Multiple actions of halothane on contractile response to noradrenaline in isolated mesenteric resistance arteries.

Halothane, a volatile anaesthetic, produces systemic hypotension and significantly alters organ blood flow. Isometric force was recorded in isolated rat small mesenteric arteries to investigate its action on contractile response to noradrenaline, the sympathetic neurotransmitter. Halothane (1-5%) enhanced contractile response to noradrenaline in the endothelium-intact arteries, but had little influence in the endothelium-denuded arteries. However, halothane consistently inhibited the noradrenaline response in the endothelium-denuded arteries pretreated with ryanodine (10 microM). The enhancement of the contractile response to noradrenaline in the endothelium-intact arteries was unaffected by treatment with N(G)-nitro L-arginine, tetraethylammonium, apamin, charybdotoxin, indomethacin, diclofenac, nordihydroguaiaretic acid, BQ-123, BQ-788, losartan, ketanserin, or superoxide dismutase. Halothane prolonged vasorelaxation after washout of noradrenaline in the endothelium-denuded arteries. Both ryanodine and vanadate (0.1-0.3 mM), a putative inhibitor of the plasma membrane Ca2+-ATPase, also prolonged the vasorelaxation. Halothane still prolonged the vasorelaxation in the ryanodine-treated arteries, but not in the vanadate-treated arteries. Halothane decreased the pD2 value for the pCa-force relation in the beta-escin-permeabilised, endothelium-denuded arteries. Halothane appears to influence contractile response to noradrenaline through multiple actions including endothelium-dependent enhancing, endothelium-independent enhancing, and endothelium-independent inhibitory actions. Nitric oxide, endothelium-derived hyperpolarising factor, cyclooxygenase products, lipoxygenase products, endothelin-1, angiotensin-II, serotonin, and superoxide anions are not involved in the endothelium-dependent enhancement. The endothelium-independent enhancement is presumably due to its ability to stimulate Ca2+ release from the ryanodine-sensitive intracellular stores, while the endothelium-independent inhibition is due, at least in part, to depressed Ca2+-activation of contractile proteins. Halothane may inhibit the plasma membrane Ca2+-ATPase of vascular smooth muscle cells.

Reliability of fingertip skin-surface temperature and its related thermal measures as indices of peripheral perfusion in the clinical setting of the operating theatre.

During the perioperative period, evaluation of digital blood flow would be useful in early detection of decreased circulating volume, thermoregulatory responses or anaphylactoid reactions, and assessment of the effects of vasoactive agents. This study was designed to assess the reliability of fingertip temperature, core-fingertip temperature gradients and fingertip-forearm temperature gradients as indices of fingertip blood flow in the clinical setting of the operating theatre. In 22 adult patients undergoing abdominal surgery with general anaesthesia, fingertip skin-surface temperature, forearm skin-surface temperature, and nasopharyngeal temperature were measured every five minutes during the surgery. Fingertip skin-surface blood flow was simultaneously estimated using laser Doppler flowmetry. These measurements were made in the same upper limb with an IV catheter (+ IV group, n=11) or without an IV catheter (-IV group, n=11). Fingertip blood flow, transformed to a logarithmic scale, significantly correlated with any of the three thermal measures in both the groups. Their rank order as an index of fingertip blood flow in the -IV group was forearm-fingertip temperature gradient (r=-0.86) > fingertip temperature (r=0.83) > nasopharyngeal-fingertip temperature gradient (r=-0.82), while that in the +IV group was nasopharyngeal-fingertip temperature gradient (r=-0.77) > fingertip temperature (r=0.71) > forearm-fingertip temperature gradient (r=-0.66). The relation of fingertip blood flow to each thermal measure in the -IV/group was stronger (P<0.05) than that in the +IV group. In the clinical setting of the operating theatre, using the upper limb without IV catheters, fingertip skin-surface temperature, nasopharyngeal-fingertip temperature gradients, and forearm-fingertip temperature gradients are almost equally reliable measures of fingertip skin-surface blood flow.

Intraoperative changes in arterial oxygenation during volume-controlled mechanical ventilation in modestly obese patients undergoing laparotomies with general anesthesia.

BACKGROUND: In obese patients, arterial oxygenation can be greatly impaired during general anesthesia. Both avoidance of denitrogenation and application of positive end-expiratory pressure (PEEP) during mechanical ventilation may be effective in preventing such impairment of arterial oxygenation. METHODS: We studied 28 obese/overweight and seven non-obese (BMI < 25 kg x m-2) patients who underwent laparotomies with general anesthesia (i.e. isoflurane with or without nitrous oxide). During anesthesia, their lungs were mechanically ventilated at a rate of 10 breaths x min-1 with a constant flow, inspiratory-to-expiratory ratio 1 : 2, and tidal volume approximately 10 ml x kg-1. The obese/overweight patients were allocated to four different groups in terms of denitrogenation and application of PEEP (7 cm H2O) during the ventilation (n = 7 each). In the non-obese patients, their denitrogenated lungs were ventilated without application of PEEP. Arterial gas analyses were performed before induction of anesthesia, and 30, 90, 150 and 210 min after tracheal intubation. The ratio of PaO2 to FiO2 was calculated as an index of arterial oxygenation. RESULTS: No significant changes in the PaO2/FiO2 ratio were observed throughout the study in the non-obese patients and in the obese/overweight patients whose non-denitrogenated lungs were ventilated with PEEP. In the obese/overweight patients whose lungs were ventilated after denitrogenation or without application of PEEP, significant decreases in the PaO2/FiO2 ratio were observed 30 and 90 min after tracheal intubation. CONCLUSIONS: In obese or overweight patients under general anesthesia, it may be advisable to avoid denitrogenation and apply PEEP during mechanical ventilation in order to minimize the impairment of arterial oxygenation.

Role of endothelium in the action of isoflurane on vascular smooth muscle of isolated mesenteric resistance arteries.

BACKGROUND: It is believed that isoflurane decreases blood pressure predominantly by decreasing systemic vascular resistance with modest myocardial depression. Nevertheless, little information is available regarding the direct action of isoflurane on systemic resistance arteries. METHODS: With use of the isometric force recording method, the action of isoflurane on contractile response to norepinephrine, a neurotransmitter that plays a central role in sympathetic maintenance of vascular tone in vivo, was investigated in isolated rat small mesenteric arteries. RESULTS: In the endothelium-intact strips, the norepinephrine response was initially enhanced after application of isoflurane (2-5%), but it was subsequently almost normalized to the control level during exposure to isoflurane. However, the norepinephrine response was notably inhibited after washout of isoflurane. In the endothelium-denuded strips, the norepinephrine response was gradually inhibited during exposure to isoflurane (> or = 3%), and the inhibition was prolonged after wash-out of isoflurane. The isoflurane-induced enhancement of norepinephrine response was still observed after inhibitions of the nitric oxide, endothelium-derived hyperpolarizing factor, cyclooxygenase and lipoxygenase pathways, or after blockade of endothelin-1, angiotensin-II, and serotonin receptors; however, it was prevented by superoxide dismutase. CONCLUSIONS: In isolated mesenteric resistance artery, the action of isoflurane on contractile response to norepinephrine consists of two distinct components: an endothelium-dependent enhancing component and an endothelium-independent inhibitory component. During exposure to isoflurane, the former counteracted the latter, preventing the norepinephrine response from being strongly inhibited. However, only the endothelium-independent component persists after washout of isoflurane, causing prolonged inhibition of the norepinephrine response. Superoxide anions may be involved in the enhanced response to norepinephrine.

Mechanisms of direct inhibitory action of ketamine on vascular smooth muscle in mesenteric resistance arteries.

BACKGROUND: Ketamine was previously suggested to relax vascular smooth muscle by reducing the intracellular Ca2+ concentration ([Ca2+]i). However, no direct evidence is available to indicate that ketamine reduces the [Ca2+]i in vascular smooth muscle of systemic resistance arteries. METHODS: Endothelium-intact or -denuded smooth muscle strips were prepared from rat small mesenteric arteries. Isometric force and [Ca2+]i were measured simultaneously in the fura-2-loaded, endothelium-denuded strips. In some experiments, only isometric force was measured in either the endothelium-intact or beta-escin-treated, endothelium-denuded strips. RESULTS: In the endothelium-intact strips, lower concentrations (< or = 30 microm) of ketamine slightly enhanced norepinephrine-induced contraction, whereas higher concentrations (> or = 100 microM) of ketamine inhibited both norepinephrine- and KCl-induced contractions. In the fura-2-loaded strips, ketamine (> or = 100 microM) inhibited the increases in both [Ca2+]i and force induced by either norepinephrine or KCl. Ketamine also inhibited the norepinephrine-induced increase in [Ca2+]i after treatment with ryanodine. In the absence of extracellular Ca2+, ketamine notably inhibited the norepinephrine-induced increase in [Ca2+]i, whereas it only minimally inhibited caffeine-induced increase in [Ca2+]i. Ketamine had little influence on the [Ca2+]i-force relation during force development to stepwise increment of extracellular Ca2+ concentration during either KCl depolarization or norepinephrine stimulation. Ketamine did not affect Ca2+-activated contractions in the beta-escin membrane-permeabilized strips. CONCLUSIONS: The action of ketamine on contractile response to norepinephrine consists of endothelium-dependent vasoconstricting and endothelium-independent vasodilating components. The direct vasorelaxation is largely a result of reduction of[Ca2+]i in vascular smooth muscle cells. The [Ca2+]i-reducing effects are caused by inhibitions of both voltage-gated Ca2+ influx and norepinephrine-induced Ca2+ release from the intracellular stores.

Comparison of volatile anesthetic actions on intracellular calcium stores of vascular smooth muscle: investigation in isolated systemic resistance arteries.

BACKGROUND: Volatile anesthetic actions on intracellular Ca2+ stores (ie., sarcoplasmic reticulum [SR]) of vascular smooth muscle have not been fully elucidated. METHODS: Using isometric force recording method and fura-2 fluorometry, the actions of four volatile anesthetics on SR were studied in isolated endothellum-denuded rat mesenteric arteries. RESULTS: Halothane (> or = 3%) and enflurane (> or = 3%), but not isoflurane and sevoflurane, increased the intracellular Ca2+ concentration ([Ca2+]i) in Ca2+-free solution. These Ca2+-releasing actions were eliminated by procaine. When each anesthetic was applied during Ca2+ loading, halothane (> or = 3%) and enflurane (5%), but not isoflurane and sevoflurane, decreased the amount of Ca2+ in the SR. However, if halothane or enflurane was applied with procaine during Ca2+ loading, both anesthetics increased the amount of Ca2+ in the SR. The caffeine-induced increase in [Ca2+], was enhanced in the presence of halothane (> or = 1%), enflurane (> or = 1%), and isoflurane (> or = 3%) but was attenuated in the presence of sevoflurane (> or = 3%). The norepinephrine-induced increase in [Ca2+], was enhanced only in the presence of sevoflurane (> or = 3%). Not all of these anesthetic effects on the [Ca2+]i were parallel with the simultaneously observed anesthetic effects on the force. CONCLUSIONS: In systemic resistance arteries, the halothane, enflurane, isoflurane, and sevoflurane differentially influence the SR functions. Both halothane and enflurane cause Ca2+ release from the caffeine-sensitive SR. In addition, both anesthetics appear to have a stimulating action on Ca2+ uptake in addition to the Ca2+-releasing action. Halothane, enflurane, and isoflurane all enhance, while sevoflurane attenuates, the Ca2+-induced Ca2+-release mechanism. However, only sevoflurane stimulates the inositol 1,4,5-triphosphate-induced Ca2+ release mechanism. Isoflurane and sevoflurane do not stimulate Ca2+ release or influence Ca2+ uptake.

Effects of changes in frequency and inspiratory time on arterial oxygenation and CO2 elimination during high-frequency jet ventilation in a child with laryngotracheal papillomata.

An 11-yr-old female without any pulmonary disorders underwent laser resections of laryngotracheal tumors using high-frequency jet ventilation (HFJV) 6 times over a period of 17 months at our institute. In this series of surgeries, we studied the effects on PaO2 and PaCO2 during HFJV of changes of either frequency or inspiratory time. Increasing the frequency from 100 to 400/min decreased the PaO2 and increased the PaCO2. Decreasing the inspiratory time from 30% to 20% increased the PaCO2, although it did not affect the PaO2. All the procedures were uneventfully carried out without critically impairing gas exchange during HFJV. In this patient with normal lung function, CO2 elimination during HFJV appeared to be facilitated by either decreasing the frequency or increasing the inspiratory time. Arterial oxygen tension during HFJV was higher at lower frequencies.

A study of the relationship between the seizure focus and 1H-MRS in temporal lobe epilepsy and frontal lobe epilepsy.

Several studies of temporal lobe epilepsy (TLE) patients have investigated the relationship between the seizure focus and 1H magnetic resonance spectroscopy (1H-MRS). There have also been a few reports in other types of partial epilepsy. We examined the relationship between the seizure focus and the reduction in N-acetylaspartate: creatine (NAA : Cr) ratio using 1H-MRS in both TLE and frontal lobe epilepsy (FLE) patients. We studied 21 patients with unilateral TLE and seven patients with unilateral FLE. We used a 1.5 Tesla magnetic resonance unit (Signa Horizon; General Electric). Approximately 15 x 15 x 20 mm3 voxel of interest (VOI) was placed over the anterior portion of the bilateral hippocampus in the TLE patients, and the anterodorsal position of bilateral frontal lobe in the FLE patients. The seizure focus was identified by interictal scalp electro-encephalogram (EEG). In the TLE patients the NAA : Cr ratios were reduced in the seizure focus, while in the FLE patients they were not always reduced in the seizure focus. In the TLE patients the coincidence rate between the seizure focus and the reduction in the NAA:Cr ratio was 90% (19 of 21 patients), while in the FLE patients the coincidence rate was only 57% (four of seven patients).

Valproic acid-induced hyperammonemic encephalopathy with triphasic waves.

PURPOSE: To examine a patient with valproic acid (VPA)-induced hyperammonemic encephalopathy accompanied by triphasic waves. METHODS: A 61-year-old male patient with epilepsy experienced disturbance of consciousness after VPA dose was increased because of poor seizure control. The electroencephalogram (EEG) taken on admission revealed triphasic waves and high-amplitude delta-activity with frontal predominance. Although serum hepatic enzymes, such as AST and ALT, were normal, serum ammonium level was high at 96 microg/dl (normal range, 3-47 microg/dl). Serum amino acid analysis showed multiple minor abnormalities. Administration of VPA was discontinued immediately after admission, while other anticonvulsants were continued. RESULTS: The patient's condition was improved on the fourth day of admission. An EEG, serum ammonium level, and amino acid profile were normal on the eighth day. Based on VPA administration, serum ammonium levels, and results of amino acid analysis, this patient had VPA-induced hyperammonemic encephalopathy. CONCLUSIONS: Our case indicates that caution is required if triphasic waves appear in VPA-induced hyperammonemic encephalopathy.

The action of sevoflurane on vascular smooth muscle of isolated mesenteric resistance arteries (part 1): role of endothelium.

BACKGROUND: The direct action of sevoflurane on systemic resistance arteries is not fully understood. METHODS: Isometric force was recorded in isolated rat small mesenteric arteries. RESULTS: Sevoflurane (2-5%) enhanced contractile response to norepinephrine only in the presence of endothelium, but inhibited it in its absence. Sevoflurane still enhanced the norepinephrine response after inhibitions of the nitric oxide, endothelium-derived hyperpolarizing factor, cyclooxygenase and lipoxygenase pathways, or after blockade of either endothelin-1 ET-1), angiotensin-II, or sevotonin receptors. Sevoflurane (3-5%) inhibited contractile response to potassium chloride only in the absence of endothelium but did not influence it in its presence. In the endothelium-intact strips, inhibition of the norepinephrine response, which was enhanced during application of sevoflurane, was observed after washout of sevoflurane and persisted for approximately 15 min. In the endothelium-denuded strips, the inhibition of norepinephrine response was similarly prolonged after washout of sevoflurane. However, no significant inhibitions of potassium chloride response were observed after washout of sevoflurane in both the endothelium-intact and the endothelium-denuded strips. CONCLUSIONS: The action of sevoflurane on norepinephrine contractile response consists of endothelium-dependent vasoconstricting and endothelium-independent vasodilating components. In the presence of endothelium, the former predominates over the latter, enhancing the norepinephrine response. The endothelium-independent component persisted after washout of sevoflurane, leading to prolonged inhibition of the norepinephrine response. The mechanisms behind the sevoflurane-induced inhibition of norepinephrine response are at least in part different from those behind its inhibition of potassium chloride response. Nitric oxide, endothelium-derived hyperpolarizing factor, cyclooxygenase products, lipoxygenase products, endothelin-1, angiotensin-II, and serotonin are not involved in the vasoconstricting action. (Key words: Halogenated volatile anesthetics; sympathetic nervous system; systemic hypotension; vascular endothelium.)

The action of sevoflurane on vascular smooth muscle of isolated mesenteric resistance arteries (part 2): mechanisms of endothelium-independent vasorelaxation.

BACKGROUND: The precise mechanisms behind the direct inhibitory action of sevoflurane on vascular smooth muscle have not been fully elucidated. METHODS: Endothelium-denuded smooth muscle strips were prepared from rat small mesenteric arteries. Isometric force and intracellular Ca2+ concentration ([Ca2+]i) were measured simultaneously in the fura-2-loaded strips. In another series of experiments, only isometric force was measured in the beta-escin-membrane-permeabilized strips. RESULTS: Sevoflurane (3-5%) inhibited the increases in both the [Ca2+]i and the force induced by either norepinephrine (0.5-10 microm) or 40 mm K+. Sevoflurane still inhibited the increase in [Ca2+]i induced by norepinephrine after depletion of intracellular Ca2+ stores with ionomycin, although it little influenced the increase in [Ca2+]i induced by norepinephrine after treatment with verapamil. In the fura-2-loaded membrane-intact muscle, sevoflurane caused a rightward shift of Ca2+-force relation during force development to stepwise increment of extracellular Ca2+ concentration during 40-mm K+ depolarization in either the presence or the absence of norepinephrine. In contrast, sevoflurane did not influence Ca2+-activated contraction in the beta-escin-permeabilized muscle, in which alpha-adrenergic receptor coupling was not retained. CONCLUSIONS: The inhibitory effects of sevoflurane on both norepinephrine- and potassium chloride (KCl)-induced contractions are caused by reduction of [Ca2+]i in vascular smooth muscle and inhibition of the myofilament Ca2+ sensitivity. The [Ca2+]i-reducing effect of sevoflurane observed in both the norepinephrine- and the K+-stimulated muscle is mainly caused by inhibition of voltage-gated Ca2+ influx. The inhibitory effect of sevoflurane on Ca2+ activation of contractile proteins seems to be mediated by the cell membrane or by some diffusible substances that are lost in the beta-escin-permeabilized cells.

Ictal brain hemodynamics in the epileptic focus caused by a brain tumor using functional magnetic resonance imaging (fMRI).

Using functional magnetic resonance imaging (fMRI) we were able to observe, in detail, ictal brain hemodynamics during epileptic seizure caused by a brain tumor. A 53-year-old man was experencing partial motor seizures of the left side of his face and neck. In a brain MR image a mass lesion was found in the subcortical area of the right frontal lobe. We found focal spikes in his right hemisphere, though dominantly in C4 and T4 regions. fMRI investigations were carried out at 1.5 T (GE Signa Horizon) using gradient-echo echo-planar neuroimaging. We were able to perform the ictal examination twice. The activated regions were focalized and clearly found only on the lateral side of the tumor base. The region was in agreement with the epileptic focus examined using an electrocorticogram (ECOG). The signal intensity in the seizure focus rapidly increased 30 seconds before the convulsion was observed. After the end of the convulsion it also took 30 seconds to restore the signal intensity to the baseline value. fMRI is a very useful tool for various studies such as the identification of the epileptic focus, the mechanism of epileptic seizure, and so on.

Life-threatening haemorrhage following obturator artery injury during transurethral bladder surgery: a sequel of an unsuccessful obturator nerve block.

In spite of prior blockade of the obturator nerve with 1% mepivacaine (8 ml) utilizing a nerve stimulator, violent leg jerking was evoked during transurethral electroresection of a bladder tumour approximately 1 h after the blockade in a 68-year-old man. The patient became severely hypotensive immediately following the jerking, and a large lower abdominal swelling concurrently developed. The urgent laparotomy indicated that the left obturator artery was severely injured by the resectoscope associated with the bladder perforation, causing acute massive haemorrhage. The patient recovered uneventfully after adequate surgery. Investigation of the literature suggested that both our nerve stimulation technique and anatomical approach were appropriate. It was therefore unlikely that our block resulted in failure because of an inappropriate site for deposition of the anaesthetic. However, consensus does not appear to have been obtained as to the concentration and volume of the anaesthetic necessary for prevention of the obturator nerve stimulation during the transurethral procedures. The concentration and volume of mepivacaine we used might have been too low and/or small, respectively, to profoundly block all the motor neuron fibres of the nerve. Alternatively, stimulation of the obturator nerve might occur because of the presence of some anatomical variant, such as the accessory obturator nerve or its abnormal branching. In conclusion, some uncertainty appears to exist in the effectiveness of the local anaesthetic blockade of the obturator nerve. In order to attain profound blockade of the motor neuron fibres of the obturator nerve and thereby prevent the thigh-adductor muscle contraction which can lead to life-threatening situations, we recommend, even with a nerve stimulator, to use a larger volume of a higher concentration of local anaesthetic with a longer duration in the obturator nerve block for the transurethral procedures.

Bone mineral density of epileptic patients on long-term antiepileptic drug therapy: a quantitative digital radiography study.

In order to assess the bone atrophy lesions of epileptic patients, the bone mineral densities (BMDs) of their lumbar spines and femoral necks were measured using quantitative digital radiography (QDR). The study groups were 44 patients on long-term medication for epilepsy and 62 healthy control subjects. We selected patients who had been taking phenytoin, barbiturates, and/or acetazolamide for at least 5 years. BMDs at both sites were significantly lower in the patient group than in the control group. No sex differences were found in BMDs. There were no significant correlations with the onset or the duration of illness and BMD. We compared BMD according to the type of epileptic drug being taken and theorized that phenytoin, barbiturates, and acetazolamide reduced BMD. BMDs of the 15 patients were measured again 7 years later, and were found to be significantly lower at both sites than in the previous examination. These results confirm the presence of bone atrophy lesions in epileptic patients on long-term antiepileptic drugs. Patients on antiepileptic therapy for long periods should have their BMDs checked, because they are prone to developing bone atrophy.

Massive retroperitoneal hemorrhage associated with femoral vein cannulation.

The right external iliac artery was inadvertently punctured during attempted right femoral vein catheterization. Severe hypotension developed several minutes after the arterial puncture. Concurrently, a large right lower abdominal quadrant swelling (approximately 5 cm in diameter) became apparent. Laparoscopic observation of the retroperitoneal region immediately revealed massive retroperitoneal hemorrhage. Abdominal computerized tomographic scan indicated development of a huge (approximately 10 cm in the maximum diameter) retroperitoneal hematoma along the right psoas muscle from the level of the right external iliac vessels up to the level of the upper pole of the right kidney. Consideration of the anatomy of the "right" femoral and retroperitoneal vessels (ie, mediolateral relationship between the vein and artery) led us to conclude that the site for insertion of the needle was too proximal and the angle for advancement of the needle too low in our patient, allowing the needle to reach and injure the "incompressible" external iliac artery, thereby causing massive retroperitoneal hemorrhage. Although femoral vein catheterization has generally been considered a relatively safe method of intravenous access, a life-threatening serious complication can occur with the inappropriate technique used in our case.

Changes in body temperature following deflation of limb pneumatic tourniquet.

STUDY OBJECTIVES: To investigate changes in both core and peripheral skin-surface temperatures during and after application of a unilateral leg pneumatic tourniquet in adult patients. DESIGN: Prospective, observational clinical study. SETTING: University hospital. PATIENTS: 21 ASA physical status I and II adult patients scheduled for elective leg orthopedic surgery with lumbar epidural anesthesia. INTERVENTIONS: Rectal and fingertip skin-surface temperatures were recorded every minute after steady-state lumbar epidural anesthesia was established. MEASUREMENTS AND MAIN RESULTS: Significant (p < 0.05) increases in both rectal and fingertip temperatures were observed during tourniquet application for 91 +/- 6 minutes from 36.5 +/- 0.14 degrees C to 37.0 +/- 0.17 degrees C and from 32.6 +/- 0.79 degrees C to 35.5 +/- 0.44 degrees C, respectively. In contrast, both rectal and fingertip temperatures progressively decreased following tourniquet release; significant (p < 0.05) decreases in the rectal and fingertip temperatures were observed 6 and 5 minutes after tourniquet release, respectively. Decreases (approximately maximum) in the rectal and fingertip temperatures 15 minutes after tourniquet release were 0.25 +/- 0.05 degrees C and 1.26 +/- 0.26 degrees C, respectively. In each case, changes in fingertip temperature were approximately six times greater than those in the rectal temperature. CONCLUSIONS: Limb tourniquets appear to cause thermal perturbations during epidural anesthesia. The progressive increases in core temperature during tourniquet application presumably resulted from constraint of metabolic heat to the core thermal compartment, and the greater increases in the skin-surface temperature during tourniquet application appear to represent vasodilation in response to the core hyperthermia. On the other hand, redistribution of body heat and the efflux of hypothermic venous blood from the tourniqueted area into systemic circulation following tourniquet deflation probably decreased the core temperature, which might switch off the thermoregulatory vasodilation, leading to the decreases in skin-surface temperature. Recognition of these thermal perturbations are useful in diagnosing intraoperative thermal perturbations.

Hemidiaphragmatic paralysis following subclavian vein catheterization.

The right subclavian artery was inadvertently punctured during attempted preoperative insertion of a right subclavian venous catheter in a 59-yr-old woman undergoing radical hysterectomy. Large supraclavicular swelling became apparent soon after the arterial puncture. The postoperative chest X-ray obtained approximately 24 h after the catheterization revealed significant elevation of the right hemidiaphragm, which was further augmented on the 2nd to 4th postoperative days; oxygenation was concurrently impaired during these days. It was clinically judged that the hemidiaphragmatic paralysis was responsible for the elevated diaphragm. Both chest roentogenogram and arterial blood gas analyses started to improve on the 5th day, finally returning to normal on the 6th day. It is unlikely that the surgical procedure caused the paralysis, because it dealt only with the lower abdomen. Rather, the attempts at the subclavian venous catheterization probably caused the phrenic nerve paralysis, because the phrenic nerve travels very close to the subclavian vessels. Both the large haematoma formation following the arterial puncture and the time course of the paralysis suggest that compression of the right phrenic nerve by the haematoma, rather than needle trauma, was responsible for the paralysis.

Is guanosine-5'-triphosphate involved in calcium-activation of contractile proteins in vascular smooth muscle?

Isometric tension was measured to investigate the effects of guanosine-5'-triphosphate (GTP) on the run-down of myofilament Ca2+ sensitivity in isolated rat mesenteric arteries permeabilized with beta-escin. The Ca2+ sensitivity assessed by the EC50 value for the Ca2+ (0.1-100 microM)-tension relationship progressively runs down in the control strips, while it was well-preserved for 5-successive Ca2+ applications in the presence of GTP (50 microM); no significant difference was found in the Ca2+ sensitivity observed with the 1st Ca2+ application between the control and GTP-treated strips. Guanosine-5'-(2-O-thio) diphosphate (GDP beta S, 100 microM) significantly decreased the Ca2+ sensitivity with the 1st Ca2+ application and eliminated the run-down of Ca2+ sensitivity. GTP (3-150 microM), applied to the strips submaximally precontracted with Ca2+, had a little effect on the Ca2+ contractions in the early stage of experiments, but dramatically enhanced the Ca2+ contractions in their later stage; its latter effect was mimicked by guanosine-5'-(3-O-thio) triphosphate (GTP gamma S) and reversed by GDP beta S (100 microM). The results suggest: 1) loss of endogenous GTP following permeabilization is involved in the run-down of Ca2+ sensitivity; and 2) activation of G-proteins is involved in Ca(2+)-activation of contractile proteins.