Inhibition of gasotransmitters production and calcium influx affect cardiodynamic variables and cardiac oxidative stress in propofol-anesthetized male Wistar rats

2019 ◽  
Vol 97 (9) ◽  
pp. 850-856 ◽  
Author(s):  
M. Djuric ◽  
T. Nikolic Turnic ◽  
S. Kostic ◽  
K. Radonjic ◽  
J. Jeremic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Mass ◽  
Coronary Flow ◽  
Wistar Rats ◽  
Calcium Influx ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Male Wistar Rats ◽  
Synthase Inhibitor

It has been assumed that the cardioprotective effects of propofol are due to its non-anesthetic pleiotropic cardiac and vasodilator effects, in which gasotransmitters (NO, H2S, and CO) as well as calcium influx could be involved. The study on isolated rat heart was performed using 4 experimental groups (n = 7 in each): (1) bolus injection of propofol (100 mg/kg body mass, i.p.); (2) L-NAME (NO synthase inhibitor, 60 mg/kg body mass, i.p.) + propofol; (3) DL-PAG (H2S synthase inhibitor, 50 mg/kg body mass, i.p.) + propofol; (4) ZnPPIX (CO synthase inhibitor, 50 μmol/kg body mass, i.p.) + propofol. Before and after the verapamil (3 μmol/L) administration, cardiodynamic parameters were recorded (dp/dtmax, dp/dtmin, systolic left ventricular pressure, diastolic left ventricular pressure, heart rate, coronary flow), as well as coronary and cardiac oxidative stress parameters. The results showed significant increases of diastolic left ventricular pressure following NO and CO inhibition, but also increases of coronary flow following H2S and CO inhibition. Following verapamil administration, significant decreases of dp/dtmax were noted after NO and CO inhibition, then increase of diastolic left ventricular pressure following CO inhibition, and increase of coronary flow following NO, H2S, or CO inhibition. Oxidative stress markers were increased but catalase activity was significantly decreased in cardiac tissue. Gasotransmitters and calcium influx are involved in pleiotropic cardiovascular effects of propofol in male Wistar rats.

Contribution of extravascular compression to reduction of maximal coronary blood flow

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

Anesthetic Preconditioning

2003 ◽  
Vol 99 (2) ◽  
pp. 385-391 ◽  
Author(s):  
Leo G. Kevin ◽  
Peter Katz ◽  
Amadou K. S. Camara ◽  
Enis Novalija ◽  
Matthias L. Riess ◽  
...  
Keyword(s):  
Coronary Flow ◽  
Vascular Dysfunction ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Ischemic Time ◽  
Langendorff Preparation ◽  
Anesthetic Preconditioning ◽  
Structural Variables ◽  
Serious Injury

Background Anesthetic preconditioning (APC) is protective for several aspects of cardiac function and structure, including left ventricular pressure, coronary flow, and infarction. APC may be protective, however, only if the duration of ischemia is within a certain, as yet undefined range. Brief ischemia causes minimal injury, and APC would be expected to provide little benefit. Conversely, very prolonged ischemia would ultimately cause serious injury with or without APC. Previous investigations used a constant ischemic time as the independent variable to assess ischemia-induced changes in dependent functional and structural variables. The purpose of the study was to define the critical limits of efficacy of APC by varying ischemic time. Methods Guinea pig hearts (Langendorff preparation; n = 96) underwent pretreatment with sevoflurane (APC) or no treatment (control), before global ischemia and 120 min reperfusion. Ischemia durations were 20, 25, 30, 35, 40, and 45 min. Results At 120 min reperfusion, developed (systolic-diastolic) left ventricular pressure was increased by APC compared with control for ischemia durations of 25-40 min. Infarction was decreased by APC for ischemia durations of 25-40 min, but not 20 or 45 min. APC improved coronary flow and vasodilator responses for all ischemia durations longer than 25 min, and decreased ventricular fibrillation on reperfusion for ischemia durations longer than 30 min. Conclusions Although APC protects against vascular dysfunction and dysrhythmias after prolonged ischemia, protection against contractile dysfunction and infarction in this model is restricted to a range of ischemia durations of 25-40 min. These results suggest that APC may be effective in a subset of patients who have cardiac ischemia of intermediate duration.

scholarly journals The Effects of Diclofenac and Ibuprofen on Heart Function and Oxidative Stress Markers in the Isolated Rat Heart

2014 ◽  
Vol 15 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Maja Jevdjevic ◽  
Ivan Srejovic ◽  
Vladimir Zivkovic ◽  
Nevena Barudzic ◽  
Anica Petkovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coronary Flow ◽  
Heart Function ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cox Inhibitors ◽  
Stress Markers ◽  
Pressure Development ◽  
And Oxidative Stress ◽  
Isolated Rat

ABSTRACT Eicosanoids lead to the promotion of inflammation, cause fever and pain and have many other eff ects. NSAIDs block the action of cyclooxygenase (COX) during the process of converting arachidonic acid into inflammatory mediators, thus reducing the symptoms of inflammation. Investigations focusing on nonselective COX inhibitors, used in high doses, revealed harmful eff ects on myocardial function. Th e aim of our study was to assess the eff ects of two nonselective NSAIDs, diclofenac and ibuprofen, on cardiodynamic parameters, coronary flow and oxidative stress biomarkers in isolated rat hearts. Th e hearts of male Wistar albino rats were excised and retrogradely perfused according to the Langendorff technique at gradually increased coronary perfusion pressures (40-120 cm H2O). Th e experiments were performed under controlled conditions (Krebs-Henseleit physiological solution). Th e hearts were perfused with 10 μmol/l diclofenac and 10 μmol/l ibuprofen. Th e heart function parameters, including the maximum rate of pressure development (dp/dt max), minimum rate of pressure development (dp/dt min), systolic left ventricular pressure (SLVP), diastolic left ventricular pressure (DLVP), mean perfusion pressure (MBP) and heart rate (HR), were continuously registered. Coronary flow (CF) was measured flowmetrically. Oxidative stress markers, including the index of lipid peroxidation measured as TBARS, nitric oxide measured through nitrites (NO2 -), superoxide anion radical (O2 -), and hydrogen peroxide (H2O2) in the coronary venous effluent, were assessed spectrophotometrically. Our results showed that diclofenac aff ected cardiodynamic parameters more significantly than did ibuprofen. Furthermore, the present data indicate that both estimated COX inhibitors do not promote the production of reactive oxygen species.

scholarly journals Coronary flow and left ventricular pressure during diastole in the anaesthetized dog

1992 ◽  
Vol 77 (2) ◽  
pp. 397-400 ◽  
Author(s):  
D Gattullo ◽  
RJ Linden ◽  
G Losano ◽  
P Pagliaro ◽  
N Westerhof
Keyword(s):  
Coronary Flow ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Anaesthetized Dog

Improved Contractility and Coronary Flow in Isolated Hearts after 1-Day Hypothermic Preservation with Isoflurane Is Not Dependent on KATPChannel Activation 

1998 ◽  
Vol 88 (1) ◽  
pp. 233-244 ◽  
Author(s):  
David F. Stowe ◽  
Satoshi Fujita ◽  
Zeljko J. Bosnjak
Keyword(s):  
Coronary Flow ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Low Flow ◽  
Control Group ◽  
Protective Effects ◽  
Isolated Hearts ◽  
Time Control ◽  
O2 Extraction

Background Isoflurane protects against reperfusion injury in isolated hearts when given before, during, and initially after hypoxia or ischemia and aids in preconditioning hearts if given before ischemia. The aims of the current study were to determine if isoflurane is cardioprotective during 1-day, severe hypothermic perfusion and if a mechanism of protection is K(ATP) channel activation. Methods Guinea pig hearts (n = 60) were isolated, perfused with Kreb's solution initially at 37 degrees C, and assigned to either a nontreated warm, time control group or one of five cold-treated groups: drug-free cold control, 1.3% isoflurane, 1.3% isoflurane plus glibenclamide (4 microM), 2.6% isoflurane, or 2.6% isoflurane plus glibenclamide. Isoflurane and glibenclamide were given 20 min before hypothermia, during low-flow hypothermia (3.8 degrees C) for 22 h, and for 30 min after rewarming to 37 degrees C. Heart rate, left ventricular pressure, %O2 extraction, and coronary flow were measured continuously, and responses to epinephrine, adenosine, 5-hydroxytryptamine, and nitroprusside were examined before and after hypothermia. Results Each group had similar initial left ventricular pressures, coronary flows, and responses to adenosine, 5-hydroxytryptamine, and nitroprusside. Before hypothermia, isoflurane with or without glibenclamide increased coronary flow while decreasing left ventricular pressure and %O2 extraction. After hypothermia, left ventricular pressure and coronary flow were reduced in all cold groups but least reduced in isoflurane-treated groups. During normothermic perfusion after isoflurane and glibenclamide, left ventricular pressure, coronary flow, %O2 extraction, and flow responses to adenosine, 5-hydroxytryptamine, and nitroprusside were similarly improved in isoflurane and isoflurane-plus-glibenclamide groups over the cold control group but not to levels observed in the warm-time control group. Conclusion Isoflurane, like halothane, given before, during, and initially after hypothermia markedly improved but did not restore cardiac perfusion and function. Protective effects of isoflurane were not concentration dependent and not inhibited by the K(ATP) channel blocker glibenclamide. Volatile anesthetics have novel cardioprotective effects when given during long-term severe hypothermia.

Intramyocardial Pressure and Coronary Extravascular Resistance

1985 ◽  
Vol 107 (1) ◽  
pp. 46-50 ◽  
Author(s):  
P. D. Stein ◽  
H. N. Sabbah ◽  
M. Marzilli
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Driving Pressure ◽  
Ventricular Pressure ◽  
Intramyocardial Pressure ◽  
Extravascular Resistance

Intramyocardial pressure is an indicator of coronary extravascular resistance. During systole, pressure in the subendocardium exceeds left ventricular intracavitary pressure; whereas pressure in the subepicardium is lower than left ventricular intracavitary pressure. Conversely, during diastole, subepicardial pressure exceeds both subendocardial pressure and left ventricular pressure. These observations suggest that coronary flow during systole is possible only in the subepicardial layers. During diastole, however, a greater driving pressure is available for perfusion of the subendocardial layers relative to the subepicardial layers. On this basis, measurements of intramyocardial pressure contribute to an understanding of the mechanisms of regulation of the phasic and transmural distribution of coronary blood flow.

Bradykinin increases myocardial contractility: relation to the Gregg phenomenon

1991 ◽  
Vol 260 (6) ◽  
pp. R1095-R1103 ◽  
Author(s):  
P. A. Munch ◽  
J. C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Coronary Flow ◽  
Wall Motion ◽  
Left Ventricular Pressure ◽  
Systemic Circulation ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Afferent Nerves ◽  
Bilateral Vagotomy ◽  
And Control

Bradykinin (BK) is reportedly produced in the heart during ischemia. Because BK has been shown to activate cardiac afferent nerves thought to be nocioceptors, we tested whether BK might alter myocardial shortening, which potentially could contribute to afferent nerve stimulation. In open-chest dogs, BK (1-10 micrograms) was injected into the left anterior descending (LAD) coronary artery while wall motion in the LAD and control circumflex regions was monitored. Wall motion was measured with midwall segment gauges (sonomicrometer crystals) placed in the hoop direction. Blood pressure, heart rate, left ventricular pressure, first derivative of left ventricular pressure, and LAD coronary flow also were monitored. At 15-20 s after injection, which was before circulation of the peptide caused blood pressure to change, BK decreased maximum end-diastolic and minimum end-systolic segment lengths and increased maximum shortening fraction in LAD region. No change was observed in circumflex region. The response was not eliminated by bilateral vagotomy or subsequent stellate ganglionectomy, indicating that it was not neurally mediated. The response closely paralleled changes in coronary flow, was mimicked by intracoronary injection of adenosine, and was reduced or absent if flow was already elevated by previous injection of adenosine. When BK eventually reached the systemic circulation, the resultant hypotension further reduced shortening in LAD region, with directionally similar effect in circumflex region. These results suggest that BK can increase regional shortening by enhancing coronary flow (Gregg phenomenon) as well as by altering global ventricular function through systemic hypotension. Such changes in shortening may contribute to stimulation of cardiac afferent nerves.

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