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Biomedical subjects

D M Philbin

Publications and source records attributed to D M Philbin.

At least 37 records · Page 2Linked to original sources
PubMed1988

Effect of hypothermic hemodilutional cardiopulmonary bypass on plasma sufentanil and catecholamine concentrations in humans.

The effect of hypothermic hemodilutional cardiopulmonary bypass (CPB) on plasma sufentanil and catecholamine concentrations was studied in four groups of ten patients each, receiving four different doses of sufentanil. Samples for measurement of sufentanil were obtained before CPB, at 15, 30, and 45 minutes of CPB, during rewarming, immediately after and 15, 60, and 240 minutes after CPB. In addition, in groups III and IV, which received the highest dose of sufentanil, blood samples were also obtained for measurement of plasma levels of epinephrine and norepinephrine. Sufentanil concentration decreased in all groups with the start of CPB (group I, 2.92 +/- 0.2 to 2.04 +/- 0.2; group II, 3.30 +/- 0.3 to 1.51 +/- 0.2; group III, 7.08 +/- 0.7 to 3.45 +/- 0.3; group IV, 10.33 +/- 0.5 to 4.59 +/- 0.5 ng/ml). No further decreases occurred during CPB but increases occurred with rewarming. The first measurement after CPB approached the concentration before CPB (group I, 2.82 +/- 0.3; group II, 2.56 +/- 0.5; group III, 4.42 +/- 0.4; group IV, 6.10 +/- 0.4 ng/ml). Norepinephrine concentrations demonstrated a wide variability with no significant changes. Epinephrine levels increased significantly during rewarming in both groups (group III, 141 +/- 23 to 279 +/- 79 pg/ml; P less than 0.05; group IV, 105 +/- 24 to 267 +/- 68 pg/ml, P less than 0.05). The stability of plasma sufentanil concentrations during CPB suggest that no measurable metabolism or excretion occurred. The increase with rewarming and after CPB suggest significant sequestration.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1988

Intravenous diltiazem worsens regional function in compromised myocardium.

The effect of intravenous diltiazem on regional myocardial function was assessed in a canine model of critical constriction of the left anterior descending coronary artery (LAD). Maintenance anesthesia with fentanyl (1.5 micrograms.kg-1.min-1), 60% inspired nitrous oxide, and 0.7% inspired halothane resulted in regional dysfunction, measured as postsystolic shortening (20.6 +/- 10.7%), which was significantly worsened after 0.1 mg/kg (48.7 +/- 12.5%, P less than 0.05) and after 0.2 mg/kg (68.8 +/- 11.7%, P less than 0.05) intravenous diltiazem. Systolic shortening in the compromised LAD territory was substantially depressed after 0.1 mg/kg diltiazem (8.2 +/- 0.6% to 5.3 +/- 1.3%, P less than 0.05) and was essentially abolished after 0.2 mg/kg diltiazem (8.2 +/- 0.6% to 0.7 +/- 2.3%, P less than 0.05). At the higher dose of diltiazem, cardiac output was substantially decreased (1.37 +/- 0.23 L/min to 0.88 +/- 0.30 L/min, P less than 0.05) and LV dP/dtmax significantly depressed (1090 +/- 90 mm Hg/sec to 744 +/- 80 mm Hg/sec, P less than 0.05). These results demonstrate significant depression of regional systolic shortening and substantial worsening of regional dysfunction in myocardium with a compromised blood supply, in association with significant depression of left ventricular performance, with intravenous diltiazem administration during anesthesia.

Anesthesia, Inhalation↗
PubMed1988

Gradual or abrupt nitrous oxide administration in a canine model of critical coronary stenosis induces regional myocardial dysfunction that is worsened by halothane.

The existence of a dose-response relation between nitrous oxide concentration and regional dysfunction in compromised myocardium, and whether or not halothane-induced myocardial depression alleviated this regional dysfunction was examined. Nitrous oxide was administered to eight dogs with experimentally induced left anterior descending coronary artery (LAD) critical stenosis during fentanyl (100 micrograms/kg bolus plus 1.5 micrograms.kg-1.min-1) anesthesia. Two modes of nitrous oxide administration were employed: gradual (in steps of 20% inspired, i.e., 0%, 20%, 40%, and 60% inspired) and abrupt (0-60% inspired). Regional myocardial function was assessed by sonomicrometry. Regional dysfunction in the compromised myocardium, in the form of postsystolic shortening (PSS), increased above baseline levels during 40% (4.2 +/- 2.3% to 12.1 +/- 3.9%, P less than 0.05) and 60% (4.2 +/- 2.3% to 12.5 +/- 3.6%, P less than 0.05) inspired nitrous oxide (gradual administration) and also during abrupt 60% nitrous oxide administration (6.4 +/- 2.6% to 9.9 +/- 3.2%, P less than 0.05). After abrupt 60% inspired nitrous oxide administration, halothane (0.7% inspired) was introduced and caused decreases in mean arterial pressure (106.1 +/- 4.5 mm Hg to 76.2 +/- 5.5 mm Hg, P less than 0.05) and peak LV dP/dt (1700 +/- 150 mm Hg/sec to 1100 +/- 100 mm Hg/sec, P less than 0.05). Halothane caused a marked increase in PSS (9.9 +/- 3.2% to 30.8 +/- 12.6%, P less than 0.05). Thus nitrous oxide administration caused regional dysfunction in myocardium supplied by a critically narrowed LAD whether administered gradually or abruptly and at concentrations as low as 40% inspired.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Histamine antagonists and d-tubocurarine-induced hypotension in cardiac surgical patients.

Hemodynamic effects and histamine release by bolus injection of 0.35 mg/kg of d-tubocurarine were studied in 24 patients. H1- and H2-histamine antagonists or placebo were given before dosing with d-tubocurarine in a randomized double-blind fashion to four groups: group 1--placebo; group 2--cimetidine, 4 mg/kg, plus placebo; group 3--chlorpheniramine, 0.1 mg/kg, plus placebo; and group 4--cimetidine plus chlorpheniramine. Histamine release occurred in most patients, the highest level 2 minutes after d-tubocurarine dosing. Group 1 had a moderate negative correlation between plasma histamine change and systemic vascular resistance (r = 0.58; P less than 0.05) not present in group 4. Prior dosing with antagonists partially prevented the fall in systemic vascular resistance. These data demonstrate that the hemodynamic changes associated with d-tubocurarine dosing are only partially explained by histamine release. Thus prior dosing with H1- and H2-antagonists provides only partial protection.

Blood Pressure↗
PubMed1986

The effect of diazepam on induction of anesthesia with alfentanil.

This study investigated the effect of intravenous diazepam on induction of anesthesia with alfentanil. Forty ASA physical status I and II patients were given one of four treatments: alfentanil 100 micrograms/kg or 200 micrograms/kg, without diazepam or preceded by 0.125 mg/kg diazepam intravenously. Blood pressure, heart rate, respiration, response to verbal command, and movement were assessed for 5 min, and blood was taken for measurement of histamine, epinephrine, and norepinephrine. All ten patients receiving 100 micrograms/kg and five of the ten patients receiving 200 micrograms/kg of alfentanil responded to voice after 5 min, but only one in each group responded when it was preceded by diazepam. There was no rigidity or serious arrhythmias in any patient. Heart rate increased in patients receiving alfentanil alone. Blood pressure increased in those receiving 100 micrograms/kg but not 200 micrograms/kg. In patients given diazepam, tachycardia did not occur, but blood pressure decreased after administration of alfentanil. There were no significant changes in plasma levels of histamine or catecholamines. Five of the six cases of inadequate postoperative ventilation were in patients given diazepam. Despite these effects, diazepam or some other hypnotic agent may be indicated when alfentanil is used for induction.

Adult↗
PubMed1986

[Coronary circulation, myocardial oxygen consumption and myocardial metabolism during enflurane-nitrous oxide anesthesia in coronary patients].

The effects of enflurane on myocardial oxygen consumption, metabolism and coronary blood flow (argon washin) were studied in 10 patients with 2- or 3-vessel coronary artery disease undergoing coronary artery bypass surgery. All patients were men with stable angina and normal left ventricular function and were on maintenance doses of beta-receptor- or calcium-antagonists. Anaesthesia consisted of enflurane and 50% nitrous oxide in oxygen. Measurements were performed and blood samples were taken with the patient awake, 30 min after induction of anaesthesia without any surgical stimulation and during sternotomy. End-tidal enflurane concentrations averaged 0.9% after induction and 2.5% during sternotomy. Enflurane decreased coronary blood flow significantly by 36% after induction, while sternotomy increased coronary blood flow by 29%. Myocardial oxygen uptake was decreased by 33% and was increased by 37% during sternotomy. Coronary vascular resistance did not change significantly during the entire observation period, while coronary sinus oxygen saturation significantly increased after induction by 20% followed by a decrease to preinduction levels during sternotomy. Myocardial glucose, free fatty acids, lactate and pyruvate uptake were significantly reduced after induction and increased to preinduction levels during sternotomy. Myocardial lactate production could not be demonstrated at any time during the observation period.

Anesthesia, Inhalation↗
PubMed1986

[Isoflurane: coronary blood flow and myocardial metabolism in patients with coronary heart disease].

The effects of isoflurane on myocardial oxygen uptake, metabolism and coronary blood flow (argon washin-technique) were studied in 10 patients undergoing three-vessel coronary artery bypass surgery. All patients were men with stable angina and normal left ventricular function and were receiving maintenance doses of beta-receptor antagonists or calcium channel blocking drugs. Anaesthesia consisted of isoflurane and 50% nitrous oxide in oxygen. Measurements were performed and blood samples were taken with the patients awake, 20 min after induction of anaesthesia without surgical stimulation, and during sternotomy and sternal spread. End-tidal isoflurane concentrations averaged 0.4% after induction of anaesthesia and 1.5% during sternotomy. Isoflurane significantly decreased myocardial blood flow by 18% following induction of anaesthesia, while sternotomy increased myocardial blood flow to pre-induction levels. Induction decreased myocardial oxygen uptake by 32%, while sternotomy increased oxygen uptake by 21% vs post-induction values. Myocardial uptake of glucose, lactate, free fatty acids and pyruvate significantly decreased after induction and increased to pre-induction levels during sternotomy. Myocardial lactate production, indicating myocardial ischaemia, was observed in 1 patient after induction and in three patients during sternotomy; three additional patients demonstrated a marked reduction in myocardial lactate uptake after induction and during sternotomy. It is concluded that all changes in myocardial metabolism, oxygen uptake and coronary blood flow were the result of a decrease in haemodynamic load on the myocardium and reduced contractility, while the increase in these parameters during sternotomy was due to an increase in myocardial work.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Regional and global myocardial function in the dog when nitrous oxide is added to halothane in the presence of critical coronary artery constriction.

The effect of substituting 66% nitrous oxide for nitrogen on global and regional myocardial function before and after critical constriction of the left anterior descending coronary artery (LAD) was studied in six open-chested dogs anesthetized with 1% halothane (inspired). Regional myocardial function was measured in the region of the LAD and in the region of the left circumflex artery using sonomicrometry, and LAD blood flow was measured. Administration of nitrous oxide produced moderate depression of global performance. Regional shortening in both myocardial segments was reduced, and dysfunction also appeared in the LAD segment. This dysfunction was observed in the presence of both normal coronary blood flow, and after critical constriction. The appearance of dysfunction when coronary blood flow was unimpaired suggests that ischemia may not be the only cause of regional myocardial dysfunction.

Animals↗
PubMed1985

Postsystolic shortening of canine left ventricle supplied by a stenotic coronary artery when nitrous oxide is added in the presence of narcotics.

The effects of fentanyl and sufentanil with and without N2O on left ventricular myocardium supplied by a critically narrowed and a normal coronary artery were studied in 16 dogs. Regional ventricular function was measured by recording ventricular segment length with the use of ultrasonic length detectors in the left anterior descending (LAD) and the left circumflex (LC) coronary artery territories before and during critical stenosis of the LAD. Critical stenosis was documented by the absence of a hyperemic response following a 10-s total occlusion of the LAD. Hemodynamic variables (aortic flow and pressure, left ventricular pressure, heart rate, and coronary blood flow) were measured and the first derivative of left ventricular pressure (LVdP/dt) and coronary perfusion pressure derived. Eight dogs received fentanyl 100 micrograms X kg-1 followed by an infusion of 1 microgram X kg-1 X min-1 while ventilated with O2:N2 (1:2), and eight dogs received sufentanil 30 micrograms X kg-1 with an infusion of 0.3 micrograms X kg-1 X min-1. Replacement of N2 with N2O produced evidence of mild systolic myocardial depression but no dysfunction in either group. After application of the critical constriction, the addition of N2O rapidly produced evidence of dysfunction with significant postsystolic shortening only in the LAD territory. This was not accompanied by hypotension or a decrease in coronary flow and was not always reversible. Higher infusion rates of either narcotic (fentanyl 2 micrograms X kg-1 X min-1, 4 micrograms X kg-1 X min-1; sufentanil 0.6 micrograms X kg-1 X min-1, 1.2 micrograms X kg-1 X min-1) in the absence of N2O did not produce dysfunction but had no protective effect when N2O was added.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1985

Prostaglandin E1. A new therapy for refractory right heart failure and pulmonary hypertension after mitral valve replacement.

Patients undergoing mitral valve replacement, particularly those with severe pulmonary hypertension and/or congestive heart failure, may develop life-threatening right heart failure in the immediate postbypass period. We have observed that such patients have intense pulmonary vasoconstriction. The markedly increased pulmonary impedance may aggravate the right heart failure and prevent recovery of right ventricular function in this setting. Therefore, we studied the effects of high-dose prostaglandin E1 (30 to 150 ng/kg/min), a potent pulmonary vasodilator, in combination with massive infusion of norepinephrine (up to 1 microgram/kg/min) into the left atrium in five consecutive patients with refractory right heart failure and pulmonary hypertension after mitral valve replacement. This pharmacologic approach takes advantage of the pulmonary vasodilating effects of prostaglandin E1, while offsetting associated systemic vasodilation and resulting hypotension. All five patients had rapid pulmonary vasodilator responses followed by marked improvement in right ventricular function. All survived the operation and none had right ventricular infarction or chronic right heart failure postoperatively.

Adult↗
PubMed1983

Pulsatile and nonpulsatile cardiopulmonary bypass: review of a counterproductive controversy.

In the controversy over pulsatile and nonpulsatile perfusion, most authors have failed to recognize the fundamental physical differences between the two methods. Pulsatile perfusion is polymorphic and its form varies with both the pulsatile source and the vascular system being perfused; nonpulsatile perfusion is by definition unvarying and uniform. While many studies of hemodynamics, metabolism, organ function, microcirculation, and histology show benefits derived from pulsatile perfusion, others do not. The simplest explanation for these conflicts is that different investigators employ different forms of pulsatile perfusion, only some of which are effective. Failure to quantitate adequately the pulsatile components of flow in these studies prevents differentiation between effective and ineffective forms of pulsatile flow and makes comparison of studies difficult. Future research in this area should be directed toward definition of effective pulsatile perfusion by adequate measurement of the pulsatile components of perfusion.

Cardiopulmonary Bypass↗
PubMed1983

Temperature gradients and rewarming time during hypothermic cardiopulmonary bypass with and without pulsatile flow.

Pulsatile perfusion during cardiopulmonary bypass (CPB) has been reported to have a number of beneficial effects, including attenuation of hormonal stress responses and improved organ blood flow and function. To determine the effect of pulsatile perfusion on temperature gradients and the time required for cooling and rewarming during CPB, we studied 21 patients scheduled for elective coronary artery operations. The patients were divided into two comparable groups: Group 1 (N = 11) had standard nonpulsatile perfusion, while in Group 2 (N = 10), a pulsatile pump was used. Rectal and esophageal temperatures were monitored, as were deltoid muscle temperatures and upper arm and finger skin temperatures in the same extremity. Ambient temperature, bypass flow and pressure, and bypass time were similar in both groups. Time required to cool to the lowest esophageal temperature was virtually identical for both groups (Group 1, 17 +/- 3 min; Group 2, 17.6 +/- 5 min), as was rewarming time (Group 1, 26.8 +/- 11 min; Group 2, 27.2 +/- 6 min). There were no significant differences in temperature measurements between groups except briefly during rewarming when finger skin temperature rose more rapidly in Group 1 (p less than 0.05). Temperature changes following CPB were the same for both groups, with rectal and esophageal temperatures showing an inverse relationships. These data demonstrate that pulsatile flow does not substantially alter rewarming time or temperature gradients during hypothermic CPB.

Aged↗
PubMed1983

Adrenocortical hormone levels during cardiopulmonary bypass with and without pulsatile flow.

To determine the effect of hypothermic pulsatile and nonpulsatile cardiopulmonary bypass (CPB) with hemodilution on adrenocortical function we measured plasma levels of adrenocorticotropic hormone (ACTH), cortisol, aldosterone, and renin in two groups of patients. Group I, comprising 11 patients had routine CPB (nonpulsatile), and Group II, comprising 12 patients, had pulsatile flow during CPB (pulsatile). Both groups demonstrated comparable increases in cortisol, ACTH, and aldosterone with operation. Levels for all three hormones appeared to decline during CPB and then rose again in the post-CPB period. There were no significant differences between groups. Plasma renin activity gradually declined in a comparable manner in both groups. In the post-CPB period, renin activity was slightly higher in the nonpulsatile group (1.7 +/- 0.5 versus 0.8 +/- 0.2 ng/ml/hr, p less than 0.05). Correction for the effect of hemodilution demonstrated no decrease in cortisol and a slight increase in ACTH in both groups during CPB. Significant increases occurred in both groups during CPB in urinary Na+ excretion rate and urinary Na+/K+ ratio, more so for the nonpulsatile group. There was no correlation between urinary Na+/K+ ratios and either plasma cortisol or aldosterone levels. Thus routine CPB demonstrates no evidence of adrenocortical hypofunction and the addition of pulsatile flow produces little improvement.

Adrenal Cortex Hormones↗