Effects of stretch or distention on phenylephrine-induced constriction of human coronary artery bypass grafts.

OBJECTIVE: To determine the effects of grafting saphenous veins into the arterial circulation and to compare the responsiveness of saphenous veins and mammary arteries to vasoconstrictors (phenylephrine or potassium) and a vasodilator (the calcium antagonist isradipine). DESIGN: Prospective, controlled, in vitro study. SETTING: Laboratory facility in a university teaching hospital. PARTICIPANTS: Small excess segments of internal mammary arteries or saphenous veins obtained from patients undergoing coronary artery bypass graft surgery. INTERVENTIONS: Vessel segments were cut into rings to measure isometric tension development in isolated tissue chambers. The law of LaPlace for a cylinder was applied to determine tensions in vitro corresponding with arterial or venous tensions in vivo or distending pressures ex vivo. MEASUREMENTS AND MAIN RESULTS: Stretching saphenous vein rings from venous to arterial tensions reduced maximal phenylephrine-induced constriction but did not alter their dose response to phenylephrine, potassium, or isradipine. At arterial tensions, potassium, but not phenylephrine, was more potent in constricting mammary artery than saphenous vein; isradipine was more potent as a vasodilator of potassium-constricted mammary artery than saphenous vein. Maximal phenylephrine-induced or potassium-induced constriction was no different for either vessel at arterial tensions; however, prior distention of veins to tensions corresponding with pressures of 200 or 300 mmHg significantly (p < 0.01, Dunnett's test) reduced subsequent constriction. CONCLUSION: Phenylephrine may be more likely to constrict native internal mammary arteries than distended autogenous saphenous vein grafts in vivo because high-pressure distention of veins markedly inhibits their vasoreactivity.

Sequestration of vecuronium bromide during extremity surgery involving use of a pneumatic tourniquet.

BACKGROUND: We hypothesized that sequestration of a neuromuscular blocking agent could occur during surgery involving use of an extremity tourniquet and cause changes in neuromuscular function after tourniquet release. METHODS: Sixteen patients scheduled for total knee replacement were randomized to one of two groups. In Group I, 10 patients were administered 0.1 mg/kg of vecuronium 5 minutes prior to inflation of a pneumatic tourniquet; in Group II, 6 patients were administered 0.1 mg/kg of vecuronium after inflation of the tourniquet. The twitch (T1) and train-of-four (TOF) were analyzed before and after release of the tourniquet, as was the rate of recovery of T1 and TOF. Serial vecuronium plasma levels were drawn during the study. RESULTS: The T1 and TOF responses and the T1 and TOF recovery rates were not significantly different between groups at tourniquet deflation. In Group I, after release of the tourniquet, T1 and TOF recovery rate decreased significantly over a 10-min period (10% +/- 3 to 4% +/- 4 and 0.12 +/- 0.06 to 0.06 +/- 0.04, mean +/- SD, respectively); in Group II, T1 and TOF recovery rate increased significantly over a 10-min period following deflation of the tourniquet (10% +/- 6 to 14% +/- 7 and 0.10 +/- 0.03 to 0.18 +/- 0.02, respectively). Changes in pharmacodynamics were temporally associated with transient but statistically significant changes in vecuronium plasma levels. Overall pharmacokinetics during the study period were comparable between groups. After administration of neostigmine 30-40 micrograms/kg i.v. all subjects in both groups showed complete TOF recovery within 15 min. CONCLUSIONS: Sequestration of a bolus dose of vecuronium, by a pneumatic tourniquet, causes transient changes in pharmacokinetics and pharmacodynamics. These changes are of limited clinical importance and do not affect reversibility of neuromuscular block.

Intravenous vitamin K1 prior to orthotopic heart transplantation: effects in vivo and in vitro.

BACKGROUND: Vitamin K1 is used to reverse warfarin's anticoagulant action. It is unclear whether intravenous vitamin K1 is safe or efficacious prior to urgent cardiac surgery. METHODS: We retrospectively and prospectively examined the effects of preoperative intravenous vitamin K1 in vivo (administered for warfarin reversal immediately before heart transplantation) on intraoperative blood product utilization, hemodynamics and coagulation parameters. We also determined the direct effects of vitamin K1 in vitro on rings of human saphenous vein and internal mammary artery. RESULTS: In the retrospective limb, 29 of 67 patients were administered vitamin K1 preoperatively via slow intravenous infusion. Vitamin K1 administration produced no adverse outcome but did not affect subsequent perioperative use of blood products. In the prospective limb (n = 10), vitamin K1 significantly (P < or = 0.01, Student t-test) altered mean arterial pressure (from 85 +/- 15 to 76 +/- 16 mmHg), systemic vascular resistance (from 1364 +/- 308 to 1078 +/- 252 dyn.s.cm-5), and cardiac index (from 2.3 +/- 0.3 to 2.7 +/- 0.3 L/min/m2) (mean +/- SD). Significant decreases in prothrombin time (19.8 +/- 2.7 to 17.7 +/- 1.8 s) and activated clotting time (164 +/- 26 to 137 +/- 24 s) were observed at 60 min. In vitro vitamin K1 (10(-7) to 10(-4) M) had no effect on the tone of noradrenaline-constricted rings. CONCLUSIONS: Vitamin K1, administered by intravenous infusion prior to heart transplantation, did not alter subsequent perioperative blood product administration. Vitamin K1 rapidly reversed the anticoagulant effect of warfarin and produced modest hemodynamic changes. The decrease in systemic vascular resistance is probably not due to a direct effect of vitamin K1 on vascular smooth muscle.

Interpleural placement of central venous catheter. Failure of preventive practices.

An attempt to access the central venous circulation in a patient with a persistent left pleural effusion resulted in positioning the catheter within the pleural space. Chest roentgenograms with injection of contrast material revealed catheter location. Compliance with standard preventive practices may not assure correct placement of a central venous catheter via the internal jugular route in a patient with a hemothorax or effusion of unknown composition.

Isradipine for treatment of acute hypertension after myocardial revascularization.

OBJECTIVE: To evaluate the efficacy and duration of action of iv isradipine in the control of postoperative hypertension immediately after myocardial revascularization. DESIGN: Prospective, phase 2 trial. SETTING: Surgical ICU, university hospital. PATIENTS: Twenty-one (15 male, six female) patients, ages 49 to 75 yr (mean 65 +/- 5), undergoing elective myocardial revascularization. INTERVENTIONS: Twenty-one patients with postoperative hypertension after coronary artery bypass graft surgery received iv isradipine, a new dihydropyridine calcium-channel antagonist. Mean duration of the isradipine infusion was 96.9 +/- 29 min. Mean dose of isradipine, indexed to weight, was 16.63 +/- 6.66 micrograms/kg (n = 20). MEASUREMENTS AND MAIN RESULTS: Twenty of the 21 patients achieved satisfactory BP control. The reduction in mean arterial pressure (MAP), first noted at the 15-min point, was maximal at 1 hr when MAP decreased from 102 +/- 9 mm Hg baseline to 81 +/- 5 mm Hg (p less than .01), accompanied by a significant (p less than .01) decrease in systemic vascular resistance from 1753 +/- 339 baseline to 1180 +/- 229 dyne.sec/cm5. The CVP, pulmonary artery diastolic pressure, and pulmonary artery occlusion pressure did not change significantly. Heart rate and cardiac index increased; however, stroke volume index did not change. CONCLUSIONS: Isradipine is an acceptable agent for the treatment of hypertension in this setting.

Wheal and flare responses to opioids in humans.

Certain opioids release histamine from cutaneous mast cells to produce local wheal and flare responses and adverse hemodynamic effects. In vivo responses to opioids suggest that cutaneous responses result from the interaction of opioids with opioid receptors on human mast cells. There are no data evaluating or comparing the opioids currently used in anesthesia. Volunteers were injected intradermally with different opioids as well as with naloxone and antihistamines to evaluate their effects on cutaneous mast cell reactivity and cutaneous vascular responses. Fentanyl and morphine produced concentration-dependent wheal and flare responses in the range of 5 X 10(-6) M to 1.5 X 10(-3) M. Volunteers were then tested intradermally with different opioids and histamine at a 5 X 10(-4) M concentration to determine their relative cutaneous effects. Morphine, meperidine, fentanyl, and sufentanil produced both wheal and flare responses that were significantly greater than those due to saline (P less than 0.05). Naloxone, alfentanil, and nalbuphine did not produce significant wheal or flare responses. Butorphenol was followed by a significant wheal but no flare. Naloxone attentuated cutaneous wheal and flare responses to fentanyl and the flare response to morphine. Intradermal antihistamines (diphenhydramine and cimetidine) produced significant wheal and flare responses. Electron micrographs of biopsies from fentanyl-induced wheals demonstrated normal mast cell architecture with no evidence of mast cell degranulation. Opioid effects on wheal and flare responses and mast cell degranulation appear independent of opioid analgesic potency. Opioids produce cutaneous vascular responses dependent on both histamine release from mast cells and direct effects on the vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)

Microsphere measurement of myocardial capillary bed in hypoxic rats.

Rats exposed to hypobaric hypoxia for 24 h showed a significant increase in the number of perfused capillaries and in the number of radioactive microspheres trapped in the coronary circulation.

Cytochemical bioassay and radioimmunoassay of ACTH in noise stressed rats.

Serum corticosterone and ACTH levels were measured in rats subjected to one and two 30 min intervals of noise (100 dB, 250--20,000 Hz). Both hormones were elevated immediately after noise exposure, dropped below pre-exposure levels after a 2 hr recovery interval and were again elevated with a second exposure. The ratio of immunoactive to bioactive ACTH was slightly depressed after one exposure and markedly depressed after two successive noise exposures (relative to controls) indicating that multiple exposure to auditory stimulation effects a proportionally greater output of bioactive ACTH.

Cytophotometric analyses of myocardial RNA in rats exposed to altitude hypoxia.

Analytical cytophotometry of azure B-stained heart sections was employed to investigate the pattern of myocardial ribonucleic acid (RNA) alterations in rats exposed to acute (1-2 days) and prolonged periods (1-8 weeks) of hypoxia exposure (380 torr). Data support the existence of a slight transient drop in myocardial RNA on day one of exposure followed by a restoration to levels slightly elevated over controls during a 1- to 8-week exposure interval. Because of the high variability in RNA levels among myocytes (coefficient of variation, ca 40%), a shift in the proportion of low and high RNA containing segments of the myocyte population proved to be a more sensitive indicator of suppression or augmentation of RNA synthesis than the use of average RNA levels of the cell population analyzed. Microscopic analyses revealed the presence of compensatory vascular responses which could be effective in ameliorating the extent of tissue hypoxemia, i.e., capillary vasodilation on day 1 with a progressive increase in vascularization with prolonged exposure.