Biomedical subjects

M Mattheussen

Publications and source records attributed to M Mattheussen.

11 recordsLinked to original sources

PubMed1996

Interaction of heart rate and hypothermia on global myocardial contraction of the isolated rabbit heart.

We studied the effects of mild hypothermia on cardiac contractility in isolated rabbit hearts perfused with Krebs-Henseleit solution according to the technique of Langendorff. Isovolumetric left ventricular pressure (LVP) was measured with a fluid-filled balloon. Hearts were paced after induction of atrioventricular block. At low heart rates ( < 30 bpm) mild hypothermia (cooling to 30 degrees C) induced a 32% increase in LVp (146.5 +/- 10 mm Hg at 30 degrees C vs 110.7 +/- 13 mm Hg at 37 degrees C) but this positive inotropic response was progressively lost by increasing heart rate. At pacing rates > or = 90 bpm, lower systolic LVP, higher diastolic LVP, and lower positive and negative LV dP/dt were obtained in hypothermic (93 +/- 12 mm Hg, 55 +/- 18 mm Hg, 584 +/- 137 mm Hg/s, and 323 +/- 57 mm Hg/s at 210 bpm, respectively) compared to normothermic hearts (123 +/- 4 mm Hg, 10 +/- 4 mm Hg, 1705 +/- 145.5 mm Hg/s, and 1155 +/- 78 mm Hg/s at 210 bpm, respectively.) The duration of mechanical diastole was reduced or suppressed in these hearts. Exposure to the beta-adrenoreceptor agonist, isoproterenol, improved this diastolic dysfunction during hypothermia and pacing at high rates, suggesting that the sarcoplasmic reticulum Ca2+ uptake might be involved. Our data are also consistent with an increase in myofilament Ca2+ sensitivity that is opposed by isoproterenol during hypothermia.

Actin Cytoskeleton↗

PubMed1996

The effect of prophylactic clonidine on postoperative shivering. A large prospective double-blind study.

The primary goal of this study was to assess the influence of clonidine administered after induction on postoperative shivering after elective peripheral surgery. The effect of clonidine on intra-operative haemodynamics (blood pressure and heart rate) during the first 30 min after induction and on the postoperative sedation of the patient was also investigated. Two hundred and eighty male ASA 1 and 2 patients, undergoing elective peripheral surgery were randomly administered either placebo or clonidine 2 micrograms.kg-1 intravenously over 10 min after induction of anaesthesia. Clonidine was found to reduce the total incidence (p = 0.024), the severity (p = 0.005) and the duration (p = 0.01) of postoperative shivering. Clonidine did not increase postoperative sedation or diminish overall consciousness. We conclude that administration of clonidine 2 micrograms.kg-1 intravenously after induction of anaesthesia is safe and reduces postoperative shivering in this group of patients.

Adrenergic alpha-Agonists↗

PubMed1993

Mechanism of the direct, negative inotropic effect of etomidate in isolated ferret ventricular myocardium.

BACKGROUND: Etomidate exerts a mild, positive inotropic effect in rat ventricular myocardium, yet has a negative inotropic effect in isolated rabbit ventricular myocardium. The aim of this study was to investigate the mechanisms of etomidate's inotropic effect and its underlying mechanism in isolated ferret ventricular myocardium (which shows similar physiologic characteristics as human ventricular myocardium) and in frog ventricular myocardium, in which Ca++ ions for myofibrillar activation are derived almost entirely from transsarcolemmal influx. METHODS: The authors analyzed the effects of etomidate after beta-adrenoceptor blockade on variables of contractility and relaxation, and on the free intracellular Ca++ transient detected with the Ca+(+)-regulated photoprotein aequorin. Etomidate's effects were also evaluated in ferret right ventricular papillary muscles in which the sarcoplasmic reticulum (SR) function was impaired by ryanodine, and in frog ventricular strips with little or no SR function. RESULTS: At concentrations > or = 3 micrograms/ml, which by far exceed the clinically useful concentration range, etomidate decreased contractility and the amplitude of the intracellular Ca++ transient. At equal peak force, control peak aequorin luminescence in [Ca++]o = 2.25 mM and peak aequorin luminescence in etomidate 10 micrograms/ml and [Ca++]o > 2.25 mM did not differ, which indicates that etomidate does not alter myofibrillar Ca++ sensitivity. After inactivation of sarcoplasmic reticulum Ca++ release with ryanodine 10(-6) M, a condition in which myofibrillar activation depends almost exclusively on transsarcolemmal Ca++ influx, etomidate caused a decrease in contractility and in the amplitude of the intracellular Ca++ transient, and etomidate's relative negative inotropic effect was not different from that in control muscles not exposed to ryanodine. Etomidate 10 micrograms/ml decreased contractility in frog ventricular myocardium. CONCLUSIONS: These findings indicate that the direct negative inotropic effect of etomidate results from a decrease in intracellular Ca++ availability with no changes in myofibrillar Ca++ sensitivity. At least part of etomidate's action is caused by inhibition of transsarcolemmal Ca++ influx. Yet, these effects become apparent only at concentrations that are at least one order of magnitude larger than those encountered in clinical practice.

Animals↗

PubMed1993

Potentiated state contractions in isolated hearts: effects of ischemia and reperfusion.

To investigate mechanisms underlying the contractile dysfunction during myocardial "stunning," potentiated contractions were studied in Langendorff-perfused rabbit hearts paced at 2.5 Hz. Isovolumetric left ventricular pressure (LVP) and the first derivative of LVP (dP/dt) were measured via a balloon. Potentiated contractions, elicited after 3 s of rest (postrest potentiation, PRP) or with paired pulses (paired-pulse potentiation, PPP) were first characterized in nonischemic conditions. Exposure to 5 nM ryanodine changed PRP into postrest depression [control, 134 +/- 1.7% (SE); ryanodine, 65 +/- 3.4%; n = 5] but did not decrease PPP (control, 125 +/- 7.2%; ryanodine, 141 +/- 14.5%). When sarcolemmal Ca2+ influx was decreased by 0.2-2 microM verapamil, PRP increased (control, 136 +/- 3.7%; 1 microM verapamil, 214 +/- 23.8%; n = 5), whereas PPP was maintained (control, 134 +/- 8.0%; 1 microM verapamil, 154 +/- 11.5%). During ischemia, both PRP and PPP were increased above preischemic values (from 128 +/- 1.9 to 355 +/- 60.4% and from 122 +/- 5.4 to 313 +/- 37.4%, respectively, n = 5). Changes of potentiation of dP/dt were qualitatively similar to those of LVP. On reperfusion, rest potentiation transiently decreased (PRP of dP/dt: 127 +/- 6% preischemia vs. 112 +/- 3% at 2 min postischemia; n = 6). However, PPP increased during the first 20 min of reperfusion (PPP of dP/dt: 184 +/- 22% preischemia vs. 236 +/- 34% postischemia; n = 6). This transient depression of PRP during reperfusion suggests an impairment of sarcoplasmic reticulum function in stunned myocardium, at least during the early phase of reperfusion.

Animals↗

PubMed1993

Recovery of function and adenosine triphosphate metabolism following myocardial ischemia induced in the presence of volatile anesthetics.

Using a normothermic isolated working rabbit heart model, experiments were performed to determine whether exposure to halothane or isoflurane prior to ischemia improved postischemic recovery of myocardial function and the preservation of myocardial high energy phosphates. After 30 min of Langendorff perfusion, hearts were perfused for 30 min in the working mode. Three groups were studied: 1) the blank undergoing no pretreatment during an additional 15 min of working mode; 2) hearts exposed to 1.5% halothane; and 3) hearts exposed to 2.3% isoflurane during the additional 15 min of working mode. Subsequently, all hearts underwent 15 min of global normothermic ischemia, followed by 5 min of Langendorff reperfusion and 15 min of working heart mode using a perfusate devoid of volatile anesthetic. Adenosine triphosphate (ATP) and catabolites were determined after 15 min exposure to volatile anesthetics or blank, after 15 min global ischemia and at the end of the recovery phase. Myocardial function was determined after 30 min of working mode, after exposure to volatile anesthetics, and at the end of the recovery phase. In nonischemic hearts, 15-min treatment with 1.5% halothane or 2.3% isoflurane resulted in a significant decrease in positive LVdP/dt, from 1858 +/- 286 to 1316 +/- 180 mm Hg.s-1 and from 1888 +/- 304 to 1541 +/- 226 mm Hg.s-1, respectively. Coronary flow was increased significantly after isoflurane but not after halothane.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1992

Effect of ischemia and reperfusion on sarcoplasmic reticulum calcium uptake.

To investigate the mechanism underlying postischemic cardiac dysfunction (myocardial stunning), contractility and adenine nucleotide metabolism were studied in three groups of isolated perfused rabbit hearts (control, ischemic, and reperfused), whereas Ca2+ uptake by the sarcoplasmic reticulum (SR) was measured in homogenates obtained from them. The hearts were Langendorff-perfused under constant pressure with Krebs-Henseleit solution at 37 degrees C. Global normothermic ischemia was produced by closing the perfusion line. In the reperfused group, after 15 minutes of ischemia, Krebs-Henseleit solution was perfused for 10 minutes. Developed left ventricular pressure (control, 104 +/- 6.3 mm Hg) and left ventricular dP/dt (2,063 +/- 256.6 mm Hg.sec-1) were significantly decreased in reperfused hearts (left ventricular pressure, 78 +/- 5.9 mm Hg; left ventricular dP/dt, 1,339 +/- 216.3 mm Hg.sec-1). Myocardial ATP content (control, 13.6 +/- 0.98 mumol/g dry wt) decreased during ischemia (4.5 +/- 1.23 mumol/g) but was restored to control level on reperfusion (11.8 +/- 0.68 mumol/g). Maximum velocity of Ca2+ uptake by the SR (Vmax) (control, 49.3 +/- 2.54 nmol.min-1 x mg-1) was significantly depressed by ischemia (36.3 +/- 1.94 nmol.min-1 x mg-1) but was restored to the control value after a 10-minute reperfusion (45.3 +/- 0.79 nmol.min-1 x mg-1). Apparent dissociation constant KCa and the Hill coefficient for Ca2+ uptake were not different between control, ischemia, and reperfusion. To test for the possible role of the SR Ca(2+)-release channel in the effect of ischemia and reperfusion, we measured Ca2+ uptake after incubation of homogenates with 610 microM ryanodine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗

PubMed1991

Mitochondrial function in myocardial stunning.

Mitochondrial respiration parameters were studied in mitochondria isolated from normal, ischemic and post-ischemic rabbit hearts. Mitochondrial function was related to tissue content of high energy phosphates (HEP) and cardiac function in the isolated working rabbit heart preparation. It was found that after 10 and 20 mins of global normothermic ischemia followed by 20 mins of Langendorff reperfusion, mitochondrial function and HEP content of the myocardium were not significantly diminished. Myocardial creatine phosphate even showed a significant overshoot as compared to the pre-ischemic condition. When these hearts were allowed to perform work, recovery of cardiac function was incomplete while mitochondrial function and HEP content remained in the normal range. Prolonged ischemia (30 mins) resulted in a significant depression of mitochondrial function and myocardial ATP content during and after ischemia. Recovery of contractile function was severely depressed. These results show that impaired cardiac function after a mild ischemic insult (myocardial stunning) can be associated with near normal mitochondrial function and HEP contents.

Adenosine Triphosphate↗

PubMed1990

Effect of propofol on cerebral circulation and autoregulation in the baboon.

The purpose of this study was to investigate the effect of propofol on cerebral blood flow, cerebral metabolism, and cerebrovascular autoregulatory capability. Seven anesthetized baboons were given propofol at three different infusion rates. An infusion of 3 mg.kg-1.h-1 caused minimal changes, but infusion rates of 6 and 12 mg.kg-1.h-1 decreased cerebral blood flow by 28% and 39%, respectively. The changes in cerebral metabolic rate of oxygen were not statistically significant. However, with the two higher infusion rates, there was a trend toward decrease, by 5% and 22%, respectively, for the cerebral metabolic rate of oxygen, and by 18% and 36% for the cerebral metabolic rate of glucose. A 25-30 mm Hg increase in arterial blood pressure had no influence on cerebral blood flow. Replacement of nitrous oxide by nitrogen had no significant influence on cerebral blood flow or metabolism. It is concluded that propofol causes a dose-dependent decrease in cerebral blood flow. However, the study does not prove that this decrease in cerebral blood flow is accompanied by the same degree of decrease in cerebral metabolism. Further studies are clearly needed to clarify propofol's influence on the coupling between cerebral metabolism and blood flow. The physiologic responsiveness of the cerebral circulation to alterations in arterial pressure is well preserved. Propofol appears to prevent the metabolic stimulation and increased cerebral blood flow that has been associated with the administration of nitrous oxide.

Animals↗

PubMed1990

[Effect of nifedipine and urapidil on autoregulation of cerebral circulation in the presence of an intracranial space occupying lesion].

We investigated in dogs with an intracranial space occupying lesion the effects of the antihypertentive agents nifedipine and urapidile on intracranial pressure (ICP) and intracerebral autoregulation. During the application of nifedipine the ICP rose significantly whereas urapidile had no influence on the ICP. By continuous angiotensin infusion the mean arterial pressure was raised by 50% by which a simultaneous increase of the ICP could be seen in the nifedipine group, whereas the urapidile group remained unaffected.

Angiotensin II↗

PubMed1989

Responsiveness of the cerebral circulation to acute alterations in mean arterial pressure during the administration of propofol.

The responsiveness of the cerebral circulation to acute increases in mean arterial pressure was studied before and during the administration of propofol 3, 6, or 12 mg/kg/h in the anaesthetised baboon. Although mean arterial pressure increased significantly on each occasion, there were no significant changes in cerebral blood flow. This indicates that the physiological responsiveness of the cerebral circulation to alterations in mean arterial pressure was preserved during the administration of propofol in the concentrations studied.

Journal Article↗

PubMed1989

The effect of sufentanil on intracranial pressure (ICP) in anesthetized dogs.

The use of sufentanil in neuroanesthesia has been questioned because of a potential increase in intracranial pressure (ICP) in dogs and humans. The effect of sufentanil administration on ICP was studied in 6 dogs with normal and elevated baseline ICP, anesthetized with nitrous oxide and an intravenous piritramide infusion. No significant change in ICP could be demonstrated over a 30 minute observation period after administration of 2 micrograms/kg of sufentanil. The results indicate that this dose of sufentanil does not increase ICP in moderately hyperventilated dogs under stable anesthetic conditions.

Analgesics, Opioid↗