minute (p = 0.044). In vitro dose–response curves to norepinephrine were shifted leftward and upwards (p = 0.0014), with an 80% increase in heart rate induced by 0.095 (0.053) norepinephrine micromole per litre perfusate in switch hearts versus 0.180 (0.035) norepinephrine micromole per litre (p = 0.023). Increase in coronary flow on norepinephrine stimulation and maximal coronary flow were significantly reduced in switch hearts: 0.3 (0.2) versus 0.8 (0.4) millilitre per gram heart weight (p = 0.045) and 2.5 (0.4) versus 3.1 (0.4) millilitre per gram heart (p = 0.030), respectively.ConclusionsA combination of increased intrinsic heart rate, increased sensitivity to chronotropic actions of norepinephrine, and a decreased maximal coronary flow creates potential for a mismatch between perfusion and energy demands.


1961 ◽  
Vol 200 (5) ◽  
pp. 1055-1062 ◽  
Author(s):  
Sidney S. Schreiber ◽  
Murray Oratz ◽  
Marcus A. Rothschild

The effect of the digitalis glycoside, ouabain, on potassium exchange in the guinea pig heart in vitro was studied with the aid of K42. With modified Ringer's solution as a perfusate at 38 C, K was found to exchange at two rates in both washout and buildup studies. In vivo equilibration studies also suggested more than one rate of exchange. Ouabain, in vitro, effected inhibition of entrance of K into the slowly exchanging compartment, but did not affect influx into the fast compartment or efflux from the fast or slow compartments. The ouabain inhibition was seen at Ringer's K concentrations of 3.8–4.3 mEq/liter was equivocal at K concentrations of 5.0–5.5 mEq/ liter and absent at K concentrations of 7.0–7.5 mEq/liter. It was postulated that ouabain inhibition was directed toward the slowly exchanging fraction of intracellular potassium.


1995 ◽  
Vol 73 (10) ◽  
pp. 1512-1518 ◽  
Author(s):  
J. Duan ◽  
J. Jaramillo ◽  
G. L. Jung ◽  
A. L. McLeod ◽  
B. H. Fernandas ◽  
...  

The present study compares the hemodynamic effects and mechanisms of action of angiotensin II (AngII) antagonists, angiotensin converting enzyme (ACE) inhibitors, and renin inhibitors in the guinea pig, an animal with high similarity to primates in terms of in vitro and in vivo responses to several human renin inhibitors. Animals were anesthetized with urethane and ketamine. The carotid artery was catheterized for monitoring blood pressure and heart rate. After 30 min stabilization, drug (or vehicle) effects were monitored for 1 h following each increasing dose (i.v. bolus injection). Drugs tested include losartan, an AngII receptor antagonist; two renin inhibitors, BILA 2157 BS and PD-134672; and captopril, an ACE inhibitor. All drugs dose dependency decreased blood pressure. Diastolic blood pressure was reduced more than systolic blood pressure, suggestive of vasodilation. The maximum decrease (32 ± 6%, p < 0.05 vs. vehicle) in mean arterial blood pressure (MABP) by losartan was achieved with a dose of 1 mg/kg. A similar decrease in MABP was observed with renin inhibitors at a dose of 3 mg/kg, without affecting heart rate. A further increase in the dose of renin inhibitors (6 mg/kg) decreased not only blood pressure but also heart rate. Captopril decreased MABP with a maximum of 48 ± 3% (p < 0.05 vs. vehicle, losartan, and PD-134672). In the presence of HOE-140, a bradykinin antagonist, the MABP decrease by captopril was only 35 ± 4%, (p < 0.05 vs. captopril alone). Bilateral nephrectomy reduced the peak MABP effect of PD-134672 by 67%, while the effects of captopril on MABP were affected to a lesser degree (57%). Therefore, captopril remains more effective in reducing MABP (p < 0.05 vs. that of PD-134672). These results suggest that renin inhibitors and AngII antagonists act more specifically on the rennin–angiotensin system cascade, while captopril acts partially by a bradykinin-dependent mechanism. The small animal model described provides a novel tool for the comparative pharmacologic assessment of different rennin–angiotensin system inhibitors.Key words: blood pressure, guinea pig, rennin–angiotensin system, rennin–angiotensin system inhibition.


1995 ◽  
Vol 82 (6) ◽  
pp. 1426-1437. ◽  
Author(s):  
Bernhard M. Graf ◽  
Martin N. Vicenzi ◽  
Eike Martin ◽  
Zeljko J. Bosnjak ◽  
David F. Stowe

Background S(+)-Ketamine is judged to produce more potent anesthesia than either the racemate or the R(-) ketamine isomer because of differential activation of specific cerebral receptors. Other than central nervous system effects, the most important side effects of ketamine occur in the cardiovascular system. We examined the direct cardiac effects of the isomers and the racemate of ketamine in the isolated perfused guinea pig heart. Methods Twenty-three guinea pig hearts were perfused by the Langendorff technique with modified 37 degrees C Krebs-Ringer's solution (97% oxygen and 3% carbon dioxide) at a constant perfusion pressure. Eight animals were pretreated with reserpine to deplete hearts of catecholamines. These pretreated hearts were also perfused with Krebs-Ringer's solution containing propranolol, phenoxybenzamine, and atropine to block any remaining effects of catecholamines and of acetylcholine. Five additional hearts were perfused with naloxone to block cardiac opioid receptors. Ten hearts were not treated. All 23 hearts were then exposed to four increasing equimolar concentrations of each isomer and the racemate of ketamine for 10 min. Heart rate, atrioventricular conduction time (AVCT), left ventricular pressure, coronary flow, and inflow and outflow oxygen tensions were measured. Percentage oxygen extraction, oxygen delivery, and oxygen consumption were calculated. Results Both isomers and the racemate caused a concentration-dependent depression of systolic left ventricular pressure and an increase in AVCT. In the untreated hearts, S(+)-ketamine decreased heart rate and left ventricular pressure and, at higher concentrations, oxygen consumption and percentage oxygen extraction significantly less than R(-)-ketamine independent of blocked or unblocked opioid receptors. Racemic ketamine depressed cardiac function to a degree intermediate to that produced by the isomers. Coronary flow and AVCT were equally affected by the isomers and by the racemic mixture. In the catecholamine-depleted hearts both isomers and the racemate caused equipotent depression of all variables. In these hearts cardiac depression was greater, and AVCT, coronary flow, and oxygen delivery were significantly greater than in untreated and opioid receptor-blocked hearts. Conclusions Lesser cardiac depression by the S(+) isomer is attributable to an increased availability of catecholamines, because previous depletion of catecholamine stores and autonomic blockade completely inhibited these differences. The inability of cardiac tissue to reuptake released catecholamines into neuronal or extraneuronal sites during exposure to ketamine is stereoselective and caused predominantly by the S(+) isomer. Cardiac opioid receptors are apparently not involved in this phenomenon.


1976 ◽  
Vol 36 (02) ◽  
pp. 401-410 ◽  
Author(s):  
Buichi Fujttani ◽  
Toshimichi Tsuboi ◽  
Kazuko Takeno ◽  
Kouichi Yoshida ◽  
Masanao Shimizu

SummaryThe differences among human, rabbit and guinea-pig platelet adhesiveness as for inhibitions by adenosine, dipyridamole, chlorpromazine and acetylsalicylic acid are described, and the influence of measurement conditions on platelet adhesiveness is also reported. Platelet adhesiveness of human and animal species decreased with an increase of heparin concentrations and an increase of flow rate of blood passing through a glass bead column. Human and rabbit platelet adhesiveness was inhibited in vitro by adenosine, dipyridamole and chlorpromazine, but not by acetylsalicylic acid. On the other hand, guinea-pig platelet adhesiveness was inhibited by the four drugs including acetylsalicylic acid. In in vivo study, adenosine, dipyridamole and chlorpromazine inhibited platelet adhesiveness in rabbits and guinea-pigs. Acetylsalicylic acid showed the inhibitory effect in guinea-pigs, but not in rabbits.


1957 ◽  
Vol 190 (3) ◽  
pp. 425-428 ◽  
Author(s):  
Richard M. Hoar ◽  
William C. Young

Oxygen consumption and heart rate during pregnancy were measured in untreated, thyroxin-injected and thyroidectomized guinea pigs given I131. From impregnation until parturition, oxygen consumption increased 7.9% in untreated females. The increase continued until 5 days postpartum when a sharp decrease occurred. The increase is not accounted for by growth of the fetal mass. Comparable increases occurred in thyroxin-injected (16.2%) and thyroidectomized (11.9%) females, although the levels throughout were higher and lower, respectively, than in intact females. Heart rate did not increase. On the contrary, statistically significant decreases occurred in the untreated and thyroxin-injected females. Although the mechanism associated with the increased metabolic rate is not known, the possibility of thyroid participation would seem to be excluded. Involvement of the adrenal cortex is suggested by morphological differences in the cells of the zona fasciculata in pregnant and nonpregnant females and by evidence cited from other studies.


Sign in / Sign up

Export Citation Format

Share Document