Cerebral and Systemic Effects of Hypotension Induced by Adenosine or ATP in Dogs

Newberg, Leslie A.; Milde, James H.; Michenfelder, John D.

doi:10.1097/00000542-198504000-00010

Cited by 31 publications

(18 citation statements)

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“…In this study, the duration or the magnitude of ATP-induced effects on haemodynamics, airway resistance or rectal temperature was not measured after the administration of a bolus dose. The earlier published data suggests that these effects are of shorter duration: profound and controlled hypotension can be induced and maintained with the infusion of ATP in dog (Boarini et al 1984;Newberg et al 1985) and in man (Sollevi et al 1978;Fukunaga et al 1982). The temporary apnea observed in this study after intravenous ATP has been reported also previously (Green & Stoner 1950).…”

Section: Results Discussionsupporting

confidence: 83%

“…In previous studies, the blocking effect of ATP on the atrioventricular nodus has been demonstrated in man (Favale et al 1985;Rinne et al 1988;, and this action has been used to treat paroxysmal supraventricular tachycardia (Tajima et al 1985;Saito et al 1986). ATP has also been shown to cause more serious cardiac arrhythmias than bradycardia (ventricular extrasystolies, bigeminy) in dog (Boarini et al 1984) and in rat (Dedrick et al 1982), possibly due to metabolic acidocis (Newberg et al 1985) and chelation of magnesium and calcium by phosphate produced by the degradation of ATP (Dedrick et al 1982). Many of the effects seen after administration of ATP, can be attributed to its metabolic product, adenosine (Newberg et al 1985).…”

Section: Results Discussionmentioning

confidence: 99%

“…ATP has also been shown to cause more serious cardiac arrhythmias than bradycardia (ventricular extrasystolies, bigeminy) in dog (Boarini et al 1984) and in rat (Dedrick et al 1982), possibly due to metabolic acidocis (Newberg et al 1985) and chelation of magnesium and calcium by phosphate produced by the degradation of ATP (Dedrick et al 1982). Many of the effects seen after administration of ATP, can be attributed to its metabolic product, adenosine (Newberg et al 1985).…”

Section: Results Discussionmentioning

confidence: 99%

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Effects of Intravenous ATP on Tracheal Ciliary Activity, Airway Resistance and Haemodynamics in Rats

Saano¹,

Muranen²,

Nuutinen³

et al. 1990

Pharmacology & Toxicology

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The effect of the intravenous administration of ATP on the airway ciliary beating frequency (CBF) of anaesthetized rat was studied by measuring CBF photoelectrically from the inner surface of incised trachea. ATP (1 or 10 mg/kg) caused no changes in the CBF, but the decrease in CBF, which was seen after 70 min. in control rats, was abolished by ATP (10 mg/kg). ATP acutely decreased blood pressure; at 10 mg/kg, the decrease was 70 mmHg in systolic, and 60 mmHg in diastolic blood pressure. ATP also tended to increase rectal temperature and airway resistance, but these effects were not significant. ECG remained normal. Intravenous administration of ATP helps to maintain the function of tracheal cilia in anaesthetized rats at doses that, although lower blood pressure, do not cause fatal untoward effects.

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Section: Results Discussionsupporting

confidence: 83%

Section: Results Discussionmentioning

confidence: 99%

Section: Results Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Intravenous ATP on Tracheal Ciliary Activity, Airway Resistance and Haemodynamics in Rats

Saano¹,

Muranen²,

Nuutinen³

et al. 1990

Pharmacology & Toxicology

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“…Recently, Vahlensieck et al [17] showed that Ap6A exerted an A 1 -receptor-mediated negative chronotropic and inotropic effect in guinea-pig and human heart preparations as well. Other members of the purine family, namely adenosine and ATP, were shown to decrease MABP as well in various anesthetized and conscious animals [18][19][20][21][22]. The observed changes in MABP in our study are certainly not a consequence of the decreases in HR and CO, as maximal reductions in these parameters were reached before MABP was minimal and, conversely, HR and CO had returned to or even above control levels before MABP started to recover.…”

Section: Systemic Hemodynamicssupporting

confidence: 54%

Effects of Diadenosine Polyphosphates on Systemic and Regional Hemodynamics in Anesthetized Rats

Khattab

Hohage²,

Hollah³

et al. 1998

Kidney Blood Press Res

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Diadenosine polyphoshates (Ap4A, Ap5A, Ap6A) induce vasodilatation or vasoconstriction in various isolated vessels and influence central and peripheral hemodynamics. The influence of diadenosine polyphoshates on hemodynamics was studied in anesthetized rats in vivo. Mean arterial blood pressure (MABP) and heart rate (HR) measured in the carotid artery decreased with Ap4A, Ap5A and Ap6A. Renal blood flow (RBF), femoral blood flow (FBF) and cardiac output (CO) were evaluated by an ultrasonic transit-time method. Renal superficial blood flow (RSBF) was measured by laser Doppler flowmetry. CO, RBF and RSBF were decreased initially by all three diadenosine polyphosphates. FBF was also slightly decreased. Total peripheral (TPR), renal (RVR) and femoral (FVR) vascular resistances were calculated. TPR was transiently increased by the dinucleotides following by a decrease. RVR and, to a lesser extent, FVR were also increased. These data show that diadenosine polyphosphates have effects on both the heart and the peripheral blood vessels. The effects on the heart and MABP were dominated by bradycardia and hypotension. In the kidney, diadenosine polyphosphates induced a predominant vascoconstriction. The effects on skeletal muscle blood flow were much smaller. Thus, the three diadenosine polyphosphates studied differ in the effects on heart and peripheral vessels.

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“…14). Experimental and clinical evidence suggests that systemic adenosine administration has a limited iriflu-ence on normal pulmonary vascular resistance at infusion rates causing a marked reduction of the systemic vascular resistance (15,16). The influence of systemic adenosine administration on acute pulmonary hypertension has not yet been investigated.…”

mentioning

confidence: 99%

Influence of adenosine and prostacyclin on hypoxia‐induced pulmonary hypertension in the anaesthetized pig

Öwall

Davilén

Sollevi

1991

Acta Anaesthesiol Scand

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The effects of adenosine and prostacyclin (PGI2) infusions on hypoxia-induced pulmonary hypertension in the pulmonary and systemic circulatory systems of nine pigs were compared. The animals received the drugs in random order, and they were allowed to recover between each experimental sequence. Hypoxia was induced by reducing FiO2 to 0.12-0.13 so as to result in an arterial PO2 of approximately 6 kPa. Dose rates of adenosine or PGI2 during hypoxia were individualized in order to achieve a maximal reduction of 15% in the mean arterial blood pressure. Adenosine and PGI2 produced a fall in pulmonary vascular resistance of 36 +/- 4% (s.e.mean P less than 0.01) and 37 +/- 6% (P less than 0.01), respectively. The mean pulmonary artery pressure was reduced by 19 +/- 3% (P less than 0.01) during adenosine infusion and by 36 +/- 4% (P less than 0.01) during PGI2 infusion. The systemic haemodynamic responses to the two drugs were similar but adenosine produced a 7 +/- 2% (P less than 0.01) increase in cardiac output. Arterial PO2 during hypoxia and vasodilator treatment did not differ from the hypoxic situation without drug infusion. It is concluded that adenosine and PGI2 counteract hypoxia-induced increases in pulmonary vascular resistance similarly, but the reduction in pulmonary artery pressure was greater with PGI2 at infusion rates, causing minor systemic haemodynamic changes.

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Cerebral and Systemic Effects of Hypotension Induced by Adenosine or ATP in Dogs

Cited by 31 publications

References 0 publications

Effects of Intravenous ATP on Tracheal Ciliary Activity, Airway Resistance and Haemodynamics in Rats

Effects of Intravenous ATP on Tracheal Ciliary Activity, Airway Resistance and Haemodynamics in Rats

Effects of Diadenosine Polyphosphates on Systemic and Regional Hemodynamics in Anesthetized Rats

Influence of adenosine and prostacyclin on hypoxia‐induced pulmonary hypertension in the anaesthetized pig

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