Search PubMed⌕ Search

Biomedical subjects

D M Philbin

Publications and source records attributed to D M Philbin.

At least 55 records · Page 3Linked to original sources
PubMed1983

Diazepam-fentanyl interaction--hemodynamic and hormonal effects in coronary artery surgery.

Diazepam has been reported to produce hypotension when administered with anesthetic doses of fentanyl. Twenty patients undergoing coronary bypass surgery were randomly assigned to one of four treatment groups: group 1, no diazepam; groups 2, 3, and 4, 0.125, 0.25, and 0.5 mg X kg -1 of diazepam, respectively. All patients then received 50 micrograms X kg -1 fentanyl at 400 micrograms X min -1 and 0.4 mg X kg -1 metocurine at 2 mg X min -1. Hemodynamic parameters were recorded and blood was sampled for measurement of plasma catecholamine and histamine concentrations. Heart rate, cardiac index, stroke volume index, central venous pressure, pulmonary arterial and wedge pressures, and pulmonary vascular resistance did not change significantly in any group. Patients in groups 2-4 had significant decreases in mean arterial pressure and systemic vascular resistance during fentanyl infusion. These hemodynamic changes were accompanied by decreases in plasma epinephrine and norepinephrine levels. These hemodynamic and hormonal changes did not occur in patients given fentanyl only. Plasma histamine levels did not change significantly in any group. Caution should be used when diazepam in doses as small as 0.125 mg X kg -1 are combined with high-dose fentanyl anesthesia.

Adult↗
PubMed1983

Temperature gradients in cardiac surgical patients--a comparison of halothane and fentanyl.

Narcotics and potent inhalation anesthetics have different effects on thermoregulation and the distribution of body heat. This study was designed to compare the effect of halothane vs fentanyl anesthesia on temperature gradients developed during and after hypothermic cardiopulmonary bypass. Twenty-two adult patients undergoing coronary artery surgery were given either fentanyl (100 micrograms/kg) or halothane (0.5-1.5%) and oxygen. Thermistor probes were inserted in rectum, esophagus, and deltoid muscle. Surface temperatures were measured on the ring finger and upper arm. All patients were cooled during cardiopulmonary bypass to 28 degrees C, and ambient temperature was maintained at 22-23 degrees C. The times to cool and rewarm were comparable in both groups. Rectal, esophageal, and skin temperatures had not reached equilibrium by 60 min after bypass, but changes in temperature were virtually identical at all sites in both groups. Regardless of differences in the effects of halothane and fentanyl on hormonal responses, blood flow, or central thermoregulation, their net effects on body temperature were the same.

Adult↗
PubMed1983

Haemodynamic effects of bolus injections of atracurium in patients with coronary artery disease.

Atracurium has been reported to have minimal haemodynamic effects in healthy patients. The purpose of this study was to determine its effects in patients with coronary artery disease. Sixteen patients scheduled for elective coronary artery surgery were studied in two equal groups. Group 1 received a bolus injection of atracurium 0.3 mgkg-1 and group 2 0.4 mgkg-1. Under local anaesthesia, radial artery, pulmonary artery thermodilution and central venous catheters were placed and the appropriate vascular pressures continuously monitored, as were leads II and V5 of the electrocardiogram. Sleep was induced with lorazepam and fentanyl while the patients were breathing nitrous oxide in oxygen (50:50). Control measurements of arterial pressure (AP) (mean, systolic, diastolic), CO (thermodilution), CVP, PA, PCW and HR were obtained. Atracurium was administered as a bolus and measurements repeated at 2, 5, and 10 min. In group 1 mean and diastolic arterial pressure decreased significantly at 2 min (73 +/- 2 to 66 +/- 3 mm Hg, P less than 0.05; 58 +/- 3 to 51 +/- 2 mm Hg, P less than 0.05). The changes were not significant at 5 or 10 min. There were no significant changes in CO or SVR. One patient in this group exhibited a typical histamine response with vasodilatation and flushing. In this patient mean arterial pressure decreased from 70 to 55 mm Hg and CO increased from 4.90 to 7.24 litre min-1. Excluding this patient from group 1 eliminated the significance of the haemodynamic changes for the rest of the group (MAP = 73 +/- 2 to 68 +/- 2 mm Hg, n.s.; mean diastolic AP = 58 +/- 3 to 53 +/- 2 mm Hg, n.s.). In group 2 none of the haemodynamic parameters measured showed significant changes. These results demonstrate minimal haemodynamic effects with 0.3- or 0.4-mgkg-1 bolus injections of atracurium in 15 patients with coronary artery disease, but in one patient doses of 0.3 mgkg-1 produced a typical histamine response with marked cardiovascular changes.

Aged↗
PubMed1982

Histamine release by neuromuscular blocking agents in man.

Several experimental and clinical studies have suggested that histamine is released following the administration of neuromuscular blocking agents, and that the histamine release is an important aspect in the hemodynamic response to the drug. We have measured plasma histamine following the administration of a series of neuromuscular blocking agents in man. Our data suggests that members of this class of drugs can cause a dose dependent release histamine release in man and that this release is hemodynamically significant. We have also evaluated the roles of rate of administration, of pretreatment with H1 and H2 antagonists and alterations in drug design as clinical strategies in attenuating the adverse reactions. The data obtained in humans can be shown to validate the cat model as a means of screening novel neuromuscular blocking agents.

Animals↗
PubMed1982

Histamine release during morphine and fentanyl anesthesia.

High doses of morphine produced peripheral vasodilation and frequently significant hypotension. These effects are thought to be due, in part, to the release of histamine. One putative advantage of high-dose fentanyl anesthesia is its relatively small effect on peripheral vascular resistance. In a randomized study, the authors examined the possibility that the hemodynamic differences between morphine and fentanyl might be attributable to histamine release. Fifteen patients were studied prior to coronary artery bypass surgery. Subjects received in infusion of morphine (1 mg . kg-1, iv at 100 micrograms . kg-1 . min-1 [n = 8]) or fentanyl (50 micrograms . kg-1 at 5 micrograms . kg-1 . min-1 [n = 7]). Patients in the morphine group had an average 750 per cent peak increase in plasma histamine accompanied by a significant decrease in mean arterial pressure (-27 mmHg- and systemic vascular resistance (-520 dyne . s . cm-5). The greatest decrease in systemic vascular resistance occurred in those patients with the highest levels of plasma histamine (r = -0.81). Patients in the fentanyl group had no change in plasma histamine and no decrease in arterial pressure or systemic vascular resistance. Cardiac output and heart rate were comparable between the two groups. Differences in the release of histamine account for most, if not all, of the different effects of morphine and fentanyl on the peripheral vasculature.

Anesthesia↗
PubMed1982

Antidiuretic and growth hormone responses during coronary artery surgery with sufentanil-oxygen and alfentanil-oxygen anesthesia in man.

Antidiuretic hormone (ADH), growth hormone (GH), and cardiovascular responses to large (anesthetic) doses of alfentanil (1.2 +/- 0.02 mg/kg) and oxygen and sufentanil (13.1 +/- 0.4 microgram/kg) and oxygen were measured before and during surgery (including cardiopulmonary bypass) and at the end of surgery in 29 patients undergoing coronary artery bypass surgery. The data demonstrate that alfentanil-O2 and sufentanil-O2 result in little change in cardiovascular dynamics throughout anesthesia and surgery, and also prevent changes in plasma levels of ADH and GH at all times during the study. Our findings contrast with previous studies with other anesthetics, including fentanyl, in which plasma levels of ADH and GH become markedly elevated during bypass. The results suggest that alfentanil and sufentanil may block hormonal stress responses to surgical stimulus better than fentanyl does. The clinical significance of the difference in ADH and GH responses during fentanyl and during alfentanil or sulfentanil anesthesia remains to be determined. However, this difference may provide part of the explanation why alfentanil and sufentanil-O2 anesthesia require less frequent employment of other anesthetic adjuvants and are easier to use than fentanyl during coronary artery surgery.

Alfentanil↗
PubMed1982

Thromboxane and prostacyclin changes during cardiopulmonary bypass with and without pulsatile flow.

Nonpulsatile cardiopulmonary bypass, in patients with coronary artery disease, produces a significant increase in thromboxane, a potent platelet aggregant and putative coronary vasoconstrictor. Pulsatile flow may decrease the incidence of perioperative infarction and the hormonal stress response to bypass. This study assessed the effect of pulsatile blood flow on plasma thromboxane and prostacyclin profiles during cardiopulmonary bypass by serial measurement of their stable metabolites, thromboxane B2 (TxB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha). Two groups of eight patients each were studied before, during, and after cardiopulmonary bypass. Eight patients had routine (nonpulsatile) bypass and eight had pulsatile flow. In the nonpulsatile group, the TxB2 concentration significantly increased during bypass (65 +/- 39 to 1,224 +/- 306 pg/ml, p less than 0.01) and rapidly returned to control. Prostacyclin also rose (53 +/- 20 to 613 +/- 132 pg/ml, p less than 0.01). In the pulsatile group, TxB2 rose during bypass (53 +/- 18 to 693 +/- 130 pg/ml, p less than 0.01), but peak concentration was significantly lower than in the nonpulsatile group (1,224 +/- 306 versus 693 +/- 130 pg/ml, p less than 0.05). Prostacyclin rose sharply during cardiopulmonary bypass in the pulsatile group (53 +/- 22 to 1,033 +/- 136 pg/ml, p less than 0.01) and was higher than in the nonpulsatile group (1,033 +/- 136 versus 325 +/- 33 pg/ml, p less than 0.01). There were no intragroup differences of plasma hemoglobin, hematocrit, or platelet count. These data demonstrate that pulsatile flow significantly alters prostacyclin and thromboxane profiles during cardiopulmonary bypass and favors production of the coronary vasodilator and platelet disaggregant prostacyclin. This may be an important factor in some of the clinical advantages previously reported with this modality.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Should we pulse?

Explore the source record for details and available documents.

Cardiopulmonary Bypass↗
PubMed1981

Plasma vasopressin levels and urinary sodium excretion during cardiopulmonary bypass with and without pulsatile flow.

The use of pulsatile perfusion during bypass should create a more physiological milieu and thus attenuate the vasopressin stress response. To determine this, 20 patients scheduled for elective coronary artery bypass operation were studied in two groups. Group 1 had a standard nonpulsatile perfusion, and in Group 2 a pulsatile pump was used. Measurements were made before and after anesthesia, after surgical incision, and at 15 and 30 minutes during and after cardiopulmonary bypass. In both groups, vasopressin levels were significantly elevated after sternotomy (4.5 +/- 1.5 to 37 +/- 10 pg/ml in Group 1 and 3.1 +/- 1.2 to 33 +/- 9 pg/ml in Group 2, p less than 0.05) and during bypass (198 +/- 19 pg/ml in Group 1 and 113 +/- 16 pg/ml in Group 2) but were higher in Group 1 (p less than 0.05). With comparable perfusion pressures in both groups, Group 2 required higher flow (4.2 +/- 0.2 versus 3.5 +/- 0.3 L/min, p less than 0.05) and had lower resistance (1,351 +/- 182 versus 1,841 +/- 229 dynes sec cm-5, p less than 0.05) and higher urine Na+ (123 +/- 5 versus 101 +/- 8 mEq/L, p less than 0.05). These data demonstrate that pulsatile flow can significantly attentuate the vasopressin stress response to bypass. Since vasopressin, at these concentrations, is a potent vasoconstrictor and is capable of producing a Na+ diuresis, this may partially explain the higher flow requirements and the decrease in Na+ excretion.

Blood Pressure↗
PubMed1981

Role of histamine in the hypotensive action of d-tubocurarine in humans.

The administration of d-tubocurarine (dTc) to animals and humans has been reported to produce hypotension. Experiments in animals suggest that the hypotension is a result of both ganglionic blockade and histamine release. In order to determine the role of histamine release in dTc-induced hypotension in humans, the authors developed a sensitive radioenzymatic assay for plasma histamine and measured plasma histamine following dTc administration (0.25-0.75 mg/kg) to 21 surgical patients. While neither fentanyl (3 microgram/kg) nor thiopental (6 mg/kg) produced a significant change in plasma histamine, dTc caused a dose-dependent increase in plasma [dose dTc vs. log (plasma histamine), r = 0.62 P less than 0.003]. The log (plasma histamine) correlated with the dTc-induced hypotension (r= 0.61, P less than 0.005). The data suggest that histamine release is an important factor in the hypotension accompanying dTc administration in humans.

Blood Pressure↗
PubMed1981

The use of H1 and H2 histamine antagonists with morphine anesthesia: a double-blind study.

High doses of morphine can produce significant cardiovascular effects generally attributed to histamine release. The authors examined the possibility that H1 and H2 histamine antagonists might prove beneficial in preventing these responses. In a randomized double-blind study, four groups of 10 patients each received 1 mg/kg morphine and either a placebo, diphenhydramine (H1), cimetidine (H2), or both of the histamine antagonists. The morphine-placebo group demonstrated a marked elevation in plasma histamine levels (880 +/- 163 to 7437 +/- 2684 pg/ml), a decrease in systemic vascular resistance (SVR) (15.5 to 9.0 l torr/(l . min-1) and diastolic BP (71 +/- 3 to 45 +/- 4 torr) and an increase in cardiac index (CI) (2.4 +/- 0.2 to 3.0 +/- 0.21 . min-1 . m-2). The administration of either cimetidine or diphenhydramine with morphine provided minimal protection. Those patients who received morphine and both antagonists demonstrated significant attenuation of these responses (CI 2.5 +/- 0.2 to 2.5 +/- 0.1 l . min-1 . m-2; SVR 17.4 to 14.6 torr/(l . min-1) although plasma histamine levels showed a comparable increase (1059 +/- 222 to 7653 +/- 4242 pg/ml). These data demonstrate directly that many of the hemodynamic effects of morphine can be attributed to histamine release. They further demonstrate that significant hemodynamic protection can be obtained by the use of histamine antagonists and the combination of H1 and H2 antagonists is superior to either given alone.

Blood Pressure↗
PubMed1981

Attenuation of the stress response to cardiopulmonary bypass by the addition of pulsatile flow.

The effect of pulsatile flow during cardiopulmonary bypass on the hormonal stress response was studied in 26 patients. Thirteen had routine and 13 had pulsatile bypass with an average pulse pressure of 30 mm Hg. Plasma vasopressin levels were significantly elevated during bypass in both groups, but were lower with pulsation (66 +/- 11 vs 36.3 pg/ml, p less than 0.05). Epinephrine levels increased in both groups during bypass, but were higher after bypass (1179 +/- 448 vs 713 +/- 140 pg/ml, p less than 0.05) and in the recovery room (1428 +/- 428 vs 699 +/- 155 pg/ml, p less than 0.05) in the nonpulsatile group. The same response was noted in the norepinephrine levels (924 +/- 225 vs 465 +/- 90 pg/ml, p less than 0.05; 1015 +/- 491 vs 717 +/- 112 pg/ml, p less than 0.05). There were no significant changes in renin activity in either group, but the increase after cardiopulmonary bypass was greater in the nonpulsatile group (2.0 +/- 0.7 vs 1.36 +/- 0.4 ng/ml/hr, NS). These data suggest that pulsatile flow significantly attenuates the vasopressin and catecholamine stress response to cardiopulmonary bypass. This may explain the increased flow requirements and better tissue perfusion and organ function and the decreased incidence of postoperative hypertension after bypass using pulsatile flow.

Blood Gas Analysis↗
PubMed1981

The effect of pulsatile perfusion on preservation of left ventricular function after aortocoronary bypass grafting.

Pulsatile perfusion has been reported to be of value in intraoperative myocardial protection. To evaluate this technique, we studied 26 patients undergoing aortocoronary bypass grafting. Ejection fraction determinations from multigated cardiac blood pool scans, serial hemodynamic monitoring, and total CPK and MB-CPK sampling were performed early (4, 6 and 8 hours after bypass) and 10 days after operation. In 12 patients, pulsatile perfusion was started immediately after aortic cannulation and continued until 10 minutes after cessation of bypass; 14 patients had standard nonpulsatile perfusion. All patients had a single aortic cross-clamping and potassium cardioplegia. Cross-clamp time (46 +/- 3 and 46 +/- 3 minutes [+/- SEM]), total bypass time (94 +/- 4 and 89 +/- 6 minutes), and mean perfusion pressure (82 +/- 5 and 83 +/- 3 mm Hg) were comparable in the pulsatile and nonpulsatile groups, respectively, as were extent of coronary disease and number of bypass grafts. Preoperative and postoperative ejection fractions for pulsatile and nonpulsatile groups, respectively, were 0.57 +/- 0.03 and 0.55 +/- 0.04 before operation, 0.37 +/- 0.03 and 0.40 +/- 0.04 4 hours after bypass, 0.40 +/- 0.03 and 0.46 +/- 0.04 at 6 hours, 0.51 +/- 0.05 and 0.52 +/- 0.07 at 8 hours and 0.56 +/- 0.05 and 0.53 +/- 0.04) 10 days after operation. Mean arterial pressure, left atrial pressure and serial cardiac indexes were similar in both groups. There were no perioperative myocardial infarctions by ECG in either group. Total CPK (586 +/- 78 and 617 +/- 140 IU/l) and peak MB-CPK (73 +/0 14 and 61 +/- 11 IU/l) were comparable in the pulsatile and nonpulsatile groups, respectively. Pulsatile perfusion offers no advantage in myocardial preservation after aortocoronary bypass grafting in patients with normal left ventricular function.

Coronary Artery Bypass↗